ANTERPARTAL HEMORRHAGIC DISORDERS.

POSTPARTUM
HEMORRHAGE.
HEMORRHAGIC SHOCK. DIC-SYNDROME. INTENSIVE CARE AND
RESUSCITATION OF OBSTETRIC HEMORRHAGES.

Prepared by Korda I.

Clinical Guideline_Antepartal hemmorrhage

https://www.rcog.org.uk/globalassets/documents/guidelines/gtg_63.pdf

Clinical Guideline_Prevention of PPH

https://rcpi-live-cdn.s3.amazonaws.com/wp-content/uploads/2016/05/14.-Prevention-
and-Management-of-Primary-Postpartum-Haemorrhage.pdf

Clinical Guideline_PPH
http://onlinelibrary.wiley.com/doi/10.1111/1471-0528.14178/epdf

Clinical Guideline_Blood Transfusion

https://www.rcog.org.uk/globalassets/documents/guidelines/gtg-47.pdf

Clinical Guideline_Placenta Previa

https://www.rcog.org.uk/globalassets/documents/guidelines/gtg_27.pdf

HEMORRHAGE IN THE SECOND HALF OF PREGNANCY

An estimated 5 % of women describe bleeding of some extent during
pregnancy. At times, the amount of bleeding is hardly more than "spotting," whereas
at other times profuse hemorrhage can lead to maternal death in a very short time. In
most cases, antepartum bleeding is minimal spotting, often following sexual
intercourse, and is thought to be related to trauma to the friable ectocervix.
The main causes of bleeding in the second half of pregnancy are:
Vulva
Varicose veins
Tears or lacerations
Vagina
Tears or lacerations
Cervix
Polyp
 Glandular tissue (normal)
Cervicitis
Carcinoma Intrauterine
Placenta previa
Abruptio placentae
Vasa previa
A previous Pap test and examination of the lower genital tract should eliminate
the likelihood of lower genital tract neoplasms in most cases. At times, patients may
mistake bleeding from hemorrhoids or even hematuria for vaginal bleeding, but the
difference is easily distinguished by examination.
The two causes of hemorrhage in the second half of pregnancy that require
greatest attention, because of the associated maternal and fetal morbidity and
mortality rates, are placenta previa and abruptio placentae. Various characteristics of
these entities are compared in Table.
Differential characteristics between placenta previa and abruptio placentae
Characteristics Placenta previa Abruptio Placenta
Magnitude of blood loss Variable Variable
Duration Often ceases within 1-2 Usually continues
hours
Abdominal discomfort None Can be severe
Absent Tachycardia, then
Fetal heart rate pattern
bradycardia; loss of
on electronic monitoring
variability; decelerations
frequently
present; intrauterine
demise not rare
Coagulation defects Rare Associated, but
infrequent; DIG often
severe when present
Cocaine use
Associated history None Abdominal trauma;
maternal hypertension;
multiple gestation;
polyhydramnios

PLACENTA PREVIA

Placenta previa refers to an abnormal location of the placenta over, or in close

proximity to, the internal cervical os. Placenta previa can be categorized as:
1. complete or total - if the entire cervical os is covered (Fig. 1);

2. partial - if the margin of the placenta extends across part but not all of the
internal os (Fig. 2);
3. marginal , if the edge of the placenta lies adjacent to the internal os;

4. low lying - if the placenta is located near but not directly adjacent to the
internal os.

Fig. 1 Total placenta previa

 Fig. 2 Partial placental previa

The etiology of placenta previa is not understood, but abnormal vascularization

has long been proposed as a mechanism for this abnormal placement of the placenta.
In some cases, such as in twin pregnancy or if it is hydropic, the placenta may extend
to the region of the internal cervical os because of its size alone. Increasing maternal
age, increasing parity, and previous cesarean delivery are factors commonly
associated with placenta previa, although recent evidence suggests that age alone is
not an important factor.

The incidence of placenta previa varies with gestational age, usually reported
overall as approximately 1 in 250 pregnancies. There is great variation in incidence,
however, with parity. The incidence in nulliparas is only 1 in 1000 to 1500, whereas
that in grandmultiparas is as high as 1 in 20. Women with the highest risk for
placenta previa are grandmultiparas, those who have had a previous placenta previa
(4% to 8%), and those who have had four or more cesarean sections. With common
use of ultrasonography examinations, it has been shown repeatedly that the placenta
may cover the internal cervical os in approximately 5% of pregnancies when
examined at midpregnancy, a finding seen even more frequently earlier in gestation.
Because of subsequent growth of both the upper and lower uterine segments, the
placenta appears to "migrate" away from the internal os in the majority of cases. The
likelihood of this apparent movement diminishes as the gestational age at first
detection increases.

Clinical findings and Diagnosis. The average gestational age at the time of the
first bleeding episode is 29 to 30 weeks. Although the bleeding may be substantial,
it almost always ceases spontaneously, unless digital examination or other trauma
occurs. The bleeding is caused by separation of part of the placenta from the lower
uterine segment and cervix, possibly in response to mild uterine contractions. The
blood that is lost is usually maternal in origin. The patient often describes a sudden
onset of bleeding without any apparent antecedent signs. There is no pain associ-
ated with placenta previa in most cases, unless coincident with labor or with an
abruptio placenta (approximately 5% to 10% of cases).
Frequently, bleeding from placenta previa has its onset without warning,
presenting without pain in a woman who has had an uneventful prenatal course.
Fortunately, the initial bleeding is rarely so profuse as to prove fatal. Usually it ceases
spontaneously, only to recur. In some cases, particularly those with a placenta
implanted near but not over the cervical os, bleeding does not appear until the onset
of labor, when it may vary from slight to profuse hemorrhage and may clinically
mimic placental abruption.

The cause of hemorrhage is reemphasized. When the placenta is located over the
internal os, the formation of the lower uterine segment and the dilatation of the
internal os result inevitably in tearing of placental attachments. The bleeding is
augmented by the inability of the myometrial fibers of the lower uterine segment to
contract and thereby constrict the torn vessels.
 Hemorrhage from the placental implantation site in the lower uterine segment
may continue after delivery of the placenta, because the lower uterine segment is
more prone to contract poorly than is the uterine body. Bleeding may also result from
lacerations in the friable cervix and lower uterine segment, especially following
manual removal of a somewhat adherent placenta.

Diagnosis

In women with uterine bleeding during the latter half of pregnancy, placenta
previa or abruptio placentae should always be suspected. The possibility of placenta
previa should not be dismissed until appropriate evaluation, including sonography,
has clearly proved its absence. The diagnosis of placenta previa can seldom be
established firmly by clinical examination unless a finger is passed through the cervix
and the placenta is palpated. Such examination of the cervix is never permissible
unless the woman is in an operating room with all the preparations for
immediate cesarean section, because even the gentlest examination of this sort
can cause torrential hemorrhage. Furthermore, such an examination should not be
made unless delivery is planned, for it may cause bleeding of such a degree that
immediate delivery becomes necessary even though the fetus is immature. Today,
however, such a “double set-up” examination is rarely necessary, as placental
location can almost always be obtained by careful sonography.

Ultrasonography has been of enormous benefit in localizing the placenta,

especially when the placenta is anterior or lateral. If the placenta lies in the posterior
portion of the lower uterine segment, its exact relation with the internal os may be
more difficult to ascertain. In most cases, though, ultrasonography examination can
accurately diagnose placenta previa or, by illustrating the placenta location away
from the cervix and lower uterine segment, exclude it as a cause for bleeding. In
some instances, transvaginal ultrasonography may be a useful adjunct to the
transabdominal approach, especially in the case of posterior placenta.
 Double setup examination can confirm the diagnosis of placenta previa. It
involves careful evaluation of the cervix in the operating room with full preparations
for rapid cesarean delivery.

Management

Includes initial hospitalization with hemodynamic stabilization, followed by

expectant management until fetal maturity has occurred. Ideal expectant
management would be continuous hospitalization with enforced bed rest and
immediate access to emergency care.

In the complete placenta previa – cesarean section in full term pregnancy. In the
case of low lying, marginal and partial placenta previa and full term pregnancy, when
blood loss is less than 250 ml – amniotomy with the following prescription of
contractile drugs. If blood loss is more than 250 ml – cesarean section.

The number of bleeding episodes is unrelated to the degree of placenta previa or

to the prognosis for fetal survival. Such expectant management combined with
appropriate use of blood transfusion and cesarean birth have resulted in the lowering
of the maternal mortality rate from !25%-30% to < 1% and the perinatal mortality
rate from 60%-70% to < 10%. If the fetus is thought to be mature by gestational
criteria or by amniocentesis for fetal lung maturity testing, there is little benefit to be
gained by a delay in delivery. The further from term that bleeding from placenta
previa occurs, the more important it is to delay delivery to allow for further fetal
growth and maturation. The degree of bleeding and the maturity of the fetus must be
constantly weighed in managing these patients. Fetal maturity is usually assessed at
approximately 36 weeks, with cesarean delivery performed once the fetus is deemed
mature.
In some cases, when the location of the placenta cannot be accurately determined
by ultrasound and delivery is required, the route of delivery is determined by a
double setup examination. This procedure involves careful evaluation of the cervix in
the oper-ating room with full preparations for rapid cesarean delivery.
 Localization by Sonography. The simplest, most precise, and safest method of
placental localization is provided by transabdominal sonography, which is used to
locate the placenta with considerable accuracy (Figs. 3, and 4 ).

Fig. 3 Partial anterior placenta previa at 36 weeks’ gestation. Placenta (P) extends
anteriorly and downward toward cervix (Cx). Fetus (F), amnionic fluid (AF), and
bladder (B) are seen. (Courtesy of Dr. R. Santos.)
 Fig. 4 Total placenta previa at 34 weeks’ gestation. Placenta (P) completely
overlies cervix (Cx). Bladder (B) and amnionic fluid (AF) are also visualized clearly.
(Courtesy of Dr. R. Santos.)
The average accuracy is about 95 percent, and rates as high as 98 percent have been
obtained. False-positive results are often a result of bladder distention. Therefore,
ultrasonic scans in apparently positive cases should be repeated after emptying the
bladder. Another source of error has been identification of abundant placenta implanted
in the uterine fundus but failure to appreciate that the placenta was large and extended
downward all the way to the internal os of the cervix. This, however is uncommon.
Farine and associates (1988) reported that the use of transvaginal ultrasonography
has substantively improved diagnostic accuracy of placenta previa. They were able to
visualize the internal cervical os in all cases with the transvaginal technique, in contrast
to only 70 percent using transabdominal equipment. An example is shown in Figure 5.
 Fig. 5 Transvaginal ultrasonic scan at 34 weeks’ gestation. Cervical canal is clearly
visible (CX) and distance from internal os to placental edge, measured between calipers
(X) is 0.75 cm. The patient was delivered by cesarean section 4 weeks later because
of vaginal bleeding. (P = placenta; B = bladder.) (Reproduced, with permission, from
Oppenheimer LW, Farine D, Ritchie JWK, Lewinsky RM, Telford J, Fairbanks LA.
What is a low-lying placenta? Am J Obstet Gynecol. 165:1035, 1991.)
Likewise, Leerentveld and colleagues (1990) studied 100 women suspected of
having placenta previa. They reported a 93 percent positive predictive value and 98
percent negative predictive value for transvaginal ultrasonography. Hertzberg and
associates (1992) demonstrated that transperineal sonography allowed visualization
of the internal os in all 164 cases examined because transabdominal sonography
disclosed a previa or was inconclusive. Placenta previa was correctly excluded in 154
women, and in 10 in whom it was diagnosed sonographically, nine had a previa
confirmed at delivery.
Magnetic Resonance Imaging.
Preliminary investigation using magnetic resonance imaging to visualize placental

abnormalities, including placenta previa, have been reported by several groups. Kay and
Spritzer (1991) discussed the many positive attributes of such technology (Fig. 6). It
is unlikely that this will replace ultrasonic scanning for routine evaluation in the near
future.

Fig. 6 A sagittal T2-weighted (2000/80 ms) image of a patient with a posterior

marginal placenta previa. The arrowhead points to the placental edge and the arrow
indicates the internal os. (F = fetal head; P = placenta; B = maternal bladder.) (From
Kay HH, Spritzer CE. Preliminary experience with magnetic resonance imaging in
patients with third-trimester bleeding. Obstet Gynecol. 78:424, 1991. Reprinted with
permission from the American College of Obstetricians and Gynecologists.)
Placental “Migration”
Since the report by King (1973), the apparent peripatetic nature of the placenta has
been well established. McClure and Dornal (1990) found a low-lying placenta in 25
percent of 1490 ultrasonic scans done at 18 weeks; however, at delivery, only 7 of these
385 low-lying placentas persisted. Sanderson and Milton (1991) found that only 12
percent of placentas were low lying in 4300 women surveyed ultrasonically at 18 to 20
weeks. Of those not covering the internal os, previa did not persist and hemorrhage was
not encountered. Conversely, of those covering the os at midpregnancy, about 40
percent persisted as a previa. Therefore, placentas that lie close to the internal
cervical os, but not over it, during the second trimester, or even early in the third
trimester, are very unlikely to persist as previas by term.
The low frequency with which placenta previa persists when it has been identified
sonographically before 30 weeks is shown in Table 32–4. It is apparent from these
data that in the absence of any other abnormality, sonography need not be frequently
repeated simply to follow placental position, and restriction of activity need not be
practiced unless the previa persists beyond 30 weeks, or becomes clinically apparent
before that time.
The mechanism of apparent placental movement is not completely understood.
The term migration is clearly a misnomer, however, as invasion of chorionic villi into
the decidua on either side of the cervical os will persist. The apparent movement of
the low-lying placenta relative to the internal os probably results from inability to
precisely define this relationship in a three-dimensional manner using two-
dimensional sonography in early pregnancy. This difficulty is coupled with
differential growth of lower and upper myometrial segments as pregnancy
progresses. Thus those placentas that “migrate” most likely never had actual
circumferential villus invasion that reached the internal cervical os in the first place.
If placental tissue is seen or palpated at the internal cervical os, prompt cesarean
delivery is performed. If the placental margin is away from the internal os, artificial
rupture of the membranes and oxytocin induction of labor may be performed in
anticipation of vaginal delivery. Before the widespread use of ultrasound, this
procedure was done more frequently than it is in modern obstetrics; nonetheless, it is
still an important tool in selected cases.
An attempt at vaginal delivery of a patient with placenta previa may be indicated if the
delivery can be accomplished with minimal blood loss and if the fetus is dead, has major
fetal malformations, or is clearly previable. If making such an attempt is appropriate,
ceasing the process and moving to cesarean delivery for a maternal indication must always
be considered. Placenta previa is associated with a nearly doubling of the rate of congenital
malformations, the most serious including major anomalies of the
central nervous system, gastrointestinal tract, cardiovascular system, and respiratory
tract. At the time of diagnosis of placenta previa, a detailed fetal survey should be
performed for anomalies.
Abnormal placental location can be further complicated by abnormal growth of the
placental mass into the substance of the uterus, a condition termed placenta previa
accreta. In placenta previa accreta, the poorly formed decidua of the lower uterine
segment offers little resistance to trophoblastic invasion. The incidence of this severe
complication is variously reported as 5% to 10% of placenta previas, although the inci-
dence is much higher in patients with multiple previous cesarean sections. At the time of
delivery, sustained and significant bleeding may ensue, often requiring hysterectomy.

ABRUPTIO PLACENTAE

Whereas placenta previa refers to the abnormal location of the placenta, abruptio
placentae, often called placental abruption, refers to the premature separation of the
normally implanted placenta from the uterine wall.
Etiology. Placental abruption occurs when there is hemorrhage into the decidua
basalis, leading to premature placental separation and further bleeding. The cause for
this bleeding is not known.
Placental abruption is associated with maternal hypertension and sudden
decompression of the uterus in cases of rupture of membranes in a patient with
excessive amniotic fluid (hydramnios) or after delivery of the first of multiple fetuses.
A more recent and serious association involves cocaine use by the mother, which
leads to intense vasoconstriction and, in some cases, sudden separation of the
placenta from the uterine wall. Placental abruption can also occur following trauma,
even when the extent of injury is not considered serious. For example, pregnant
women involved in motor vehicle accidents can sustain placental abruption even
though lap belts and shoulder strap restraints are used. Moreover, direct trauma to the
abdomen is not required, because sudden force applied elsewhere to the body can
result in coup and countercoup injury.
 Fig. 7. Types of placental abruption
Clinical findings and Diagnosis
The signs and symptoms can vary considerable. External bleeding can be profuse
or there may be no external bleeding (concealed hemorrhage) but the placenta is
completely sheared off and the fetus dead. Besides, common findings are uterine
tenderness, back pain, fetal distress, uterine hypertonus or high-frequently
contractions, idiopathic preterm labor, and a dead fetus.
Because the separation of the placenta from the uterus interferes with oxygénation
of the fetus, a nonreassuring fetal status is quite common in cases of significant
placental abruption. Thus, in any patient in whom placental abruption is suspected,
electronic fetal monitoring should be included in the initial management.
Placental abruption may be total and partial.
.
 Fig. 8 Total placental abruption
Coagulation abnormalities may also be found, thereby compounding the patient's
already compromised status. Placental abruption is the most common cause of
consump-tive coagulopathy in pregnancy and is manifested by hypofibrinogenemia
as well as by increased levels of fibrin degradation products. The platelet count can
also be decreased, and prothrombin time and partial thromboplastin time can be
increased as well. Such coagulopathy is a result of intravascular and retroplacental
coagulation. The intravascular fibrinogen is converted to fibrin by way of the
extrinsic clotting cascade. Thus not only is serum fibrinogen decreased but platelets
and other clotting factors are thereby also depleted.
Ultrasound is of little benefit in diagnosing placental abruption, except to exclude
placenta previa as a cause for the hemorrhage. Relatively large retroplacental clots
may be detected on ultrasound examination, but the absence of ultrasonographically
identified retroplacental clots does not rule out the possibility of placental abruption,
and conversely, a retroplacental echogenic area can be seen in patients without
placental abruption. The diagnosis rests on the classic clinical presentation of vaginal
bleeding, a tender uterus, and frequent uterine contractions with some evidence of
fetal distress. The extravasation of blood into the uterine muscle causes contractions
such that the resting intrauterine pressure, when measured with an intrauterine pres-
sure catheter, is often elevated; this sign can be helpful in making the diagnosis. The
entire uterus has a purplish or bluish appearance, owing to such extravasation of
blood (Couvelaire uterus) – Fig. 9.

Fig. 9 Couvelaire uterus

Management of a patient with placental abruption when the fetus is mature is
hemodynamic stabilization and delivery. Appropriate facilities and staff for cesarean
section must be continuously available whenever placental abruption is suspected
Careful attention to blood component therapy is critical, and the coagulation status must
be followed closely. Unless there is evidence of fetal distress or hemodynamic
instability, vaginal delivery by oxytocin induction of labor is preferable to a cesarean
delivery, although the maternal or fetal status may require that abdominal delivery be
performed. When the fetus is not mature and the placental abruption is limited and not
associated with premature labor or fetal or maternal distress, observation with close
monitoring of both fetal and maternal well-being may be considered while awaiting fetal
maturity. In the case of Couvelaire uterus total hysterectomy is performed because of
danger of uterine hypotony and disseminated intravascular clotting syndrome.

AMNIOTOMY. Rupture of the membranes as early as possible has long been

championed in the management of placental abruption. The rationale for amniotomy
is that the escape of amnionic fluid might both decrease bleeding from the
implantation site and reduce the entry into the maternal circulation of thromboplastin
and perhaps activated coagulation factors from the retroplacental clot. There is no
evidence, however, that either is accomplished by amniotomy. If the fetus is
reasonably mature, rupture of the membranes may hasten delivery. If the fetus is
immature, the intact sac may be more efficient in promoting cervical dilatation than
will a small fetal part poorly applied to the cervix.

LABOR. With slight degrees of placental separation, uterine contractions are

usually of normal frequency, duration, and intensity. With extensive placental
abruption, the uterus will likely be persistently hypertonic. The baseline intra-
amnionic pressure may be 25 to 50 mm Hg or higher, with rhythmic increases up to
75 to 100 mm Hg. Because of persistent hypertonus, it may be difficult at times to
determine by palpation if the uterus is contracting and relaxing to any degree (Fig.
32–9 ).

OXYTOCIN. Although hypertonicity characterizes myometrial function in most

cases of severe placental abruption, if no rhythmic uterine contractions are
superimposed, then oxytocin is given in standard doses. Uterine stimulation to effect
vaginal delivery provides benefits that override the risks. The use of oxytocin has
been challenged on the basis that it might enhance the escape of thromboplastin into
the maternal circulation and thereby initiate or enhance consumptive coagulopathy or
amnionic fluid embolism syndrome. There is no evidence to support this fear (Clark
and colleagues, 1995; Pritchard and Brekken, 1967).
 VASA PREVIA

Although rarely encountered, vasa previa presents significant risk to the fetus. In
vasa previa (Fig. 10), the umbilical cord inserts into the membranes of the placenta
(rather than into the central mass of the placental tissue), and one such vessel lies
below the presenting fetal part in the vicinity of the internal os. If this vessel ruptures,
fetal bleeding occurs. Because of the low blood volume of the fetus, seemingly
insignificant amounts of blood may place the fetus in jeopardy. A small amount of
vaginal bleeding associated with fetal tachycardia may be the clinical presentation. A
test to distinguish fetal blood from maternal blood, such as the Kleihauer-Betke or the
Apt test, can be of value when such a condition is suspected. These tests distinguish
between maternal and fetal blood on the basis of the marked resistance to pH changes
in fetal red cells compared with the friable nature of adult red cells in the presence of
strong bases. Immediate cesarean section is the only way to save the fetus in vasa
previa.

Fig. 10 Sonogram showing placenta (P), succenturiate lobe (S), and leading fetal

vessels in vasa previa (arrow). (From Gianopoulas J, Carver T, Tomich PG, Karlman
 R, Gadwood K. Diagnosis of vasa previa with ultrasonography. Obstet Gynecol.
69:488, 1987).

APPROACH TO A PATIENT WITH VAGINAL BLEEDING IN THE

SECOND HALF OF GESTATION
In any woman with vaginal bleeding during the second half of pregnancy, fetal
and maternal status should be evaluated promptly. At the same time that a search is
undertaken for the cause of the bleeding, attention must be directed toward stabiliza-
tion of the maternal hemodynamic state. The approach is not unlike that for any
hemorrhaging patient and includes ready access for fluid replacement through one or
more large-bore intravenous catheters, serial complete blood counts, type and cross-
match of ample amounts of blood, and if the condition is unstable, intracardiac
monitoring. Attention to urinary output is a simple and important reflection of the
volume status of a patient. Because normal antepartum blood volume expansion is
substantial, pregnant women may lose considerable amounts of blood before vital
sign changes are apparent. In more than half of the cases of significant vaginal
bleeding in pregnancy, no specific cause can be discovered despite careful evaluation.
In general, patients with significant bleeding should remain hospitalized until
delivery, although in some cases minimal bleeding ceases, and the patient appears
normal in every way. Caution is advised, however, because patients with bleeding of
undetermined etiology can be at greater risk for preterm delivery, intrauterine growth
restriction, and fetal distress than patients with bleeding of known cause.
HEMORRHAGE IN THE THIRD STAGE OF LABOR AND EARLY
PUERPERAL PERIOD
Postpartum hemorrhage is defined as blood loss in excess of 400 mL at the
time of vaginal delivery.
Postpartum hemorrhage before delivery of the placenta is called third-stage
hemorrhage.
Postpartum hemorrhage after delivery of placenta during the first two hours is
called as hemorrhage in early puerperal stage.
Hemorrhage after placental separation is stopped thanks to:
 1. uterine contractions – caliberes of ruptured vessels decreases during
uterine contractions;
2. formation of thrombs, especially in the region of placental site;
3. torsion of thin septs in which vessels are situated.

Causes of Postpartum Hemorrhage:

1. uterine atony,
2. genital tract trauma,
3. bleeding from the placental site (retained placental tissue, low
placental implantation, placental adherence, uterine inversion)
4. coagulation disorders.

The main causes of third-stage bleeding are genital tract trauma

and bleeding from placental site.
The main causes of hemorrhage in early puerperal stage are all of the
above causes of Postpartum hemorrhage.
Predisposing factors and causes of immediate postpartum hemorrhage:
Uterine atony:
1. Overdistended uterus – multiple fetuses, Hydramnios, distention with
clots.
2. Anesthesia or analgesia – halogenated agents, conducted analgesia with
hypertension.
3. Exhausted myometrium – rapid labor, prolonged labor, oxytocin
or prostaglandin stimulation.
4. Chrionamnionitis.
4. Previous uterine atony.
Genital tract trauma:
1. Complicated vaginal delivery.
2. Cesarean section or hysterectomy, forceps or vacuum.
3. Uterine rupture; risk increased by: previously scarred uterus, high
parity, hyperstimulation, obstructed labor, intrauterine manipulation.
 4. Large episiotomy, including extensions.
5. Lacerations of the perineum, vagina or cervix.

Bleeding form placental implantation cite:

1. Retained placental tissue – avulsed cotyledon, succentuariate lobe
2.Abnormally adherent – accreta, increta, percreta.
Coagulation defects – intensifies other causes:
1. Placental abruption.
2. Prolonged retention of dead fetus.
3. Amnionic fluid embolism.
4. Saline-induced abortion.
5. Sepsis with endotoxemia.
6. Severe intravescular hemolysis.
7. Massive transfusions.
8. Severe preeclampsia or eclampsia.
9. Congenital coagulopathies.
Clinical findings and diagnosis
The two most common causes of immediate hemorrhage are hypotonic
myometrium (uterine atony) and lacerations of the vagina and cervix. Retention
of part or all of the placenta, a less common cause, may produce either immediate
or delayed hemorrhage (or both).
Uterine atony is called as total absence of uterine contractions into the
external irritation. Uterine hypotony is called as presence of inadequate uterine
contractions on the external irritation. In the pauses between uterine contractions a
uterus is soft. But blood form clots in the case of uterine hypo- or atony. These
clots are stored in the uterine cavity that’s why a uterus is enlarged in sizes.
The differentiation between bleeding from uterine atony and from lacerations
is tentatively based on the condition of the uterus. If bleeding persists despite a firm,
well-contracted uterus, the cause of the hemorrhage most probably lacerations.
Bright red blood also suggests lacerations. To ascertain the role of lacerations as a
cause of bleeding, careful inspection of the vagina, cervix, and uterus is essential.
 Placental accreta is any implantation of the placenta in which there is
abnormally firm adherence to the uterine wall. As a consequence of partial or
total absence of the decidua basalis and imperfect development of the
fibrinoid layer (Nitabush’s membrane):
1. the placental villi are attached into the basal layer - placenta adhaerens;
2. the placental villi are attached to the myometrium - placenta accreta (Fig.
11);
3. extensive growth of placental tissue into the uterine muscle itself – placenta
increta;
4. complete invasion through the sickness of the uterine muscle to the serosa or
beyond – placenta percreta (Fig. 12, 13 ).

Fig. 11 A fatal case of inverted uterus associated with placenta

accreta following delivery at home.
 Fig. 12 Placenta percreta in a woman at term with a known placenta previa.
The placenta had grown into the entire lower uterine segment. (Photograph
courtesy of Dr. Tom Dowd.)
 Fig. 13 Placenta percreta. On the left, the placenta is fungating through the
fundus above the old classical cesarean section scar. In the opened specimen on
the right, the variable penetration of the fundus by the placenta is evident.
(From Morison, 1978.)
Complete or total placenta accreta will not cause bleeding because the placenta
remains attached, but partial ( the abnormal adherence involves a few to several
cotyledons) or focal ( the abnormal adherence involves a single cotyledon) type
may cause profuse bleeding, as the normal part of the placenta separates and the
myometrium cannot contract sufficiently to occlude the placental site vessels.
The abnormal placental adherence is diagnosed by:
1. Absence of the signs of placental separation during
30 minutes. Signs of placental separation:
1. the uterus rises in the abdomen;
2. the shape of the uterus changes from discoid to globular
3. the umbilical cord lengthens.
 2. External bleeding – in the case of partial adherence, absence of the bleeding
– in the case of total placenta accreta.
3. Manual removal of the placenta confirms the diagnosis of different types
of abnormal placental adherence. In the case of partial placental adhaerence it
stops bleeding, but in the case of placenta accreta, increta and percrata it increases
bleeding. Attempts at manual removal are futile. That’s why in these cases
manual removal of the placenta should be stopped immediately and hysterectomy
should be performed.
Coagulation disorders are recognized thanks to coagulation
studies and inspection for clot formation.
MANAGEMENT OF THE PATIENTS IN THE THIRD-STAGE
BLEEDING
UTERINE ATONY
1. Catheterization of the urinary bladder.
2. Cold on the lower abdomen.
3. Manual massage of the uterine corpus: one hand gently massages the uterus
from the abdomen while the other is inserted so that the cervix is cradled in the
fingers and thumb to allow maximal compression and massage.
4. Prescription of the uterine contracting drugs: oxytocin – 5 units,
methylergonovine (Methergine) – 1mL intramuscularly or in intravenous infusion. If
the uterus remains atonic and the placental site bleeding continuos during the
oxytocin infusion, a rapid continuos intravenous infusion of dilute oxytocin (20 units
in 1L of normal saline) should be given to increase uterine tone. Analogues of
prostaglandin F2 alpha (Hemabate) in a dose 5 mg given intramuscularly or
intravenously are quite effective in controlling postpartum hemorrhage caused by
uterine atony. Large-bore intravenous catheters – 1 or 2 well functioning lines.
Mifipristone – 800 mkg per rectum, enzaprost – 5 mg into anterior abdominal wall.
5. Manual exploration of the uterine cavity under the general anesthesia,
bimanual uterine compression. (fig. 14)
6. A tampon with ether is inserted into the posterior fornix.
7. Clemmas on the parametrium or into the cervix of the uterus are putted on.
 8. Aorta compression to the spinal column.
In a case if blood loss increase 800 mL and bleeding continuos - surgery
management should be perform:
1.Uterine artery ligation;
2. Hypogastric artery ligation;
3. Hysterectomy.

Fig.14 Bimanual compression of the uterus and massage with the

abdominal hand usually will effectively control hemorrhage from uterine atony.

GENITAL TRACT TRAUMA – ligation and suturing of all ruptures of the

vagina, cervix and perineum. In the case of uterine rupture – hysterectomy should
be performed.
BLEEDING FROM PLACENTAL IMPLANTATION CITE
1) placental separation signs are absent – manual separation and removal of
the placenta and exploration of the uterine cavity, uterine massage, uterine
contracting drugs are prescribed;
2) complete and partial placenta adhaerens - manual separation and removal
of the placenta (Fig. 15);
 3) placenta accreta, increta and percreta – hysterectomy. With more
extensive involvement, however, hemorrhage becomes profuse as manual
removal of the placenta is attempted.

Fig. 15 Technique of manual removal of the placenta

Technique of Manual Removal. Adequate analgesia or anesthesia is mandatory.
Aseptic surgical technique should be employed. After grasping the fundus through the
abdominal wall with one hand, the other hand is introduced into the vagina and passed
into the uterus, along the umbilical cord. As soon as the placenta is reached, its margin is
located and the ulnar border of the hand insinuated between it and the uterine wall. Then
with the back of the hand in contact with the uterus, the placenta is peeled off its uterine
attachment by a motion similar to that employed in separating the leaves of a book.
After its complete separation, the placenta should be grasped with the entire hand, which
is then gradually withdrawn. Membranes are removed at the same time by carefully
teasing them from the decidua, using ring forceps to grasp them as necessary. Some
prefer to wipe out the uterine
cavity with a sponge. If this is done, it is imperative that a sponge not be left in the
uterus or vagina.
Placenta Accreta, Increta, and Percreta
In most instances, the placenta separates spontaneously from its implantation
site during the first few minutes after delivery of the infant. The precise reason for
delay in detachment beyond this time is not obvious always, but quite often it seems
to be due to inadequate uterine contraction. Very infrequently, the placenta is
unusually adherent to the implantation site, with scanty or absent decidua, so that
the physiological line of cleavage through the decidual spongy layer is lacking. As a
consequence, one or more cotyledons are firmly bound to the defective decidua
basalis or even to the myometrium. When the placenta is densely anchored in this
fashion, the condition is called placenta accreta.
The term placenta accreta is used to describe any placental implantation in
which there is abnormally firm adherence to the uterine wall. As the consequence of
partial or total absence of the decidua basalis and imperfect development of the
fibrinoid layer (Nitabuch layer), placental villi are attached to the myometrium in
placenta accreta, actually invade the myometrium in placenta increta, or penetrate
through the myometrium in placenta percreta. The abnormal adherence may involve
all of the cotyledons (total placenta accreta), a few to several cotyledons (partial
placenta accreta), or a single cotyledon (focal placenta accreta).
Significance
An abnormally adherent placenta, although an uncommon condition, assumes
considerable significance clinically because of morbidity and, at times, mortality from
severe hemorrhage, uterine perforation, and infection. The true frequencies of
placenta accreta, increta, and percreta are unknown. Breen and associates (1977)
reviewed reports published since 1891. The incidence varied from 1 in 540 deliveries
to 1 in 70,000 deliveries, with an average incidence of about 1 in 7000. Read and co-
workers (1980) reported an incidence of about 1 per 2500 deliveries and concluded
that today there is a higher reported incidence, lower parity, and greater incidence of
associated placenta previa, as well as decreasing maternal and perinatal mortality.
 Abnormal placental adherence is found most often in circumstances where
decidual formation was likely to have been defective. Associated conditions include
implantation in the lower uterine segment, over a previous cesarean section scar or
other previous uterine incisions, or after uterine curettage. In his review of 622
reported cases of placenta accreta collected between 1945 and 1969, Fox (1972)
noted the following characteristics: (1) placenta previa was identified in a third of
affected pregnancies, (2) one fourth of the women had been previously delivered by
cesarean section, (3) nearly one fourth had previously undergone curettage, and (4)
one fourth were gravida 6 or more. Read and co-workers (1980) reported similar
findings for women studied in the 1970s; however, the overall incidence and parity
had decreased. In a preliminary investigation, Hardardottir and colleagues (1996)
found that almost half of placentas in women with a prior cesarean section had
adherent myometrial fibers detected microscopically.
Antepartum hemorrhage is common, but in the great majority of cases, bleeding
before delivery is the consequence of coexisting placenta previa. Myometrial
invasion by placental villi at the site of a previous cesarean section scar may lead to
uterine rupture during labor or even before (Berchuck and Sokol, 1983). Archer and
Furlong (1987) described a woman who presented with an acute abdomen from
massive hemoperitoneum caused by placenta percreta at 21 weeks’ gestation. In
women whose pregnancies go to term, however, labor will most likely be normal in
the absence of an associated placenta previa or an involved uterine scar.
The problems associated with delivery of the placenta and subsequent
developments vary appreciably, depending upon the site of implantation, depth of
myometrial penetration, and number of cotyledons involved. It is very likely that
focal placenta accreta with implantation in the upper uterine segment develops much
more often than is recognized. The involved cotyledon is either pulled off the
myometrium with perhaps somewhat excessive bleeding, or the cotyledon is torn
from the placenta and adheres to the implantation site with increased bleeding,
immediately or later.
 With more extensive involvement, hemorrhage becomes profuse as delivery of
the placenta is attempted. Successful treatment depends upon immediate blood
replacement therapy, and nearly always prompt hysterectomy.
With total placenta accreta, there may be very little or no bleeding, at least until
manual placental removal is attempted. At times, traction on the umbilical cord will
invert the uterus, as will be described in the next section. Moreover, usual attempts at
manual removal will not succeed, because a cleavage plane between the maternal
placental surface and the uterine wall cannot be developed. The safest treatment in
this circumstance is prompt hysterectomy.
In the 622 cases reviewed by Fox (1972), the most common form of
“conservative” management was manual removal of as much placenta as possible and
then packing of the uterus. One fourth of the women died, which was four times as
many as when treatment consisted of immediate hysterectomy. So-called
“conservative” treatment in at least four instances was followed by an apparently
normal pregnancy.
The possibility exists that placenta increta might be diagnosed antepartum. Cox
and associates (1988) described a case of placenta previa in which they also were
able to identify placenta increta ultrasonically from the lack of the usual subplacental
sonolucent space. They hypothesize that the presence of this normal subplacental
sonolucent area represents the decidual basalis and the underlying myometrial tissue.
The absence of this sonolucent area is consistent with the presence of a placenta
increta. Pasto and associates (1983) confirmed that the absence of a subplacental
sonolucent or “hypoechoic retroplacental zone” is consistent with placenta increta.
Inversion of the Uterus
Complete uterine inversion after delivery of the infant is almost always the
consequence of strong traction on an umbilical cord attached to a placenta implanted
in the fundus (Fig. 16).
Most likely site of placental implantation in cases of uterine inversion. With
traction on the cord and the placenta still attached, the likelihood of inversion is
obvious.
 Fig. 16 Contributing to uterine inversion is a tough cord that does not readily
break away from the placenta, combined with fundal pressure and a relaxed uterus,
including the lower segment and cervix.
Placenta accreta may be implicated although uterine inversion can occur
without the placenta being so firmly adherent. At times, the inversion may be
incomplete (Fig. 11).
Shah-Hosseini and Evrard (1989) reported an incidence of about 1 in 6400
deliveries at the Women and Infants Hospital of Rhode Island. Of the 11 inversions
identified, most were in primiparous women and immediate vaginal replacement of
the inverted uterus was successful in nine instances. Platt and Druzin (1981) reported
28 cases in over 60,000 deliveries, for an incidence of about 1 in 2100. These same
investigators suggested that parenteral magnesium sulfate, which was administered to
women with pregnancy-induced hypertension, might have played a role in the
etiology of this complication.
Uterine inversion is most often associated with immediate life-threatening
hemorrhage, and without prompt treatment it may be fatal (Fig. 11).
 In the past it was stated that shock tends to be disproportionate to blood loss.
Careful evaluation of the effects from transfusion of large volumes of blood in such
cases does not support this concept, but instead makes it very apparent that blood loss
in such circumstances was often massive but greatly underestimated (Watson and
associates, 1980).
Treatment
Delay in treatments increases the mortality rate appreciably. It is imperative that
a number of steps be taken immediately and simultaneously:
1. Assistance, including an anesthesiologist, is summoned immediately.
2. The freshly inverted uterus with placenta already separated from it may often
be replaced simply by immediately pushing up on the fundus with the palm of the
hand and fingers in the direction of the long axis of the vagina.
3. Preferably two intravenous infusion systems are made operational, and
lactated Ringer solution and whole blood are given to reverse hypovolemia.
4. If attached, the placenta is not removed until the infusion systems are
operational, fluids are being given, and anesthesia, preferably halothane or enflurane,
has been administered. Tocolytic drugs have also been used successfully for this
purpose. Terbutaline, ritodrine, or magnesium sulfate have been used for uterine
relaxation and repositioning (Catanzarite and associates, 1986; Kovacs and DeVore,
1984; Thiery and Delbeke, 1985). To remove the placenta before this time increases
hemorrhage. In the meantime, the inverted uterus, if prolapsed beyond the vagina, is
replaced within the vagina.
5. After removing the placenta, the palm of the hand is placed on the center of
the fundus with the fingers extended to identify the margins of the cervix. Pressure is
then applied with the hand so as to push the fundus upward through the cervix.
6. Oxytocin is not given until after the uterus is restored to its normal
configuration.
As soon as the uterus is restored to its normal configuration, the agent used to
provide relaxation is stopped and simultaneously oxytocin is started to contract the
uterus while the operator maintains the fundus in normal relationship. Initially,
bimanual compression will aid in the control of further hemorrhage until uterine tone
is recovered.

Fig.17 Uterine replacement

After the uterus is well contracted, the operator continues to monitor the uterus
transvaginally for any evidence of subsequent inversion.
Surgical Intervention. Most often, the inverted uterus can be restored to its
normal position by the techniques described. If the uterus cannot be reinverted by
vaginal manipulation because of a dense constriction ring (Fig. 18), laparotomy is
imperative.
 Fig. 18 Completely inverted uterus viewed from above.
The fundus then may be simultaneously pushed upward from below and pulled
from above. A traction suture well placed in the inverted fundus may be of aid. If the
constriction ring still prohibits reposition, it is carefully incised posteriorly to expose
the fundus. A graphic outline of this surgical technique was described by Van Vugt
and associates (1981). After replacement of the fundus, the anesthetic agent used to
relax the myometrium is stopped, oxytocin infusion is begun, and the uterine incision
repaired. Following restoration of the uterus, the adjacent viscera are carefully
examined for trauma.
Attention ! Irrespective of the apparent cause, whenever there is any suggestion at
the delivery or postpartum of excessive blood loss from the genital tract,
immediate steps must be taken to identify the presence of uterine atony, retained
placental fragments, and trauma.
1. At least one or, in the presence of frank hemorrhage, two
intravenous infusion systems of large caliber must be established right
away to permit rapid administration of aqueous electrolyte solutions and
blood as nedded
 2. An operating room and a surgical team, including
an anesthesiologist, must be immediate available.
COAGULATION DEFECTS
The treatment of coagulation defects is aimed at correcting the
coagulation defects and include infusion of:
1. platelet concentrate – increases platelet count by about 20 000 to 25 000;
1. cryoprecipitate – supplies fibrinogen, factor VIII, and factor XIII (3 to
10 times more concentrated than the equivalent volume of fresh plasma);
2. fresh-frozen plasma – supplies all factors except platelets (1 g of fibrinogen);
3. packed red blood cells – raises hematocrit 3 % to 4 %.

OBSTETRIC SHOCK. TERMINAL STATES IN OBSTETRICS

Shock encompasses various pathophysiological aberrations that lead to
inadequate tissue perfusion and impaired cellular metabolism. Although hypotension
often is the most obvious clinical sign in shock of any cause, such blood pressure
changes are the final common manifestation of a number of distinct pathologic
processes. The successful clinical management of patients in shock depends on the
proper definition of the underlying pathophysiology as well as an under of the unique
effects of pregnancy on such conditions.
Uterine bleeding (hemorrhage) during labor and early puerperal stage play an
important role among different kinds of severe obstetrics pathology, such as
hemorrhagic shock, disseminated intravascular coagulopathy, sepsis and other.
Uterine bleeding is the leading cause of maternal death.
Uterine bleeding frequency is 8,0 – 11, 0 %.
The main causes of uterine bleeding are:
During pregnancy: placenta praevia, placenta abruptio.
During labor: placenta praevia, placenta abruptio, uterine rupture, traumatization
of the soft birth canal tissues.
In the third period of labor and early puerperal stage: uterine hypo- and atony;
uterine rupture and traumatization of the soft birth canal tissues; placenta accreta,
increta, and percreta; retention of some parts of afterbirth in the uterine cavity;
thrombohemorrhagic bleeding.
Methods of blood loss determination
1. Libov’s method.
After surgical intervention the napkins, which are filling by blood, should be
weighted.
Blood loss volume = Weight x 15 % ( if blood loss is < 1000 ml);
2
Blood loss volume = Weight x 30 % ( if blood loss is > 1000 ml).
2
2. By hematocrit
Hematocr Blood
it, % loss
volume,
ml
44–40 500
38–32 1000
30–22 1500
< 22 >
1500
3. Algover’s index
Shock’ index = Heart rate
Systolic arterial blood pressure
In normal Algover’s index is < 1.
Algov
Blood loss
er’s index volume, %
out of
circulating
blood volume
0,8 10 %
and <
 0,9 – 20 %
1,2

1,3 – 30 %
1,4
1,5 40 %
and >

HEMORRHAGIC (HYPOVOLEMIC) SHOCK

Hemorrhagic shock is a very serious complication in the case of pathological
hemorrhage.
Physiological blood loss during labor is 0, 5 % out of puerperant’ weight.
Physiological blood loss is 350, 0 – 400, 0 ml.in the puerperant with 70-75 kg of
weight. If blood loss predominate physiological one, hemorrhagic shock have been
occurred.
There are 4 stages of hemorrhagic shock according to Baker classification.
Evaluation of hemorrhagic shock stage severity is presented in the table.
Evaluation of hemorrhagic shock stage severity
Shock Hypovolemia Circulating Blood loss, % from body weight Hemodynamic
stage stage blood ml diuresis
volume
deficiency
I Mild 10 %-20% 500 – 1,0 – 1,5 % Ps – 90-100 be
1000,0 Arterial blood
Central Venou
Diuresis – N.
II Moderate 20%-30% 1000,0- 1,5 - Ps – 120 beats
1500,0 2,0 % BP - <100 mm
CVP – < 60 m
Diuresis – < 5
III Severe 30%-40% 1500,0– 2,0 – Ps – 140 beats
2000,0 2,5 % BP - < 70 mm
 CVP – < 40 m
Diuresis – < 3
IV Considerable 40% and > 2000,0 and > > Ps – 140 beats
2,5 % BP – < 50 mm
CVP – 0;
Diuresis– anur

The main principles of obstetrics hemorrhage and hemorrhagic

shock treatment:
1. Hemorrhage stopping.
2. Determination of blood loss stage.
3. Restoration of the circulating blood volume.
4. Normalization of vascular tone.
5. Blood reology, its structural, biochemical, and electrolytes compounds
correction.
6. Detoxication therapy.
7. Desensibilizing therapy.
8. Correction of clotting, antyclotting, fibrinolitic systems functions.
9. Regulation of the main human organs functions.
10. Prevention of infectious complications.
INTERM restoration of the circulating blood volume – is the main step in the
treatment of acute blood loss. Human organism should be survived in the case of 2/3-
erythrocytes volume loss, but it doesn’t survive in the case of 1/3 plasma volume
loss. That’s why it should be remembered that in considerable blood loss the first step
is the transfusion not only blood, but also кровозамінники, which eliminate
hypovolemia very quickly.
Transfusion therapy in obstetrics hemorrhages

Blood Volume Crysta- Refortan, Fresh- Albumin Erythro-

loss of infusion lloids Gelofusin frozen (10-20 massa
Stabisol plasma %)
 10-20 10-15 10 ml /kg - -
% 2500 ml/
500- ml kg
1000ml

20-30 10 ml 10 ml /kg 5-10 - 5 ml /kg

% 3000 /kg ml /kg
1000- ml
1500
ml

30-40 7 ml/kg 7 ml/kg 10 - 200 ml 10-20

% 4000 15 ml /kg ml /kg
1500- ml
2000
ml

40- 7 ml/kg 10 ml /kg 15 - 200 ml 30 ml

and > > 6000 20 ml /kg /kg
> ml
2000 ml
The volume of infusion therapy in hemorrhagic shock should be predominated in
1,5-2,5 times its real blood loss.
Glucose transfusion doesn’t administrated in blood loss, because it very quickly
enter intracellular space and doesn’t increase circulating blood volume, it caused
metabolic acidosis.
Attention! Erythrocyte transfusion has value only after hemodynamics and
peripheral blood circulation normalization. Only in these conditions erythrocytes
should be taken oxygen.
Attention ! In all stages of hemorrhagic shock 2-4 veins should be catheterized
in one moment (one or two of them are central, such as v. subclavia).
Infusion speed depends on blood loss volume and patient state. In the case of
hemorrhagic shock and low arterial blood pressure it should be reach 200 ml per
minute. The infusion speed gradually decreased to 150-100-50 ml-per minute in the
case of increasing arterial blood pressure to 80-90 mm Hg.
The main prescription of infusion therapy in the case of acute blood lose is the
stabilization of central hemodynamics which lead to cerebral and coronary blood
circulation stabilization.
Vascular tone normalization.
In the first stage of hemorrhagic shock because of vascular spasm presence
spasmolitics drugs are used, such as Nospani, Papaverini hydrochloridi. On the II-III-
IV stages because of vascular dilation glucocorticoids are prescribed. They are:
Prednisoloni, Hydrocortisone – in the dose 1,5-2 g/ daily, Dexametazoni.
If intravenous insertion 800-1000 ml any solution with the speed of 50-100
ml/per minute doesn’t change (increase) arterial blood pressure – vasopressors agents
should be prescribed, such as Remestip – in the dose 0,2-1,0 mg; Dopamine –
5mkg/kg/minute or glucocrticoids.
In considerable infusion therapy after circulating blood volume normalization
diuresis stimulation is recommended. For this purpose Euphillini in the dose 3 mh per
kg, lazix – 2-4 mg/kg or furosemidi in the dose 6-8 mg/kg have been used.
Structural, biochemical, electrolytes compounds correction of blood,
detoxycation, desensibilizing therapy and normalization of clotting, antyclotting,
fibrinolytic systems functions and functions of the main human organs is obligatory
in the treatment of hemorrhagic shock.
Introduction of cardiologic drugs is possible only after blood loss restoration.
For this purpose such agents have been used as Corgliconi –0, 6 % - 0,5 –1 ml;
Cocarboxylase – 50 mg twice a day.
Prevention of infectious complications by prescription of wide spectrum
antibiotics (cefalosporines, aminoglycozides) in the daily dose is recommended also.

Main steps of urgent medical care in the obstetrics bleeding

during pregnancy, labor, and puerperal stage
1. Blood loss is 0, 8 – 1, 0 % of body weight
1. To determine the cause of hemorrhage
 Pla Uterine Uterine
centa cervix hypo- and
praevia, rupture, deep atony; uterine
placenta vagival rupture and
abruptio, ruptures, traumatization
uterine traumatization of the soft
rupture of the soft birth canal
birth canal tissues;
tissues. placenta
accreta,
increta, and
percreta;
retention of
some parts of
afterbirth in
the uterine
cavity

Bleeding stopping

Urgent Rupture Manual

cesarean suture uterine
section revision

2. To start intravenous infusion: crystalloids (0,9 % NaCl + 10

Units of oxytocin), colloids – Refortan, Stabisol, Poliglucin.

2. Blood loss is 1, 0 %– 1, 5 % of body weight.

1. Injection of 250 – 1000 mkg Prostin F2a intramuscularly or 0,4 mg Remestip
+ 10 ml 0,9 % NaCl into uterine cervix.
 2. Catheterization of two veins (one of them is v. subclavia), intravenous
transfusion of autoblood, plasma, erythrocyte massa, Refortan, Stabisol.

Attention! Surgical intervention should be performed in continuing

bleeding! (if blood loss is more than 1, 0 % - 800 ml of body weight ).

3. Blood loss is > 1, 5 % of body weight.

1. Laparotomy. Total hysterectomy without adnexa (adnexa are removed
if inflammatory, degenerative changes are presented).

2. Restoration of the blood circulating volume: autoblood, donor’s blood – 100

% from blood loss, cryoprecipitate, albumin.
DISSEMINATED INTRAVASCULAR COAGULOPATHY (DIC)
DIC is not a distinct clinical entity; rather, it represents a manifestation of
various disease processes that have in common activation of intravascular clotting
and fibrinolysis, resulting in excess consumption of solutable coagulation
components. In obstetrics, secondary fibrinogenolysis commonly dominates the
clotting aberration and results in the circulation of fibrin and fibrinolytic split
products, which further accentuates the clinical presentation of henorrhage. In
addition, sometimes a dilutional coagulopathy is encountered in pregnancy. This
condition obtains when massive hemorrhage is teplaced only by red blood cells and
crystalloids solution, resulting in a dilutional depletion of platelets and soluble
clotting factors.. In practice, the hemorrhage associated with dilutional coagulopathy
often results in hypotension and shock. The tissue hypoxia that accompanies shock of
any cause is well known to potentially activate the coagulation-fibrinolysis cycle
associated with DIC.
DIC is the pathological complex, which is characterized by blood clotting that
has been leading to microcirculation blockade by fibrin in the main human organs
(lungs, kidneys, liver). Dysfunction of these organs is the result of their damage. In
the end of this process thrombohemorrhagic disorders have been developed.
 The main causes of DIC in the obstetrics are:
1. All kinds of shock (hemorrhagic, septic, anaphylactic);
2. Placenta abruption;
3. Embolic fluid embolism;
4. OPH – hestosis;
5. Hypotonic bleeding;
6. Uterine ruptures;
7. Excessive labor induction;
8. Cesarean section;
9. Extragenital pathology;
10.Septic abortion;
11.Puerperal endometritis;
12.Intensive uterine massage;
13. dead fetus syndrome
Classification of thrombohemorrhagic syndrome
1. By clinical duration:
1. Acute;
2. Subacute;
3. Chronic.
2. By stages:
I stage – hypercoagulation;
II stage – hypocoagulation without generalizing fibrinolysis
activation; III stage – hypocoagulation with generalizing
fibrinolysis activation; IV stage – total fibronolysis.
Clinical manifestatiuon.
Clinical manifestation of DIC is connected with ischemic and hemorrhagic
changes in human organs and tissues. They are:
1. Hemorrhages into skin and mucous membranes;
2. Hemorrhages from the places of injections, incisions, uterus.
3. Necrosis of some areas of skin and mucous membranes;
4. Central nervous system impairment;
 5. Acute renal, liver, lung insufficiency.

Laboratory diagnosis of DIC

The main laboratory data
Blood Spontaneous Thrombin Throm- Thrombin
Stages clotting thrombus test bocytes time,
time, lisis number, seconds
minutes 10x9/l
I.Hypercoagulation <5(N) absent (N) 7-11 (N) 175-425 < 24
(N)
II.Hypocoagulation 5 -12 absent 7-11 < 120 >60
without
generalizing
fibrinolysis

III Hypocoagu- >12 quick 20-60 < 100 >100

lation with
generalizing
fibrinolysis
IV. Total > 60 Thrombus >60 <60 >180
fibrinolysis doesn’t
formed

General principles of DIC treatment are:

1. Heparin,fibrinogen are contraindicated inall stagesof
thrombohemorrhagic syndrome.
2. Proteolytic enzymes inhibitors in the dose of 10 mg/kg/hour have been used
for inhibit excessive fibrinolysis and prevention of intracellular clotting.
3. Early and quick introduction of fresh frozen donor’s plasma. The main aim of
its usage is the restoration of haemostatic potential of blood (it contains all
soluble clotting factors, similar to whole blood). It has been used in all stages of
 thrombohemorrhagic syndrome. Initially the dose of intravenous introduction is 6-12
ml/kg. After it dose is 300-400 ml each 6-8 hours.
4. Stimulation of vascular-thrombocytes link of hemostasis (dicinone, etamsilat).
5. Transamacha acid usage – in the dose 500-750 mg on 0,9 % NaCl. This
medicine inhibits plasmine activity, stabilizes coagulate factors and fibrin, decreases
vascular permeability and gives permanent hemostatic action, which have been
prevented fibrinogen degradation.
Treatment of thrombhemorrhagic syndrome in obstetric hemorrhagic
shock in different stages
Stages Treatment
I.Hypercoagulation For normalization blood reology: Trental – 100mg on
100 ml 0,9 % NaCl, Curantill – 0,5 – 2, %
II.Hypocoagulation without Procoagulants: fresh frozen plasma 500,0, blood of 3-
generalizing fibrinolysis 5 days of conservation. Transamacha – antyplasmin
drug – 500-750 mg on 0, 9 % NaCl.
Fibrinolysis inhibitors: Contrical in the dose 10-
20.000 units/ daily dose 100-200.000 units; Trasilol –
40.000 units or Gordox – 100-200.000 units.
Cortycosteroids – Prednisolone – 10mg/kg/hour or
Hydrocortisone – 100 mg/kg.
III Hypocoagulation with Proteolytic enzymes inhibitors: Contrycal 40.000 units
generalizing fibrinolysis (daily dose 500.000 units)
Procoagulants – fresh frozen plasma, blood, albumin.
Cortycosteroids.Cryoprecipitate–200-400,0,
Transamcha – 500-700 mg.
IV. Total fibrinolysis The treatment should be started from the large doses
of proteolytic enzymes inhibitors – Contrical 100.000
units to 500.000 units. Blood, albumin, plasma,
cryoprecipitate, cortycosteroids.

AMNIOTIC FLUID EMBOLISM (AFE)

 Amniotic fluid embolism is a rare, sudden, and often fatal obstetric
complication caused by entry of amniotic fluid into the maternal venous circulation.
The initial physiological disturbances involve profound alterations in
hemodynamics and oxygenation, often followed by the development of a
consumptive coagulopathy.
The main pathogenetical factors that have been predisposing to amniotic fluid
embolism are predomination of amniotic pressure over venous and traumatization of
venous uterine vessels.
Predomination of amniotic pressure over venous is presented in excessive labor
contractions, breach presentation, postdate pregnancy, multiple pregnancy, uterine
cervix dystocia, hypovolemia of different etiology.
Traumatization of venous uterine vessels is presented in placenta abruption,
cesarean section, manual removal of placenta, puerperal hypotonic hemorrhage.

Clinical manifestation
The condition results in severe cardiorespiratory collapse and usually a
coagulopathy.
Cardiorespiratory collapse is the result of entry large amount of amniotic fluid
into the maternal circulation and characterized by severe pain in the chest, cough,
feeling of the death. The most common presentation is that of sudden dyspnea and
hypotension commonly followed within minutes by cardiorespiratory arrest. Heart
fibrillation and sudden death are the results of this disorder. In 10 % to 20 % of cases,
these initial events accompanied by seizure activity. In 70 % of cases, a chest
radiography reveals some degree of pulmonary edema. One half of the patients with
AFE die within 1 hour after the onset of symptoms; in survivors, neurologic damage
or brain death secondary to the initial severe hypoxia is not uncommon..
In the case of entering of small number of amniotic fluid into the maternal
circulation disseminated intravascular coagulopathy is common.
The definitive diagnosis of AFE has classically been made at autopsy with the
demonstration of fetal squamosus cells, mucin, hair, or vernix in the pulmonary
artery vasculature.
 Treatment is directed toward total support of the cardiovascular and
coagulation systems and include:
I. 1. Assisted pulmonary ventilation, oxygen therapy, closed chest massage.
Intravenous 10 % 10,0 ml Calcii chloridi and intracardiac 0.1 % - 0,5 ml adrenalin
hydrochloridi are indicated.
2. Sedative drugs: Droperidol – 4-5 ml intravenous, 20 % - 20, 0 ml
Natrii oxybuturate, 2, 0 ml Diazepame.
3. Spasmolytic agents are prescribed: Euphyllini – 2,4 % 10, 0 ml
intravenous, Nospani – 2 % - 4 ml, Papaverini hydrochloridi – 2 % - 4 ml.
4. Cardiovascular drugs: Corglyconi 0, 06 % - 0,5 ml or Strophantini – 0,05 %
- 0, 5 ml intravenous on 20 ml 10 % glucose.
5. Drugs that have been increasing arterial pressure and vascular tone:
hydrocortizone 250 mg, dopamine infusion.
6. Elimination of acute hypovolemia and metabolic acidosis, initial optimization of
cardiac preload: polyglucin 400 ml, Natrii hydrocarbonatis 200 ml intravenous.
7. Disseminated intravascular coagulopathy treatment.
II. Immediate delivery: by cesarean section or by forceps.

SEPTIC SHOCK
Septic shock is the result of entering of infective agents into the maternal
circulation in different obstetrics and gynecologic conditions. It is a serious
complication that requires aggressive management. Pregnancy is classically thought
to be a factor that predisposes a patient to septic shock. In obstetrics, septic abortion,
chorionamnionitis, pyelonephritis, and endometritis are the most common conditions
associated with septic shock.
Pathogenesis. Septic shock in obstetrics most commonly is associated with
infection caused by endotoxin-releasing gram-negative aerobic coliform organisms.
Endotoxin, a complex cell wall-associated lipopolysaccharide, is released into the
circulation at the time of bacterial death, resulting in multiple hemodynamic effects.
Early septic shock is a classic example of distributive shock, related to a
systemic maldistribution of relatively normal or even increased output. Clinical
findings include hypotension, fever, and chills. Initial hemodynamic findings include
decreased systemic vascular resistance and high normal or elevated cardiac output
The continued maldistribution of cardiac output leads to local tissue hypoxia and the
development of lactic acidosis and end-organ dysfunction. This decrease in systemic
vascular resistance is caused by the release of vasoactive substances as well as by
vascular endothelial cell injury, which promotes capillary plugging secondary to
complement induced leukocyte aggregation. These factors lead to increased
arteriovenous shunting.

These patients are acutely ill, with fevers of up to 39,5 0 C, general weakness,
tachycardia, severe pelvic and abdominal pain, and nausea and vomiting.
On physical examination patients may exhibit muscular guarding, and or
rebound tenderness. A purulent cervical discharge is often seen and uterus or adnexa
are usually moderately to exquisitely tender.
Such phases of septic shock have been distinguished as:
1. hyperdynamic or “warm” phase (systolic arterial blood pressure is
decreased to 80-90 mm. Hg durinh 1-2 hours);
2. hypodynamic or “cold” phase (continuous decreasing of arterial blood
pressure; shock’ index is more than 1,5; chest, abdominal, back pain;
oliguria, consciousness impairment, dyspnea; mulberry rash; skin
necrosis);
3. irreversible shock (anuria, respiratory and heart insufficiency, coma).
The treatment of septic shock in this early phase involves optimizing preload by
restoring relative intravascular volume with crystalloid infusion as well as aggressive
treating the underlying infection. If the offending organism is known, single-agent
antibiotic therapy may be used. More commonly in obstetrics, the infection is
polymicrobial, and broad-spectrum coverage for gram-negative and gram-positive
aerobic and anaerobic organisms is most appropriate.. If an abscess is involved,
prompt surgical drainage after initial resuscitation is mandatory.
If the process should continue, the patient may enter a second hemodynamic
phase of septic shock. Of primary importance in this late phase is the development
and progression of myocardial dysfunction leading to ventricular failure.
 Patients who recover from the initial hemodynamic instability of septic shock
may suffer prolonged morbidity secondary to endotoxin-mediated pulmonary
capillary injury and noncardiogenic pulmonary capillary edema. Such lung failure is
a major cause of death in patients with septic shock. Similarly, pregnant patients
whose hypotension was prolonged may experience acute tubular necrosis. Endotoxin-
mediated endothelial cell injury and associated tyhromboplastin-like activity as well
as prolonged shock from any cause may also lead to activation of the coagulation
cascade and a clinical picture of disseminated intravascular coagulation. Although the
use of high-dose corticosteroids has been advocated in the acute management of
septic shock, reports have failed to demonstrate a benefit from such therapy.
Aggressive therapy for patients with septic shock should be tailored the site of
infection and the individual patient. Hospitalized patients require high dose
intravenous antibiotic therapy with an antimicrobial spectrum that covers aerobic and
anaerobic organisms (Tienam – 1000 mg 4 times a day intravenous each 6 hours. Its
daily dose is 4 gram. Cyprinol – intravenous administration 400 mg twice a day).
Surgical intervention - hysterectomy should be performed immediately. Pulmonary
ventilation, disseminated intravascular coagulopathy elimination, normalization of
vascular tone, immunocorrection, detoxycation therapy have been prescribed.

ANAPHYLACTIC SHOCK
Anaphylactic shock is a allergic reaction of human organism as result of
bounding of different origin antigens with antibodies which are fixed on the cell
membranes. It is leading to cell’ membranes destruction and excessive entering into
the blood such substances as histamine, serotonin, acetylcholine, and some
substances of anaphylaxia. The last ones effect into the vessels and provoke arterial
blood pressure decreasing and , as result, development of hypovolemia and tissual
hypoxia. Human reaction should be general and local. Local reaction is characterized
by edema in the site of drug’ injection, its chills, and hyperemia (allergic
manifestation after drug’s administration). General reaction is manifested by
respiratory, cardiovascular disorders.
 Such forms of anaphylactic shock have been distinguished as typical,
hemodynamics, asphyxial, cerebral, and abdominal.
The management of the patients with anaphylactic shock consists of medicines
that have been eliminated cardiovascular, respiratory, epileptic disorders, antyallergic
drugs.
The urgent care in the case of anaphylactic shock include:
1. Intravenous administration of adrenalini hydrochloridu 0.1 % - 1, 0.
In cardiac arrest – this drug is injected intracardiac.
2. Injection in the place of allergen’ entering adrenalini hydrtochloridi also.
3. The place above the allergic drug injection should be pressed obligatory.
3. For elimination respiratory disorders (asphyxia) intravenous (or
intramuscular) administration of Cordiamine 4 ml, Coffeini benzoate Natrii – 10 %
- 10. 0 ml, Euphylline – 2,4 % - 10, 0 ml have been prescribed.
4. Cortycosteroids are very effective for allergic manifestations elimination.
Prednizolone in the dose 0,005 g/kg intravenous, Dexamatazone – 0,02 g
intravenous, Hydrocortizone – 0,5 g into 0,9 % Nacl have been prescribed.
4. Antyhistaminic drugs are indicated also – Diphynylhydramine hydrochloride
– 1, 0 % - 5 ml, Suprastin – 2-6 ml 2 % intravenous or intramuscular.
5. Epileptic state is eliminated by intravenous administration of Aminazine – 2,5
% - 2 ml or Sibazone – 0,5 % - 2-4 ml.
Introduction of detoxycative, hypoallergenic, dehydrative drugs and
glucocorticoids is prescribed during 8-10 days after anaphylactic reaction.

Hemorrhagic shock.DIC-syndrome. Terminal states in

obstetrics.
Prepared by I. Kuziv
Shock encompasses various pathophysiological aberrations that lead to
inadequate tissue perfusion and impaired cellular metabolism. Although hypotension
often is the most obvious clinical sign in shock of any cause, such blood pressure
changes are the final common manifestation of a number of distinct pathologic
processes. The successful clinical management of patients in shock depends on the
proper definition of the underlying pathophysiology as well as an under of the unique
effects of pregnancy on such conditions.
Uterine bleeding (hemorrhage) during labor and early puerperal stage play an
important role among different kinds of severe obstetrics pathology, such as
hemorrhagic shock, disseminated intravascular coagulopathy, sepsis and other.
Uterine bleeding is the leading cause of maternal death.
Uterine bleeding frequency is 8,0 – 11, 0 %.
The main causes of uterine bleeding are:
During pregnancy: placenta praevia, placenta abruptio.
During labor: placenta praevia, placenta abruptio, uterine rupture, traumatization
of the soft birth canal tissues.
In the third period of labor and early puerperal stage: uterine hypo- and atony;
uterine rupture and traumatization of the soft birth canal tissues; placenta accreta,
increta, and percreta; retention of some parts of afterbirth in the uterine cavity;
thrombohemorrhagic bleeding.
Methods of blood loss determination
4. Libov’s method.
After surgical intervention the napkins, which are filling by blood, should be
weighted.
Blood loss volume = Weight x 15 % ( if blood loss is < 1000
ml); 2
Blood loss volume = Weight x 30 % ( if blood loss is > 1000 ml).
2
5. By hematocrit
Hematocr Blood
it, % loss
volume,
ml
44–40 500
38–32 1000
 30 – 22 1500
<22 >
1500
6. Algover’s index
Shock’ index = Heart rate
Systolic arterial blood pressure
In normal Algover’s index is < 1.
Algov Blood loss
er’s index volume, %
out of
circulating
blood volume
0,8 10 %
and <
0,9– 20%
1,2

1,3– 30%

1,4
1,5 40 %
and >

HEMORRHAGIC (HYPOVOLEMIC) SHOCK

Hemorrhagic shock is a very serious complication in the case of pathological
hemorrhage.
Physiological blood loss during labor is 0, 5 % out of puerperant’ weight.
Physiological blood loss is 350, 0 – 400, 0 ml.in the puerperant with 70-75 kg of
weight. If blood loss predominate physiological one, hemorrhagic shock have been
occurred.
There are 4 stages of hemorrhagic shock according to Baker classification.
Evaluation of hemorrhagic shock stage severity is presented in the table.
Evaluation of hemorrhagic shock stage severity
Shock Hypovolemia Circulating Blood loss, % from body weight Hemodynamic
stage stage blood ml diuresis
volume
deficiency
I Mild 10 %-20% 500 – 1,0 – 1,5 % Ps – 90-100 be
1000,0 Arterial blood
Central Venou
Diuresis – N.
II Moderate 20%-30% 1000,0- 1,5 - Ps – 120 beats
1500,0 2,0 % BP - <100 mm
CVP – <60 m
Diuresis – < 5
III Severe 30%-40% 1500,0– 2,0 – Ps – 140 beats
2000,0 2,5 % BP - <70 mm
CVP – <40 m
Diuresis – < 3
IV Considerable 40% and > 2000,0 and > > Ps – 140 beats
2,5 % BP – <50 mm
CVP – 0;
Diuresis– anur

The main principles of obstetrics hemorrhage and hemorrhagic

shock treatment:
11. Hemorrhage stopping.
12. Determination of blood loss stage.
13.Restoration of the circulating blood volume.
14.Normalization of vascular tone.
15.Blood reology, its structural, biochemical, and electrolytes compounds
correction.
16. Detoxication therapy.
17. Desensibilizing therapy.
 18.Correction of clotting, antyclotting, fibrinolitic systems functions.
19.Regulation of the main human organs functions.
20.Prevention of infectious complications.
INTERM restoration of the circulating blood volume – is the main step in the
treatment of acute blood loss. Human organism should be survived in the case of 2/3-
erythrocytes volume loss, but it doesn’t survive in the case of 1/3 plasma volume
loss. That’s why it should be remembered that in considerable blood loss the first step
is the transfusion not only blood, but also кровозамінники, which eliminate
hypovolemia very quickly.
Transfusion therapy in obstetrics hemorrhages

Blood Volume Crysta- Refortan, Erythro

loss of infusion lloids Gelofusin Fresh- Albumin -

Stabisol frozen (10-20 massa

plasma %)
10-20 10-15 10 ml /kg
% 2500 ml/ - -

500- ml kg
1000ml
20-30 10 ml 10 ml /kg
% 3000 /kg 5-10 - 5 ml /kg
ml /kg
1000- ml
1500
ml
30-40 7 ml/kg 7 ml/kg
% 4000 10 - 200 ml 10-20
1500- ml 15 ml /kg ml /kg

2000
ml
40- 7 ml/kg 10 ml /kg
and > > 6000 15 - 200 ml 30 ml
> ml 20 ml /kg /kg
2000 ml

The volume of infusion therapy in hemorrhagic shock should be predominated

in 1,5-2,5 times its real blood loss.
Glucose transfusion doesn’t administrated in blood loss, because it very quickly
enter intracellular space and doesn’t increase circulating blood volume, it caused
metabolic acidosis.
Attention! Erythrocyte transfusion has value only after hemodynamics and
peripheral blood circulation normalization. Only in these conditions erythrocytes
should be taken oxygen.
Attention ! In all stages of hemorrhagic shock 2-4 veins should be catheterized
in one moment (one or two of them are central, such as v. subclavia).
Infusion speed depends on blood loss volume and patient state. In the case of
hemorrhagic shock and low arterial blood pressure it should be reach 200 ml per
minute. The infusion speed gradually decreased to 150-100-50 ml-per minute in the
case of increasing arterial blood pressure to 80-90 mm Hg.
The main prescription of infusion therapy in the case of acute blood lose is the
stabilization of central hemodynamics which lead to cerebral and coronary blood
circulation stabilization.
Vascular tone normalization.
In the first stage of hemorrhagic shock because of vascular spasm presence
spasmolitics drugs are used, such as Nospani, Papaverinihydrochloridi. On the II-III-
IV stages because of vascular dilation glucocorticoids are prescribed. They are:
Prednisoloni, Hydrocortisone – in the dose 1,5-2 g/ daily, Dexametazoni.
If intravenous insertion 800-1000 ml any solution with the speed of 50-100
ml/per minute doesn’t change (increase) arterial blood pressure – vasopressors agents
should be prescribed, such as Remestip – in the dose 0,2-1,0 mg; Dopamine –
5mkg/kg/minute or glucocrticoids.
In considerable infusion therapy after circulating blood volume normalization
diuresis stimulation is recommended. For this purpose Euphillini in the dose 3 mh per
kg, lazix – 2-4 mg/kg or furosemidi in the dose 6-8 mg/kg have been used.
 Structural, biochemical, electrolytes compounds correction of blood,
detoxycation, desensibilizing therapy and normalization of clotting, antyclotting,
fibrinolytic systems functions and functions of the main human organs is obligatory
in the treatment of hemorrhagic shock.
Introduction of cardiologic drugs is possible only after blood loss restoration.
For this purpose such agents have been used as Corgliconi –0, 6 % - 0,5 –1 ml;
Cocarboxylase – 50 mg twice a day.
Prevention of infectious complications by prescription of wide spectrum
antibiotics (cefalosporines, aminoglycozides) in the daily dose is recommended also.

Main steps of urgent medical care in the obstetrics bleeding

during pregnancy, labor, and puerperal stage
4. Blood loss is 0, 8 – 1, 0 % of body weight
1. To determine the cause of hemorrhage

Pla Uterine Uterine

centa cervix hypo- and
praevia, rupture, deep atony; uterine
placenta vagival rupture and
abruptio, ruptures, traumatization
uterine traumatization of the soft
rupture of the soft birth canal
birth canal tissues;
tissues. placenta
accreta,
increta, and
percreta;
retention of
some parts of
afterbirth in
the uterine
 cavity

Bleeding stopping

Urgent Rupture Manual

cesarean suture uterine
section revision

2. To start intravenous infusion: crystalloids (0,9 % NaCl + 10

Units of oxytocin), colloids – Refortan, Stabisol, Poliglucin.

5. Blood loss is 1, 0 %– 1, 5 % of body weight.

1. Injection of 250 – 1000 mkgProstin F2a intramuscularly or 0,4 mg
Remestip + 10 ml 0,9 % NaCl into uterine cervix.

2. Catheterization of two veins (one of them is v. subclavia), intravenous

transfusion of autoblood, plasma, erythrocyte massa, Refortan, Stabisol.

Attention! Surgical intervention should be performed in continuing

bleeding! (if blood loss is more than 1, 0 % - 800 ml of body weight ).

6. Blood loss is > 1, 5 % of body weight.

1. Laparotomy. Total hysterectomy without adnexa (adnexa are removed
if inflammatory, degenerative changes are presented).

2. Restoration of the blood circulating volume: autoblood, donor’s blood – 100

% from blood loss, cryoprecipitate, albumin.
DISSEMINATED INTRAVASCULAR COAGULOPATHY (DIC)
DIC is not a distinct clinical entity; rather, it represents a manifestation of
various disease processes that have in common activation of intravascular clotting
and fibrinolysis, resulting in excess consumption of solutable coagulation
components. In obstetrics, secondary fibrinogenolysis commonly dominates the
clotting aberration and results in the circulation of fibrin and fibrinolytic split
products, which further accentuates the clinical presentation of henorrhage. In
addition, sometimes a dilutional coagulopathy is encountered in pregnancy. This
condition obtains when massive hemorrhage is teplaced only by red blood cells and
crystalloids solution, resulting in a dilutional depletion of platelets and soluble
clotting factors.. In practice, the hemorrhage associated with dilutional coagulopathy
often results in hypotension and shock. The tissue hypoxia that accompanies shock of
any cause is well known to potentially activate the coagulation-fibrinolysis cycle
associated with DIC.
DIC is the pathological complex, which is characterized by blood clotting that
has been leading to microcirculation blockade by fibrin in the main human organs
(lungs, kidneys, liver). Dysfunction of these organs is the result of their damage. In
the end of this process thrombohemorrhagic disorders have been developed.
The main causes of DIC in the obstetrics are:
14.All kinds of shock (hemorrhagic, septic, anaphylactic);
15.Placenta abruption;
16. Embolic fluid embolism;
17. OPH – hestosis;
18. Hypotonic bleeding;
19. Uterine ruptures;
20. Excessive labor induction;
21. Cesarean section;
22.Extragenital pathology;
23.Septic abortion;
24.Puerperal endometritis;
25.Intensive uterine massage;
26.dead fetus syndrome
Classification of thrombohemorrhagic syndrome
3. By clinical duration:
1. Acute;
 2. Subacute;
3. Chronic.
4. By stages:
I stage – hypercoagulation;
II stage – hypocoagulation without generalizing fibrinolysis
activation; III stage – hypocoagulation with generalizing
fibrinolysis activation; IV stage – total fibronolysis.
Clinical manifestatiuon.
Clinical manifestation of DIC is connected with ischemic and
hemorrhagic changes in human organs and tissues. They are:
6. Hemorrhages into skin and mucous membranes;
7. Hemorrhages from the places of injections, incisions, uterus.
8. Necrosis of some areas of skin and mucous membranes;
9. Central nervous system impairment;
10. Acute renal, liver, lung insufficiency.

Laboratory diagnosis of DIC

The main laboratory data
Blood Spontaneous Thrombin Throm- Thrombin
Stages clotting thrombus test bocytes time,
time, lisis number, seconds
minutes 10x9/l
I.Hypercoagulation <5(N) absent (N) 7-11 (N) 175-425 < 24
(N)
II.Hypocoagulation 5 -12 absent 7-11 < 120 >60
without
generalizing
fibrinolysis

III Hypocoagu- >12 quick 20-60 < 100 >100

lation with
 generalizing
fibrinolysis
IV. Total > 60 Thrombus >60 <60 >180
fibrinolysis doesn’t
formed

General principles of DIC treatment are:

6. Heparin, fibrinogen are contraindicated in all stages of
thrombohemorrhagic syndrome.
7. Proteolytic enzymes inhibitors in the dose of 10 mg/kg/hour have been used
for inhibit excessive fibrinolysis and prevention of intracellular clotting.
8. Early and quick introduction of fresh frozen donor’s plasma. The main aim of
its usage is the restoration of haemostatic potential of blood (it contains all soluble
clotting factors, similar to whole blood). It has been used in all stages of
thrombohemorrhagic syndrome. Initially the dose of intravenous introduction is 6-12
ml/kg. After it dose is 300-400 ml each 6-8 hours.
9. Stimulation of vascular-thrombocytes link of hemostasis (dicinone, etamsilat). 10.
Transamacha acid usage – in the dose 500-750 mg on 0,9 % NaCl. This medicine
inhibits plasmine activity, stabilizes coagulate factors and fibrin, decreases
vascular permeability and gives permanent hemostatic action, which have been
prevented fibrinogen degradation.
Treatment of thrombhemorrhagic syndrome in obstetric hemorrhagic
shock in different stages
Stages Treatment
I.Hypercoagulation For normalization blood reology: Trental – 100mg on
100 ml 0,9 % NaCl, Curantill – 0,5 – 2, %
II.Hypocoagulation without Procoagulants: fresh frozen plasma 500,0, blood of 3-
generalizing fibrinolysis 5 days of conservation. Transamacha – antyplasmin
drug – 500-750 mg on 0, 9 % NaCl.
Fibrinolysis inhibitors: Contrical in the dose 10-
20.000 units/ daily dose 100-200.000 units; Trasilol –

III Hypocoagulation with
generalizing fibrinolysis
IV. Total fibrinolysis
40.000 units or Gordox – 100-200.000 units.
Cortycosteroids – Prednisolone – 10mg/kg/hour or
Hydrocortisone – 100 mg/kg.
Proteolytic enzymes inhibitors:Contrycal 40.000 units
(daily dose 500.000 units)
Procoagulants – fresh frozen plasma, blood, albumin.
Cortycosteroids.Cryoprecipitate–200-400,0,
Transamcha – 500-700 mg.
The treatment should be started from the large doses
of proteolytic enzymes inhibitors – Contrical 100.000
units to 500.000 units. Blood, albumin, plasma,
cryoprecipitate, cortycosteroids.

AMNIOTIC FLUID EMBOLISM (AFE)

Amniotic fluid embolism is a rare, sudden, and often fatal obstetric
complication caused by entry of amniotic fluid into the maternal venous circulation.
The initial physiological disturbances involve profound alterations in
hemodynamics and oxygenation, often followed by the development of a
consumptive coagulopathy.
The main pathogenetical factors that have been predisposing to amniotic fluid
embolism are predomination of amniotic pressure over venous and traumatization of
venous uterine vessels.
Predomination of amniotic pressure over venous is presented in excessive labor
contractions, breach presentation, postdate pregnancy, multiple pregnancy, uterine
cervix dystocia, hypovolemia of different etiology.
Traumatization of venous uterine vessels is presented in placenta abruption,
cesarean section, manual removal of placenta, puerperal hypotonic hemorrhage.

Clinical manifestation
The condition results in severe cardiorespiratory collapse and usually a
coagulopathy.
 Cardiorespiratory collapse is the result of entry large amount of amniotic fluid
into the maternal circulation and characterized by severe pain in the chest, cough,
feeling of the death. The most common presentation is that of sudden dyspnea and
hypotension commonly followed within minutes by cardiorespiratory arrest. Heart
fibrillation and sudden death are the results of this disorder. In 10 % to 20 % of cases,
these initial events accompanied by seizure activity. In 70 % of cases, a chest
radiography reveals some degree of pulmonary edema. One half of the patients with
AFE die within 1 hour after the onset of symptoms; in survivors, neurologic damage
or brain death secondary to the initial severe hypoxia is not uncommon..
In the case of entering of small number of amniotic fluid into the maternal
circulation disseminated intravascular coagulopathy is common.
The definitive diagnosis of AFE has classically been made at autopsy with the
demonstration of fetal squamosus cells, mucin, hair, or vernix in the pulmonary
artery vasculature.
Treatmentis directed toward total support of the cardiovascular and coagulation
systems and include:
I. 1. Assisted pulmonary ventilation, oxygen therapy, closed chest massage.
Intravenous 10 % 10,0 ml Calciichloridi and intracardiac 0.1 % - 0,5 ml adrenalin
hydrochloridi are indicated.
2. Sedative drugs: Droperidol – 4-5 ml intravenous, 20 % - 20, 0
ml Natriioxybuturate, 2, 0 ml Diazepame.
3. Spasmolytic agents are prescribed: Euphyllini – 2,4 % 10, 0 ml
intravenous, Nospani – 2 % - 4 ml, Papaverinihydrochloridi – 2 % - 4 ml.
4. Cardiovascular drugs: Corglyconi 0, 06 % - 0,5 ml or Strophantini – 0,05 %
- 0, 5 ml intravenous on 20 ml 10 % glucose.
5. Drugs that have been increasing arterial pressure and vascular tone:
hydrocortizone 250 mg, dopamine infusion.
6. Elimination of acute hypovolemia and metabolic acidosis, initial optimization of
cardiac preload: polyglucin 400 ml, Natriihydrocarbonatis 200 ml intravenous.
7. Disseminated intravascular coagulopathy treatment.
II. Immediate delivery: by cesarean section or by forceps.
 SEPTIC SHOCK
Septic shock is the result of entering of infective agents into the maternal
circulation in different obstetrics and gynecologic conditions. It is a serious
complication that requires aggressive management. Pregnancy is classically thought
to be a factor that predisposes a patient to septic shock. In obstetrics, septic abortion,
chorionamnionitis, pyelonephritis, and endometritis are the most common conditions
associated with septic shock.
Pathogenesis. Septic shock in obstetrics most commonly is associated with
infection caused by endotoxin-releasing gram-negative aerobic coliform organisms.
Endotoxin, a complex cell wall-associated lipopolysaccharide, is released into the
circulation at the time of bacterial death, resulting in multiple hemodynamic effects.
Early septic shock is a classic example of distributive shock, related to a
systemic maldistribution of relatively normal or even increased output. Clinical
findings include hypotension, fever, and chills. Initial hemodynamic findings include
decreased systemic vascular resistance and high normal or elevated cardiac output
The continued maldistribution of cardiac output leads to local tissue hypoxia and the
development of lactic acidosis and end-organ dysfunction. This decrease in systemic
vascular resistance is caused by the release of vasoactive substances as well as by
vascular endothelial cell injury, which promotes capillary plugging secondary to
complement induced leukocyte aggregation. These factors lead to increased
arteriovenous shunting.

These patients are acutely ill, with fevers of up to 39,50 C, general weakness,
tachycardia, severe pelvic and abdominal pain, and nausea and vomiting.
On physical examination patients may exhibit muscular guarding, and or
rebound tenderness. A purulent cervical discharge is often seen and uterus or adnexa
are usually moderately to exquisitely tender.
Such phases of septic shock have been distinguished as:
4. hyperdynamic or “warm” phase (systolic arterial blood pressure is
decreased to 80-90 mm. Hg durinh 1-2 hours);
 5. hypodynamic or “cold” phase (continuous decreasing of arterial blood
pressure; shock’ index is more than 1,5; chest, abdominal, back pain;
oliguria, consciousness impairment, dyspnea; mulberry rash; skin
necrosis);
6. irreversible shock (anuria, respiratory and heart insufficiency, coma).
The treatment of septic shock in this early phase involves optimizing preload by
restoring relative intravascular volume with crystalloid infusion as well as aggressive
treating the underlying infection. If the offending organism is known, single-agent
antibiotic therapy may be used. More commonly in obstetrics, the infection is
polymicrobial, and broad-spectrum coverage for gram-negative and gram-positive
aerobic and anaerobic organisms is most appropriate.. If an abscess is involved,
prompt surgical drainage after initial resuscitation is mandatory.
If the process should continue, the patient may enter a second hemodynamic
phase of septic shock. Of primary importance in this late phase is the development
and progression of myocardial dysfunction leading to ventricular failure.
Patients who recover from the initial hemodynamic instability of septic shock
may suffer prolonged morbidity secondary to endotoxin-mediated pulmonary
capillary injury and noncardiogenic pulmonary capillary edema. Such lung failure is
a major cause of death in patients with septic shock. Similarly, pregnant patients
whose hypotension was prolonged may experience acute tubular necrosis. Endotoxin-
mediated endothelial cell injury and associated tyhromboplastin-like activity as well
as prolonged shock from any cause may also lead to activation of the coagulation
cascade and a clinical picture of disseminated intravascular coagulation. Although the
use of high-dose corticosteroids has been advocated in the acute management of
septic shock, reports have failed to demonstrate a benefit from such therapy.
Aggressive therapy for patients with septic shock should be tailored the site of
infection and the individual patient. Hospitalized patients require high dose
intravenous antibiotic therapy with an antimicrobial spectrum that covers aerobic and
anaerobic organisms (Tienam – 1000 mg 4 times a day intravenous each 6 hours. Its
daily dose is 4 gram. Cyprinol – intravenous administration 400 mg twice a day).
Surgical intervention - hysterectomy should be performed immediately. Pulmonary
ventilation, disseminated intravascular coagulopathy elimination, normalization of
vascular tone, immunocorrection, detoxycation therapy have been prescribed.

ANAPHYLACTIC SHOCK
Anaphylactic shock is a allergic reaction of human organism as result of
bounding of different origin antigens with antibodies which are fixed on the cell
membranes. It is leading to cell’ membranes destruction and excessive entering into
the blood such substances as histamine, serotonin, acetylcholine, and some
substances of anaphylaxia. The last ones effect into the vessels and provoke arterial
blood pressure decreasing and , as result, development of hypovolemia and tissual
hypoxia. Human reaction should be general and local. Local reaction is characterized
by edema in the site of drug’ injection, its chills, and hyperemia (allergic
manifestation after drug’s administration). General reaction is manifested by
respiratory, cardiovascular disorders.
Such forms of anaphylactic shock have been distinguished as typical,
hemodynamics, asphyxial, cerebral, and abdominal.
The management of the patients with anaphylactic shock consists of medicines
that have been eliminated cardiovascular, respiratory, epileptic disorders, antyallergic
drugs.
The urgent care in the case of anaphylactic shock include:
1. Intravenous administration of adrenalinihydrochloridu 0.1 % - 1, 0. In cardiac
arrest – this drug is injected intracardiac.
2. Injection in the place of allergen’ entering adrenalinihydrtochloridi also.
3. The place above the allergic drug injection should be pressed obligatory.
3. For elimination respiratory disorders (asphyxia) intravenous (or
intramuscular) administration of Cordiamine 4 ml, Coffeini benzoate Natrii – 10 % -
10. 0 ml, Euphylline – 2,4 % - 10, 0 ml have been prescribed.
4. Cortycosteroids are very effective for allergic manifestations elimination.
Prednizolone in the dose 0,005 g/kg intravenous, Dexamatazone – 0,02 g
intravenous, Hydrocortizone – 0,5 g into 0,9 % Nacl have been prescribed.
 4. Antyhistaminic drugs are indicated also – Diphynylhydramine hydrochloride
– 1, 0 % - 5 ml, Suprastin – 2-6 ml 2 % intravenous or intramuscular.
5. Epileptic state is eliminated by intravenous administration of Aminazine – 2,5
% - 2 ml or Sibazone – 0,5 % - 2-4 ml.
Introduction of detoxycative, hypoallergenic, dehydrative drugs and
glucocorticoids is prescribed during 8-10 days after anaphylactic reaction.

HEMORRHAGE IN THE SECOND HALF OF PREGNANCY

An estimated 5 % of women describe bleeding of some extent during pregnancy.
At times, the amount of bleeding is hardly more than "spotting," whereas at other
times profuse hemorrhage can lead to maternal death in a very short time. In most
cases, antepartum bleeding is minimal spotting, often following sexual intercourse,
and is thought to be related to trauma to the friable ectocervix.
The main causes of bleeding in the second half of pregnancy are:
Vulva
Varicose veins
Tears or lacerations
Vagina
Tears or lacerations
Cervix
Polyp
Glandular tissue (normal)
Cervicitis
Carcinoma Intrauterine
Placenta previa
Abruptio placentae
Vasa previa
A previous Pap test and examination of the lower genital tract should eliminate
the likelihood of lower genital tract neoplasms in most cases. At times, patients may
mistake bleeding from hemorrhoids or even hematuria for vaginal bleeding, but the
difference is easily distinguished by examination.
The two causes of hemorrhage in the second half of pregnancy that require
greatest attention, because of the associated maternal and fetal morbidity and
mortality rates, are placenta previaand abruptio placentae. Various characteristics of
these entities are compared in Table.
Differential characteristics between placenta previaand abruptio placentae
Characteristics Placenta previa Abruptio Placenta
Magnitudeofbloodloss Variable Variable
Duration Often ceases within 1-2 Usually continues
hours
Abdominal discomfort None Can be severe
Absent Tachycardia, then
Fetal heart rate pattern
bradycardia; loss of
on electronic monitoring
variability; decelerations
frequently
present; intrauterine
demise not rare
Coagulation defects Rare Associated, but
infrequent; DIG often
severe when present
Cocaine use
Associated history None Abdominal trauma;
maternal hypertension;
multiple gestation;
polyhydramnios

PLACENTA PREVIA

Placenta previa refers to an abnormal location of the placenta over, or in

close proximity to, the internal cervical os. Placenta previa can be categorized as:
5. complete or total - if the entire cervical os is covered (Fig. 1);

6. partial - if the margin of the placenta extends across part but not all of the
internal os (Fig. 2);
7. marginal , if the edge of the placenta lies adjacent to the internal os;

8. low lying - if the placenta is located near but not directly adjacent to the
internal os.

Fig. 1 Total placenta previa

 Fig. 2 Partial placental previa

The etiology of placentaprevia is not understood, but abnormal vascularization

has long been proposed as a mechanism for this abnormal placement of the placenta.
In some cases, such as in twin pregnancy or if it is hydropic, the placenta may extend
to the region of the internal cervical os because of its size alone. Increasing maternal
age, increasing parity, and previous cesarean delivery are factors commonly
associated with placenta previa, although recent evidence suggests that age alone is
not an important factor.

The incidence of placenta previa varies with gestational age, usually reported
overall as approximately 1 in 250 pregnancies. There is great variation in incidence,
however, with parity. The incidence in nulliparasis only 1 in 1000 to 1500, whereas
that in grandmultiparas is as high as 1 in 20. Women with the highest risk for
placenta previa are grandmultiparas, those who have had a previous placenta previa
(4% to 8%), and those who have had four or more cesarean sections. With common
use of ultrasonography examinations, it has been shown repeatedly that the placenta
may cover the internal cervical os in approximately 5% of pregnancies when
examined at midpregnancy, a finding seen even more frequently earlier in gestation.
Because of subsequent growth of both the upper and lower uterine segments, the
placenta appears to "migrate" away from the internal os in the majority of cases. The
likelihood of this apparent movement diminishes as the gestational age at first
detection increases.

Clinical findings and Diagnosis.The average gestational age at the time of the
first bleeding episode is 29 to 30 weeks. Although the bleeding may be substantial,
it almost always ceases spontaneously, unless digital examination or other trauma
occurs. The bleeding is caused by separation of part of the placenta from the lower
uterine segment and cervix, possibly in response to mild uterine contractions. The
blood that is lost is usually maternal in origin. The patient often describes a sudden
onset of bleeding without any apparent antecedent signs. There is no pain associ-
ated with placenta previa in most cases, unless coincident with labor or with an
abruptio placenta (approximately 5% to 10% of cases).
Frequently, bleeding from placenta previa has its onset without warning,
presenting without pain in a woman who has had an uneventful prenatal course.
Fortunately, the initial bleeding is rarely so profuse as to prove fatal. Usually it ceases
spontaneously, only to recur. In some cases, particularly those with a placenta
implanted near but not over the cervical os, bleeding does not appear until the onset
of labor, when it may vary from slight to profuse hemorrhage and may clinically
mimic placental abruption.

The cause of hemorrhage is reemphasized. When the placenta is located over the
internal os, the formation of the lower uterine segment and the dilatation of the
internal os result inevitably in tearing of placental attachments. The bleeding is
augmented by the inability of the myometrial fibers of the lower uterine segment to
contract and thereby constrict the torn vessels.
 Hemorrhage from the placental implantation site in the lower uterine segment
may continue after delivery of the placenta, because the lower uterine segment is
more prone to contract poorly than is the uterine body. Bleeding may also result from
lacerations in the friable cervix and lower uterine segment, especially following
manual removal of a somewhat adherent placenta.

Diagnosis

In women with uterine bleeding during the latter half of pregnancy, placenta
previa or abruptio placentae should always be suspected. The possibility of placenta
previa should not be dismissed until appropriate evaluation, including sonography,
has clearly proved its absence. The diagnosis of placenta previa can seldom be
established firmly by clinical examination unless a finger is passed through the cervix
and the placenta is palpated. Such examination of the cervix is never permissible
unless the woman is in an operating room with all the preparations for
immediate cesarean section, because even the gentlest examination of this sort
can cause torrential hemorrhage. Furthermore, such an examination should not be
made unless delivery is planned, for it may cause bleeding of such a degree that
immediate delivery becomes necessary even though the fetus is immature. Today,
however, such a “double set-up” examination is rarely necessary, as placental
location can almost always be obtained by careful sonography.

Ultrasonography has been of enormous benefit in localizing the placenta,

especially when the placenta is anterior or lateral. If the placenta lies in the posterior
portion of the lower uterine segment, its exact relation with the internal os may be
more difficult to ascertain. In most cases, though, ultrasonography examination can
accurately diagnose placenta previaor, by illustrating the placenta location away from
the cervix and lower uterine segment, exclude it as a cause for bleeding. In some
instances, transvaginal ultrasonography may be a useful adjunctto the
transabdominalapproach, especially in the case of posterior placenta.
 Double setup examination can confirm the diagnosis of placenta previa. It
involves careful evaluation of the cervix in the operating room with full preparations
for rapid cesarean delivery.

Management

Includes initial hospitalization with hemodynamic stabilization, followed by

expectant management until fetal maturity has occurred. Ideal expectant
management would be continuous hospitalization with enforced bed rest and
immediate access to emergency care.

In the complete placenta previa – cesarean section in full term pregnancy. In the
case of low lying, marginal and partial placenta previa and full term pregnancy, when
blood loss is less than 250 ml – amniotomy with the following prescription of
contractile drugs. If blood loss is more than 250 ml – cesarean section.

The number of bleeding episodes is unrelated to the degree of placenta previa or

to the prognosis for fetal survival. Such expectant management combined with
appropriate use of blood transfusion and cesarean birth have resulted in the lowering
of the maternal mortality rate from !25%-30% to < 1% and the perinatal mortality
rate from 60%-70% to < 10%. If the fetus is thought to be mature by gestational
criteria or by amniocentesis for fetal lung maturity testing, there is little benefit to be
gained by a delay in delivery. The further from term that bleeding from placenta
previa occurs, the more important it is to delay delivery to allow for further fetal
growth and maturation. The degree of bleeding and the maturity of the fetus must be
constantly weighed in managing these patients. Fetal maturity is usually assessed at
approximately 36 weeks, with cesarean delivery performed once the fetus is deemed
mature.
In some cases, when the location of the placenta cannot be accurately determined
by ultrasound and delivery is required, the route of delivery is determined by a
double setup examination. This procedure involves careful evaluation of the cervix in
the oper-ating room with full preparations for rapid cesarean delivery.
 Localization by Sonography. The simplest, most precise, and safest method of
placental localization is provided by transabdominalsonography, which is used to
locate the placenta with considerable accuracy (Figs. 3, and 4 ).

Fig. 3 Partial anterior placenta previa at 36 weeks’ gestation. Placenta (P) extends
anteriorly and downward toward cervix (Cx). Fetus (F), amnionic fluid (AF), and
bladder (B) are seen. (Courtesy of Dr. R. Santos.)
 Fig. 4 Total placenta previa at 34 weeks’ gestation. Placenta (P) completely
overlies cervix (Cx). Bladder (B) and amnionic fluid (AF) are also visualized clearly.
(Courtesy of Dr. R. Santos.)
The average accuracy is about 95 percent, and rates as high as 98 percent have been
obtained. False-positive results are often a result of bladder distention. Therefore,
ultrasonic scans in apparently positive cases should be repeated after emptying the
bladder. Another source of error has been identification of abundant placenta implanted
in the uterine fundus but failure to appreciate that the placenta was large and extended
downward all the way to the internal os of the cervix. This, however is uncommon.
Farine and associates (1988) reported that the use of transvaginal ultrasonography
has substantively improved diagnostic accuracy of placenta previa. They were able to
visualize the internal cervical os in all cases with the transvaginal technique, in contrast
to only 70 percent using transabdominal equipment. An example is shown in Figure 5.
 Fig. 5 Transvaginal ultrasonic scan at 34 weeks’ gestation. Cervical canal is clearly
visible (CX) and distance from internal os to placental edge, measured between calipers
(X) is 0.75 cm. The patient was delivered by cesarean section 4 weeks later because
of vaginal bleeding. (P = placenta; B = bladder.) (Reproduced, with permission, from
Oppenheimer LW, Farine D, Ritchie JWK, Lewinsky RM, Telford J, Fairbanks LA.
What is a low-lying placenta? Am J Obstet Gynecol. 165:1035, 1991.)
Likewise, Leerentveld and colleagues (1990) studied 100 women suspected of
having placenta previa. They reported a 93 percent positive predictive value and 98
percent negative predictive value for transvaginal ultrasonography. Hertzberg and
associates (1992) demonstrated that transperinealsonography allowed visualization of
the internal os in all 164 cases examined because transabdominalsonography
disclosed a previa or was inconclusive. Placenta previa was correctly excluded in 154
women, and in 10 in whom it was diagnosed sonographically, nine had a previa
confirmed at delivery.
Magnetic Resonance Imaging.
Preliminary investigation using magnetic resonance imaging to visualize placental

abnormalities, including placenta previa, have been reported by several groups. Kay and
Spritzer (1991) discussed the many positive attributes of such technology (Fig. 6). It
is unlikely that this will replace ultrasonic scanning for routine evaluation in the near
future.

Fig. 6 A sagittal T2-weighted (2000/80 ms) image of a patient with a posterior

marginal placenta previa. The arrowhead points to the placental edge and the arrow
indicates the internal os. (F = fetal head; P = placenta; B = maternal bladder.) (From
Kay HH, Spritzer CE.Preliminary experience with magnetic resonance imaging in
patients with third-trimester bleeding.Obstet Gynecol. 78:424, 1991.Reprinted with
permission from the AmericanCollege of Obstetricians and Gynecologists.)
Placental “Migration”
Since the report by King (1973), the apparent peripatetic nature of the placenta has
been well established. McClure and Dornal (1990) found a low-lying placenta in 25
percent of 1490 ultrasonic scans done at 18 weeks; however, at delivery, only 7 of these
385 low-lying placentas persisted. Sanderson and Milton (1991) found that only 12
percent of placentas were low lying in 4300 women surveyed ultrasonically at 18 to 20
weeks. Of those not covering the internal os, previa did not persist and hemorrhage was
not encountered. Conversely, of those covering the os at midpregnancy, about 40
percent persisted as a previa. Therefore, placentas that lie close to the internal
cervical os, but not over it, during the second trimester, or even early in the third
trimester, are very unlikely to persist as previas by term.
The low frequency with which placenta previa persists when it has been identified
sonographically before 30 weeks is shown in Table 32–4. It is apparent from these
data that in the absence of any other abnormality, sonography need not be frequently
repeated simply to follow placental position, and restriction of activity need not be
practiced unless the previa persists beyond 30 weeks, or becomes clinically apparent
before that time.
The mechanism of apparent placental movement is not completely understood.
The term migration is clearly a misnomer, however, as invasion of chorionic villi into
the decidua on either side of the cervical os will persist. The apparent movement of
the low-lying placenta relative to the internal os probably results from inability to
precisely define this relationship in a three-dimensional manner using two-
dimensional sonography in early pregnancy. This difficulty is coupled with
differential growth of lower and upper myometrial segments as pregnancy
progresses. Thus those placentas that “migrate” most likely never had actual
circumferential villus invasion that reached the internal cervical os in the first place.
If placental tissue is seen or palpated at the internal cervical os, prompt cesarean
delivery is performed. If the placental margin is away from the internal os, artificial
rupture of the membranes and oxytocin induction of labor may be performed in
anticipation of vaginal delivery. Before the widespread use of ultrasound, this
procedure was done more frequently than it is in modern obstetrics; nonetheless, it is
still an important tool in selected cases.
An attempt at vaginal delivery of a patient with placenta previa may be indicated if the
delivery can be accomplished with minimal blood loss and if the fetus is dead, has major
fetal malformations, or is clearly previable. If making such an attempt is appropriate,
ceasing the process and moving to cesarean delivery for a maternal indication must always
be considered. Placenta previa is associated with a nearly doubling of the rate of congenital
malformations, the most serious including major anomalies of the
central nervous system, gastrointestinal tract, cardiovascular system, and respiratory
tract. At the time of diagnosis of placenta previa, a detailed fetal survey should be
performed for anomalies.
Abnormal placental location can be further complicated by abnormal growth of the
placental mass into the substance of the uterus, a condition termed placenta previaaccreta.
In placenta previaaccreta, the poorly formed decidua of the lower uterine segment offers
little resistance to trophoblastic invasion. The incidence of this severe complication is
variously reported as 5% to 10% of placenta previas, although the incidence is much higher
in patients with multiple previous cesarean sections. At the time of delivery, sustained and
significant bleeding may ensue, often requiring hysterectomy.

ABRUPTIO PLACENTAE

Whereas placenta previa refers to the abnormal location of the placenta, abruptio
placentae, often called placental abruption, refers to the premature separation of the
normally implanted placenta from the uterine wall.
Etiology. Placental abruption occurs when there is hemorrhage into the decidua
basalis, leading to premature placental separation and further bleeding. The cause for
this bleeding is not known.
Placental abruption is associated with maternal hypertension and sudden
decompression of the uterus in cases of rupture of membranes in a patient with
excessive amniotic fluid (hydramnios) or after delivery of the first of multiple fetuses.
A more recent and serious association involves cocaine use by the mother, which
leads to intense vasoconstriction and, in some cases, sudden separation of the
placenta from the uterine wall. Placental abruption can also occur following trauma,
even when the extent of injury is not considered serious. For example, pregnant
women involved in motor vehicle accidents can sustain placental abruption even
though lap belts and shoulder strap restraints are used. Moreover, direct trauma to the
abdomen is not required, because sudden force applied elsewhere to the body can
result in coup and countercoup injury.
 Fig. 7. Types of placental abruption
Clinical findings and Diagnosis
The signs and symptoms can vary considerable. External bleeding can be profuse
or there may be no external bleeding (concealed hemorrhage) but the placenta is
completely sheared off and the fetus dead. Besides, common findings are uterine
tenderness, back pain, fetal distress, uterine hypertonus or high-frequently
contractions, idiopathic preterm labor, and a dead fetus.
Because the separation of the placenta from the uterus interferes with
oxygénationof the fetus, a nonreassuring fetal status is quite common in cases of
significant placental abruption. Thus, in any patient in whom placental abruption is
suspected, electronic fetal monitoring should be included in the initial management.
Placental abruption may be total and partial.
.
 Fig. 8 Total placental abruption
Coagulation abnormalities may also be found, thereby compounding the patient's
already compromised status. Placental abruption is the most common cause of
consump-tive coagulopathy in pregnancy and is manifested by hypofibrinogenemia
as well as by increased levels of fibrin degradation products. The platelet count can
also be decreased, and prothrombin time and partial thromboplastin time can be
increased as well. Such coagulopathy is a result of intravascular and retroplacental
coagulation. The intravascular fibrinogen is converted to fibrin by way of the
extrinsic clotting cascade. Thus not only is serum fibrinogen decreased but platelets
and other clotting factors are thereby also depleted.
Ultrasound is of little benefit in diagnosing placental abruption, except to exclude
placenta previa as a cause for the hemorrhage. Relatively large retroplacentalclots may
be detected on ultrasound examination, but the absence of ultrasonographically
identified retroplacental clots does not rule out the possibility of placental abruption, and
conversely, a retroplacentalechogenic area can be seen in patients without placental
abruption. The diagnosis rests on the classic clinical presentation of vaginal bleeding, a
tender uterus, and frequent uterine contractions with some evidence of fetal distress.
The extravasation of blood into the uterine muscle causes contractions such that the
resting intrauterine pressure, when measured with an intrauterine pressure catheter, is
often elevated; this sign can be helpful in making the diagnosis. The entire uterus has
a purplish or bluish appearance, owing to such extravasation of blood (Couvelaire
uterus) – Fig. 9.

Fig. 9 Couvelaire uterus

Management of a patient with placental abruption when the fetus is mature is
hemodynamic stabilization and delivery. Appropriate facilities and staff for cesarean
section must be continuously available whenever placental abruption is suspected
Careful attention to blood component therapy is critical, and the coagulation status must
be followed closely. Unless there is evidence of fetal distress or hemodynamic
instability, vaginal delivery by oxytocin induction of labor is preferable to a cesarean
delivery, although the maternal or fetal status may require that abdominal delivery be
performed. When the fetus is not mature and the placental abruption is limited and not
associated with premature labor or fetal or maternal distress, observation with close
monitoring of both fetal and maternal well-being may be considered while awaiting fetal
maturity. In the case of Couvelaire uterus total hysterectomy is performed because of
danger of uterine hypotony and disseminated intravascular clotting syndrome.

AMNIOTOMY.Rupture of the membranes as early as possible has long been

championed in the management of placental abruption. The rationale for amniotomy
is that the escape of amnionic fluid might both decrease bleeding from the
implantation site and reduce the entry into the maternal circulation of thromboplastin
and perhaps activated coagulation factors from the retroplacental clot. There is no
evidence, however, that either is accomplished by amniotomy. If the fetus is
reasonably mature, rupture of the membranes may hasten delivery. If the fetus is
immature, the intact sac may be more efficient in promoting cervical dilatation than
will a small fetal part poorly applied to the cervix.

LABOR. With slight degrees of placental separation, uterine contractions are usually
of normal frequency, duration, and intensity. With extensive placental abruption, the
uterus will likely be persistently hypertonic. The baseline intra-amnionic pressure
may be 25 to 50 mm Hg or higher, with rhythmic increases up to 75 to 100 mm Hg.
Because of persistent hypertonus, it may be difficult at times to determine by
palpation if the uterus is contracting and relaxing to any degree (Fig. 32–9 ).

OXYTOCIN. Although hypertonicity characterizes myometrial function in most

cases of severe placental abruption, if no rhythmic uterine contractions are
superimposed, then oxytocin is given in standard doses. Uterine stimulation to effect
vaginal delivery provides benefits that override the risks. The use of oxytocin has
been challenged on the basis that it might enhance the escape of thromboplastin into
the maternal circulation and thereby initiate or enhance consumptive coagulopathy or
amnionic fluid embolism syndrome. There is no evidence to support this fear (Clark
and colleagues, 1995; Pritchard and Brekken, 1967).

VASA PREVIA

Although rarely encountered, vasa previapresents significant risk to the fetus. In

vasa previa (Fig. 10), the umbilical cord inserts into the membranes of the placenta
(rather than into the central mass of the placental tissue), and one such vessel lies
below the presenting fetal part in the vicinity of the internal os. If this vessel ruptures,
fetal bleeding occurs. Because of the low blood volume of the fetus, seemingly
insignificant amounts of blood may place the fetus in jeopardy. A small amount of
vaginal bleeding associated with fetal tachycardia may be the clinical presentation. A
test to distinguish fetal blood from maternal blood, such as the Kleihauer-Betke or the
Apt test, can be of value when such a condition is suspected. These tests distinguish
between maternal and fetal blood on the basis of the marked resistance to pH changes
in fetal red cells compared with the friable nature of adult red cells in the presence of
strong bases. Immediate cesarean section is the only way to save the fetus in vasa
previa.

Fig. 10 Sonogram showing placenta (P), succenturiate lobe (S), and leading fetal
vessels in vasa previa (arrow). (From Gianopoulas J, Carver T, Tomich PG,
Karlman R, Gadwood K. Diagnosis of vasa previa with ultrasonography.
ObstetGynecol. 69:488, 1987).
 APPROACH TO A PATIENT WITH VAGINAL BLEEDING IN THE
SECOND HALF OF GESTATION
In any woman with vaginal bleeding during the second half of pregnancy, fetal
and maternal status should be evaluated promptly. At the same time that a search is
undertaken for the cause of the bleeding, attention must be directed toward stabiliza-
tion of the maternal hemodynamic state. The approach is not unlike that for any
hemorrhaging patient and includes ready access for fluid replacement through one or
more large-bore intravenous catheters, serial complete blood counts, type and cross-
match of ample amounts of blood, and if the condition is unstable, intracardiac
monitoring. Attention to urinary output is a simple and important reflection of the
volume status of a patient. Because normal antepartum blood volume expansion is
substantial, pregnant women may lose considerable amounts of blood before vital
sign changes are apparent. In more than half of the cases of significant vaginal
bleeding in pregnancy, no specific cause can be discovered despite careful evaluation.
In general, patients with significant bleeding should remain hospitalized until
delivery, although in some cases minimal bleeding ceases, and the patient appears
normal in every way. Caution is advised, however, because patients with bleeding of
undetermined etiology can be at greater risk for preterm delivery, intrauterine growth
restriction, and fetal distress than patients with bleeding of known cause.
HEMORRHAGE IN THE THIRD STAGE OF LABOR AND EARLY
PUERPERAL PERIOD
Postpartum hemorrhage is defined as blood loss in excess of 400 mL at the
time of vaginal delivery.
Postpartum hemorrhage before delivery of the placenta is called third-stage
hemorrhage.
Postpartum hemorrhage after delivery of placenta during the first two hours is
called as hemorrhage in early puerperal stage.
Hemorrhage after placental separation is stopped thanks to:
4. uterine contractions – caliberes of ruptured vessels decreases during
uterine contractions;
5. formation of thrombs, especially in the region of placental site;
 6. torsion of thin septs in which vessels are situated.

Causes of Postpartum Hemorrhage:

5. uterine atony,
6. genital tract trauma,
7. bleeding from the placental site (retained placental tissue, low
placental implantation, placental adherence, uterine inversion)
8. coagulation disorders.

The main causes of third-stage bleeding are genital tract trauma

and bleeding from placental site.
The main causes of hemorrhage in early puerperal stage are all of the
above causes of Postpartum hemorrhage.
Predisposing factors and causes of immediate postpartum hemorrhage:
Uterine atony:
1. Overdistended uterus – multiple fetuses, Hydramnios, distention with
clots.
2. Anesthesia or analgesia – halogenated agents, conducted analgesia with
hypertension.
3. Exhausted myometrium – rapid labor, prolonged labor, oxytocin
or prostaglandin stimulation.
4. Chrionamnionitis.
4. Previous uterine atony.
Genital tract trauma:
1. Complicated vaginal delivery.
2. Cesarean section or hysterectomy, forceps or vacuum.
3. Uterine rupture; risk increased by: previously scarred uterus, high
parity, hyperstimulation, obstructed labor, intrauterine manipulation.
4. Large episiotomy, including extensions.
5. Lacerations of the perineum, vagina or cervix.
 Bleeding form placental implantation cite:
1. Retained placental tissue – avulsed cotyledon, succentuariate lobe
2.Abnormally adherent – accreta, increta, percreta.
Coagulation defects – intensifies other causes:
1. Placental abruption.
2. Prolonged retention of dead fetus.
3. Amnionic fluid embolism.
4. Saline-induced abortion.
5. Sepsis with endotoxemia.
6. Severe intravescular hemolysis.
7. Massive transfusions.
8. Severe preeclampsia or eclampsia.
9. Congenital coagulopathies.
Clinical findings and diagnosis
The two most common causes of immediate hemorrhage are hypotonic
myometrium (uterine atony) and lacerations of the vagina and cervix. Retention
of part or all of the placenta, a less common cause, may produce either immediate
or delayed hemorrhage (or both).
Uterine atony is called as total absence of uterine contractions into the
external irritation. Uterine hypotony is called as presence of inadequate uterine
contractions on the external irritation. In the pauses between uterine contractions a
uterus is soft. But blood form clots in the case of uterine hypo- or atony. These
clots are stored in the uterine cavity that’s why a uterus is enlarged in sizes.
The differentiation between bleeding from uterine atony and from lacerations
is tentatively based on the condition of the uterus. If bleeding persists despite a firm,
well-contracted uterus, the cause of the hemorrhage most probably lacerations.
Bright red blood also suggests lacerations. To ascertain the role of lacerations as a
cause of bleeding, careful inspection of the vagina, cervix, and uterus is essential.
Placental accretais any implantation of the placenta in which there is

abnormally firm adherence to the uterine wall. As a consequence of partial or total

absence of the decidua basalis and imperfect development of the fibrinoid
layer (Nitabush’s membrane):
5. the placental villi are attached into the basal layer - placenta adhaerens;
6. the placental villi are attached to the myometrium - placenta accreta (Fig.
11);
7. extensive growth of placental tissue into the uterine muscle itself – placenta
increta;
8. complete invasion through the sickness of the uterine muscle to the serosa or
beyond – placenta percreta (Fig. 12, 13 ).

Fig. 11 A fatal case of inverted uterus associated with placenta

accreta following delivery at home.
 Fig. 12 Placenta percreta in a woman at term with a known placenta previa.
The placenta had grown into the entire lower uterine segment. (Photograph
courtesy of Dr. Tom Dowd.)
 Fig. 13 Placenta percreta. On the left, the placenta is fungating through the
fundus above the old classical cesarean section scar. In the opened specimen on
the right, the variable penetration of the fundus by the placenta is evident.
(From Morison, 1978.)
Complete or total placenta accreta will not cause bleeding because the placenta
remains attached, but partial ( the abnormal adherence involves a few to several
cotyledons) or focal ( the abnormal adherence involves a single cotyledon) type
may cause profuse bleeding, as the normal part of the placenta separates and the
myometrium cannot contract sufficiently to occlude the placental site vessels.
The abnormal placental adherence is diagnosed by:
1. Absence of the signs of placental separation during
30 minutes. Signs of placental separation:
4. the uterus rises in the abdomen;
5. the shape of the uterus changes from discoid to globular
6. the umbilical cord lengthens.
 2. External bleeding – in the case of partial adherence, absence of the bleeding
– in the case of total placenta accreta.
3. Manual removal of the placenta confirms the diagnosis of different types of
abnormal placental adherence. In the case of partial placental adhaerence it stops
bleeding, but in the case of placenta accreta, increta and percrata it increases
bleeding. Attempts at manual removal are futile. That’s why in these cases manual
removal of the placenta should be stopped immediately and hysterectomy
should be performed.
Coagulation disorders are recognized thanks to coagulation
studies and inspection for clot formation.
MANAGEMENT OF THE PATIENTS IN THE THIRD-STAGE
BLEEDING
UTERINE ATONY
9. Catheterization of the urinary bladder.
10. Cold on the lower abdomen.
11. Manual massage of the uterine corpus: one hand gently massages the
uterus from the abdomen while the other is inserted so that the cervix is cradled in the
fingers and thumb to allow maximal compression and massage.
12. Prescription of the uterine contracting drugs: oxytocin – 5 units,
methylergonovine (Methergine) – 1mL intramuscularly or in intravenous infusion. If
the uterus remains atonic and the placental site bleeding continuos during the
oxytocin infusion, a rapid continuos intravenous infusion of dilute oxytocin (20 units
in 1L of normal saline) should be given to increase uterine tone. Analogues of
prostaglandin F2 alpha (Hemabate) in a dose 5 mg given intramuscularly or
intravenously are quite effective in controlling postpartum hemorrhage caused by
uterine atony. Large-bore intravenous catheters – 1 or 2 well functioning lines.
Mifipristone – 800 mkg per rectum, enzaprost – 5 mg into anterior abdominal wall.
13. Manual exploration of the uterine cavity under the general anesthesia,
bimanual uterine compression. (fig. 14)
14. A tampon with ether is inserted into the posterior fornix.
 15. Clemmas on the parametrium or into the cervix of the uterus are putted
on.
16. Aorta compression to the spinal column.
In a case if blood loss increase 800 mL and bleeding continuos - surgery
management should be perform:
1.Uterine artery ligation;
2. Hypogastric artery ligation;
3. Hysterectomy.

Fig.14 Bimanual compression of the uterus and massage with the

abdominal hand usually will effectively control hemorrhage from uterine atony.

GENITAL TRACT TRAUMA – ligation and suturing of all ruptures of the

vagina, cervix and perineum. In the case of uterine rupture – hysterectomy should
be performed.
BLEEDING FROM PLACENTAL IMPLANTATION CITE
1) placental separation signs are absent – manual separation and removal of
the placenta and exploration of the uterine cavity, uterine massage, uterine
contracting drugs are prescribed;
 2) complete and partial placenta adhaerens - manual separation and
removal of the placenta (Fig. 15);
3) placentaaccreta, increta and percreta – hysterectomy. With more
extensive involvement, however, hemorrhage becomes profuse as
manual removal of the placenta is attempted.

Fig. 15 Technique of manual removal of the placenta

Technique of Manual Removal. Adequate analgesia or anesthesia is
mandatory. Aseptic surgical technique should be employed. After grasping the
fundus through the abdominal wall with one hand, the other hand is introduced into
the vagina and passed into the uterus, along the umbilical cord. As soon as the
placenta is reached, its margin is located and the ulnar border of the hand insinuated
between it and the uterine wall. Then with the back of the hand in contact with the
uterus, the placenta is peeled off its uterine attachment by a motion similar to that
employed in separating the leaves of a book. After its complete separation, the
placenta should be grasped with the entire hand, which is then gradually withdrawn.
Membranes are removed at the same time by carefully teasing them from the
decidua, using ring forceps to grasp them as necessary. Some prefer to wipe out the
uterine cavity with a sponge. If this is done, it is imperative that a sponge not be left
in the uterus or vagina.
Placenta Accreta, Increta, and Percreta
In most instances, the placenta separates spontaneously from its implantation
site during the first few minutes after delivery of the infant. The precise reason for
delay in detachment beyond this time is not obvious always, but quite often it seems
to be due to inadequate uterine contraction. Very infrequently, the placenta is
unusually adherent to the implantation site, with scanty or absent decidua, so that
the physiological line of cleavage through the decidual spongy layer is lacking. As a
consequence, one or more cotyledons are firmly bound to the defective decidua
basalis or even to the myometrium. When the placenta is densely anchored in this
fashion, the condition is called placenta accreta.
The term placenta accreta is used to describe any placental implantation in
which there is abnormally firm adherence to the uterine wall. As the consequence of
partial or total absence of the decidua basalis and imperfect development of the
fibrinoid layer (Nitabuch layer), placental villi are attached to the myometrium in
placenta accreta, actually invade the myometrium in placenta increta, or penetrate
through the myometrium in placenta percreta. The abnormal adherence may involve
all of the cotyledons (total placenta accreta), a few to several cotyledons (partial
placenta accreta), or a single cotyledon (focal placenta accreta).
Significance
An abnormally adherent placenta, although an uncommon condition, assumes
considerable significance clinically because of morbidity and, at times, mortality from
severe hemorrhage, uterine perforation, and infection. The true frequencies of
placenta accreta, increta, and percreta are unknown. Breen and associates (1977)
reviewed reports published since 1891. The incidence varied from 1 in 540 deliveries
to 1 in 70,000 deliveries, with an average incidence of about 1 in 7000. Read and co-
workers (1980) reported an incidence of about 1 per 2500 deliveries and concluded
that today there is a higher reported incidence, lower parity, and greater incidence of
associated placenta previa, as well as decreasing maternal and perinatal mortality.

Abnormal placental adherence is found most often in circumstances where

decidual formation was likely to have been defective. Associated conditions include
implantation in the lower uterine segment, over a previous cesarean section scar or
other previous uterine incisions, or after uterine curettage. In his review of 622
reported cases of placenta accreta collected between 1945 and 1969, Fox (1972)
noted the following characteristics: (1) placenta previa was identified in a third of
affected pregnancies, (2) one fourth of the women had been previously delivered by
cesarean section, (3) nearly one fourth had previously undergone curettage, and (4)
one fourth were gravida 6 or more. Read and co-workers (1980) reported similar
findings for women studied in the 1970s; however, the overall incidence and parity
had decreased. In a preliminary investigation, Hardardottir and colleagues (1996)
found that almost half of placentas in women with a prior cesarean section had
adherent myometrial fibers detected microscopically.
Antepartum hemorrhage is common, but in the great majority of cases, bleeding
before delivery is the consequence of coexisting placenta previa. Myometrial
invasion by placental villi at the site of a previous cesarean section scar may lead to
uterine rupture during labor or even before (Berchuck and Sokol, 1983). Archer and
Furlong (1987) described a woman who presented with an acute abdomen from
massive hemoperitoneum caused by placenta percreta at 21 weeks’ gestation. In
women whose pregnancies go to term, however, labor will most likely be normal in
the absence of an associated placenta previa or an involved uterine scar.
The problems associated with delivery of the placenta and subsequent
developments vary appreciably, depending upon the site of implantation, depth of
myometrial penetration, and number of cotyledons involved. It is very likely that
focal placenta accreta with implantation in the upper uterine segment develops much
more often than is recognized. The involved cotyledon is either pulled off the
myometrium with perhaps somewhat excessive bleeding, or the cotyledon is torn
from the placenta and adheres to the implantation site with increased bleeding,
immediately or later.
 With more extensive involvement, hemorrhage becomes profuse as delivery of
the placenta is attempted. Successful treatment depends upon immediate blood
replacement therapy, and nearly always prompt hysterectomy.
With total placenta accreta, there may be very little or no bleeding, at least until
manual placental removal is attempted. At times, traction on the umbilical cord will
invert the uterus, as will be described in the next section. Moreover, usual attempts at
manual removal will not succeed, because a cleavage plane between the maternal
placental surface and the uterine wall cannot be developed. The safest treatment in
this circumstance is prompt hysterectomy.
In the 622 cases reviewed by Fox (1972), the most common form of
“conservative” management was manual removal of as much placenta as possible and
then packing of the uterus. One fourth of the women died, which was four times as
many as when treatment consisted of immediate hysterectomy. So-called
“conservative” treatment in at least four instances was followed by an apparently
normal pregnancy.
The possibility exists that placenta increta might be diagnosed antepartum. Cox
and associates (1988) described a case of placenta previa in which they also were
able to identify placenta increta ultrasonically from the lack of the usual
subplacentalsonolucent space. They hypothesize that the presence of this normal
subplacentalsonolucent area represents the decidualbasalis and the underlying
myometrial tissue. The absence of this sonolucent area is consistent with the presence
of a placenta increta. Pasto and associates (1983) confirmed that the absence of a
subplacentalsonolucent or “hypoechoicretroplacental zone” is consistent with
placenta increta.
Inversion of the Uterus
Complete uterine inversion after delivery of the infant is almost always the
consequence of strong traction on an umbilical cord attached to a placenta implanted
in the fundus (Fig. 16).
Most likely site of placental implantation in cases of uterine inversion. With
traction on the cord and the placenta still attached, the likelihood of inversion is
obvious.
 Fig. 16 Contributing to uterine inversion is a tough cord that does not readily
break away from the placenta, combined with fundal pressure and a relaxed uterus,
including the lower segment and cervix.
Placenta accreta may be implicated although uterine inversion can occur without
the placenta being so firmly adherent. At times, the inversion may be incomplete
(Fig. 11).
Shah-Hosseini and Evrard (1989) reported an incidence of about 1 in 6400
deliveries at the Women and Infants Hospital of Rhode Island. Of the 11 inversions
identified, most were in primiparous women and immediate vaginal replacement of
the inverted uterus was successful in nine instances. Platt and Druzin (1981) reported
28 cases in over 60,000 deliveries, for an incidence of about 1 in 2100. These same
investigators suggested that parenteral magnesium sulfate, which was administered to
women with pregnancy-induced hypertension, might have played a role in the
etiology of this complication.
Uterine inversion is most often associated with immediate life-threatening
hemorrhage, and without prompt treatment it may be fatal (Fig. 11).
 In the past it was stated that shock tends to be disproportionate to blood loss.
Careful evaluation of the effects from transfusion of large volumes of blood in such
cases does not support this concept, but instead makes it very apparent that blood loss
in such circumstances was often massive but greatly underestimated (Watson and
associates, 1980).
Treatment
Delay in treatments increases the mortality rate appreciably. It is imperative that
a number of steps be taken immediately and simultaneously:
1. Assistance, including an anesthesiologist, is summoned immediately.
2. The freshly inverted uterus with placenta already separated from it may often
be replaced simply by immediately pushing up on the fundus with the palm of the
hand and fingers in the direction of the long axis of the vagina.
3. Preferably two intravenous infusion systems are made operational, and
lactated Ringer solution and whole blood are given to reverse hypovolemia.
4. If attached, the placenta is not removed until the infusion systems are
operational, fluids are being given, and anesthesia, preferably halothane or enflurane,
has been administered. Tocolytic drugs have also been used successfully for this
purpose. Terbutaline, ritodrine, or magnesium sulfate have been used for uterine
relaxation and repositioning (Catanzarite and associates, 1986; Kovacs and DeVore,
1984; Thiery and Delbeke, 1985). To remove the placenta before this time increases
hemorrhage. In the meantime, the inverted uterus, if prolapsed beyond the vagina, is
replaced within the vagina.
5. After removing the placenta, the palm of the hand is placed on the center of
the fundus with the fingers extended to identify the margins of the cervix. Pressure is
then applied with the hand so as to push the fundus upward through the cervix.
6. Oxytocin is not given until after the uterus is restored to its normal
configuration.
As soon as the uterus is restored to its normal configuration, the agent used to
provide relaxation is stopped and simultaneously oxytocin is started to contract the
uterus while the operator maintains the fundus in normal relationship. Initially,
bimanual compression will aid in the control of further hemorrhage until uterine tone
is recovered.

Fig.17 Uterine replacement

After the uterus is well contracted, the operator continues to monitor the uterus
transvaginally for any evidence of subsequent inversion.
Surgical Intervention. Most often, the inverted uterus can be restored to its
normal position by the techniques described. If the uterus cannot be reinverted by
vaginal manipulation because of a dense constriction ring (Fig. 18), laparotomy is
imperative.
 Fig. 18 Completely inverted uterus viewed from above.
The fundus then may be simultaneously pushed upward from below and pulled
from above. A traction suture well placed in the inverted fundus may be of aid. If the
constriction ring still prohibits reposition, it is carefully incised posteriorly to expose
the fundus. A graphic outline of this surgical technique was described by Van Vugt
and associates (1981). After replacement of the fundus, the anesthetic agent used to
relax the myometrium is stopped, oxytocin infusion is begun, and the uterine incision
repaired. Following restoration of the uterus, the adjacent viscera are carefully
examined for trauma.
Attention ! Irrespective of the apparent cause, whenever there is any suggestion at
the delivery or postpartum of excessive blood loss from the genital tract,
immediate steps must be taken to identify the presence of uterine atony, retained
placental fragments, and trauma.
3. At least one or, in the presence of frank hemorrhage, two
intravenous infusion systems of large caliber must be established right
away to permit rapid administration of aqueous electrolyte solutions and
blood as nedded
 4. An operating room and a surgical team, including
an anesthesiologist, must be immediate available.
COAGULATION DEFECTS
The treatment of coagulation defects is aimed at correcting the
coagulation defects and include infusion of:
2. platelet concentrate – increases platelet count by about 20 000 to 25 000;
4. cryoprecipitate – supplies fibrinogen, factor VIII, and factor XIII (3 to
10 times more concentrated than the equivalent volume of fresh plasma);
5. fresh-frozen plasma – supplies all factors except platelets (1 g of fibrinogen);
6. packed red blood cells – raises hematocrit 3 % to 4 %.

OBSTETRIC SHOCK. TERMINAL STATES IN OBSTETRICS

Shock encompasses various pathophysiological aberrations that lead to
inadequate tissue perfusion and impaired cellular metabolism. Although hypotension
often is the most obvious clinical sign in shock of any cause, such blood pressure
changes are the final common manifestation of a number of distinct pathologic
processes. The successful clinical management of patients in shock depends on the
proper definition of the underlying pathophysiology as well as an under of the unique
effects of pregnancy on such conditions.
Uterine bleeding (hemorrhage) during labor and early puerperal stage play an
important role among different kinds of severe obstetrics pathology, such as
hemorrhagic shock, disseminated intravascular coagulopathy, sepsis and other.
Uterine bleeding is the leading cause of maternal death.
Uterine bleeding frequency is 8,0 – 11, 0 %.
The main causes of uterine bleeding are:
During pregnancy: placenta praevia, placenta abruptio.
During labor: placenta praevia, placenta abruptio, uterine rupture, traumatization
of the soft birth canal tissues.
In the third period of labor and early puerperal stage: uterine hypo- and atony;
uterine rupture and traumatization of the soft birth canal tissues; placenta accreta,
increta, and percreta; retention of some parts of afterbirth in the uterine cavity;
thrombohemorrhagic bleeding.
Methods of blood loss determination
7. Libov’s method.
After surgical intervention the napkins, which are filling by blood, should be
weighted.
Blood loss volume = Weight x 15 % ( if blood loss is < 1000
ml); 2
Blood loss volume = Weight x 30 % ( if blood loss is > 1000 ml).
2
8. By hematocrit
Hematocr Blood
it, % loss
volume,
ml
44–40 500
38–32 1000
30–22 1500
< 22 >
1500
9. Algover’s index
Shock’ index = Heart rate
Systolic arterial blood pressure
In normal Algover’s index is < 1.
Algover’si Blood
ndex loss
volume,
% out of
circulatin
g blood
volume
 0,8 and < 10 %
0,9 – 1,2 20 %
1,3 – 1,4 30 %
1,5 and > 40 %

HEMORRHAGIC (HYPOVOLEMIC) SHOCK

Hemorrhagic shock is a very serious complication in the case of pathological
hemorrhage.
Physiological blood loss during labor is 0, 5 % out of puerperant’ weight.
Physiological blood loss is 350, 0 – 400, 0 ml.in the puerperant with 70-75 kg of
weight. If blood loss predominate physiological one, hemorrhagic shock have been
occurred.
There are 4 stages of hemorrhagic shock according to Baker classification.
Evaluation of hemorrhagic shock stage severity is presented in the table.
Evaluation of hemorrhagic shock stage severity
Shock Hypovolemia Circulating Blood loss, % from body weight Hemodynamic
stage stage blood ml diuresis
volume
deficiency
I Mild 10 %-20% 500 – 1,0 – 1,5 % Ps – 90-100 be
1000,0 Arterial blood
Central Venou
Diuresis – N.
II Moderate 20%-30% 1000,0- 1,5 - Ps – 120 beats
1500,0 2,0 % BP - <100 mm
CVP – <60 m
Diuresis – < 5
III Severe 30%-40% 1500,0– 2,0 – Ps – 140 beats
2000,0 2,5 % BP - <70 mm
CVP – <40 m
Diuresis – < 3
IV Considerable 40% and > 2000,0 and > > Ps – 140 beats
2,5 % BP – <50 mm
CVP – 0;
Diuresis– anur

The main principles of obstetrics hemorrhage and hemorrhagic shock

treatment:
21. Hemorrhage stopping.
22. Determination of blood loss stage.
23. Restoration of the circulating blood volume.
24. Normalization of vascular tone.
25. Blood reology, its structural, biochemical, and electrolytes compounds
correction.
26. Detoxication therapy.
27.Desensibilizing therapy.
28.Correction of clotting, antyclotting, fibrinolitic systems functions.
29.Regulation of the main human organs functions.
30.Prevention of infectious complications.
INTERM restoration of the circulating blood volume – is the main step in the
treatment of acute blood loss. Human organism should be survived in the case of 2/3-
erythrocytes volume loss, but it doesn’t survive in the case of 1/3 plasma volume
loss. That’s why it should be remembered that in considerable blood loss the first step
is the transfusion not only blood, but also кровозамінники, which eliminate
hypovolemia very quickly.
Transfusion therapy in obstetrics hemorrhages

Blood Volume Crysta- Refortan, Fresh- Albumin Erythro-

loss of infusion lloids Gelofusin frozen (10-20 massa
Stabisol plasma %)

10-20 10-15 10 ml /kg - -

% 2500 ml/
 500- ml kg
1000ml

20-30 10 ml 10 ml /kg 5 - 10 - 5 ml /kg ml /kg

% 3000 /kg
1000- ml
1500
ml
30-40 7 ml/kg 7 ml/kg 10 - 200 ml 10-20
% 4000 15 ml /kg ml /kg
1500- ml
2000
ml
40- 7 ml/kg 10 ml /kg 15 - 200 ml 30 ml
and > > 6000 20 ml /kg /kg
> ml
2000 ml

The volume of infusion therapy in hemorrhagic shock should be predominated

in 1,5-2,5 times its real blood loss.
Glucose transfusion doesn’t administrated in blood loss, because it very quickly
enter intracellular space and doesn’t increase circulating blood volume, it caused
metabolic acidosis.
Attention! Erythrocyte transfusion has value only after hemodynamics and
peripheral blood circulation normalization. Only in these conditions erythrocytes
should be taken oxygen.
Attention ! In all stages of hemorrhagic shock 2-4 veins should be catheterized
in one moment (one or two of them are central, such as v. subclavia).
Infusion speed depends on blood loss volume and patient state. In the case of
hemorrhagic shock and low arterial blood pressure it should be reach 200 ml per
minute. The infusion speed gradually decreased to 150-100-50 ml-per minute in the
case of increasing arterial blood pressure to 80-90 mm Hg.
 The main prescription of infusion therapy in the case of acute blood lose is the
stabilization of central hemodynamics which lead to cerebral and coronary blood
circulation stabilization.
Vascular tone normalization.
In the first stage of hemorrhagic shock because of vascular spasm presence
spasmolitics drugs are used, such as Nospani, Papaverinihydrochloridi. On the II-III-
IV stages because of vascular dilation glucocorticoids are prescribed. They are:
Prednisoloni, Hydrocortisone – in the dose 1,5-2 g/ daily, Dexametazoni.
If intravenous insertion 800-1000 ml any solution with the speed of 50-100
ml/per minute doesn’t change (increase) arterial blood pressure – vasopressors agents
should be prescribed, such as Remestip – in the dose 0,2-1,0 mg; Dopamine –
5mkg/kg/minute or glucocrticoids.
In considerable infusion therapy after circulating blood volume normalization
diuresis stimulation is recommended. For this purpose Euphillini in the dose 3 mh per
kg, lazix – 2-4 mg/kg or furosemidi in the dose 6-8 mg/kg have been used.
Structural, biochemical, electrolytes compounds correction of blood,
detoxycation, desensibilizing therapy and normalization of clotting, antyclotting,
fibrinolytic systems functions and functions of the main human organs is obligatory
in the treatment of hemorrhagic shock.
Introduction of cardiologic drugs is possible only after blood loss restoration.
For this purpose such agents have been used as Corgliconi –0, 6 % - 0,5 –1 ml;
Cocarboxylase – 50 mg twice a day.
Prevention of infectious complications by prescription of wide spectrum
antibiotics (cefalosporines, aminoglycozides) in the daily dose is recommended also.

Main steps of urgent medical care in the obstetrics bleeding

during pregnancy, labor, and puerperal stage
7. Blood loss is 0, 8 – 1, 0 % of body weight
1. To determine the cause of hemorrhage

Placenta Uterine cervix Uterine hypo-

 praevia, rupture, deep and atony;
placenta vagival uterine
abruptio, ruptures, rupture and
uterine traumatization traumatization
rupture of the soft of the soft
birth canal birth canal
tissues. tissues;
placenta
accreta,
increta, and
percreta;
retention of
some parts of
afterbirth in
the uterine
cavity

Bleeding stopping

Urgent Rupture Manual

cesarean suture uterine
section revision

2. To start intravenous infusion: crystalloids (0,9 % NaCl + 10

Units of oxytocin), colloids – Refortan, Stabisol, Poliglucin.

8. Blood loss is 1, 0 %– 1, 5 % of body weight.

1. Injection of 250 – 1000 mkgProstin F2a intramuscularly or 0,4 mg
Remestip + 10 ml 0,9 % NaCl into uterine cervix.
 2. Catheterization of two veins (one of them is v. subclavia), intravenous
transfusion of autoblood, plasma, erythrocyte massa, Refortan, Stabisol.

Attention! Surgical intervention should be performed in continuing

bleeding! (if blood loss is more than 1, 0 % - 800 ml of body weight ).

9. Blood loss is > 1, 5 % of body weight.

1. Laparotomy. Total hysterectomy without adnexa (adnexa are removed
if inflammatory, degenerative changes are presented).

2. Restoration of the blood circulating volume: autoblood, donor’s blood – 100

% from blood loss, cryoprecipitate, albumin.
DISSEMINATED INTRAVASCULAR COAGULOPATHY (DIC)
DIC is not a distinct clinical entity; rather, it represents a manifestation of
various disease processes that have in common activation of intravascular clotting
and fibrinolysis, resulting in excess consumption of solutable coagulation
components. In obstetrics, secondary fibrinogenolysis commonly dominates the
clotting aberration and results in the circulation of fibrin and fibrinolytic split
products, which further accentuates the clinical presentation of henorrhage. In
addition, sometimes a dilutional coagulopathy is encountered in pregnancy. This
condition obtains when massive hemorrhage is teplaced only by red blood cells and
crystalloids solution, resulting in a dilutional depletion of platelets and soluble
clotting factors.. In practice, the hemorrhage associated with dilutional coagulopathy
often results in hypotension and shock. The tissue hypoxia that accompanies shock of
any cause is well known to potentially activate the coagulation-fibrinolysis cycle
associated with DIC.
DIC is the pathological complex, which is characterized by blood clotting that
has been leading to microcirculation blockade by fibrin in the main human organs
(lungs, kidneys, liver). Dysfunction of these organs is the result of their damage. In
the end of this process thrombohemorrhagic disorders have been developed.
The main causes of DIC in the obstetrics are:
 27.All kinds of shock (hemorrhagic, septic, anaphylactic);
28.Placenta abruption;
29. Embolic fluid embolism;
30. OPH – hestosis;
31. Hypotonic bleeding;
32. Uterine ruptures;
33. Excessive labor induction;
34. Cesarean section;
35.Extragenital pathology;
36.Septic abortion;
37.Puerperal endometritis;
38.Intensive uterine massage;
39.dead fetus syndrome
Classification of thrombohemorrhagic syndrome
5. By clinical duration:
1. Acute;
2. Subacute;
3. Chronic.
6. By stages:
I stage – hypercoagulation;
II stage – hypocoagulation without generalizing fibrinolysis
activation; III stage – hypocoagulation with generalizing
fibrinolysis activation; IV stage – total fibronolysis.
Clinical manifestatiuon.
Clinical manifestation of DIC is connected with ischemic and
hemorrhagic changes in human organs and tissues. They are:
11. Hemorrhages into skin and mucous membranes;
12. Hemorrhages from the places of injections, incisions, uterus.
13. Necrosis of some areas of skin and mucous membranes;
14.Central nervous system impairment;
15.Acute renal, liver, lung insufficiency.
 Laboratory diagnosis of DIC

The main laboratory data

Blood Spontaneous Thrombin Throm- Thrombin
Stages clotting thrombus test bocytes time,
time, lisis number, seconds
minutes 10x9/l
I.Hypercoagulation <5(N) absent (N) 7-11 (N) 175-425 < 24
(N)
II.Hypocoagulation 5 -12 absent 7-11 < 120 >60
without
generalizing
fibrinolysis

III Hypocoagu- >12 quick 20-60 < 100 >100

lation with
generalizing
fibrinolysis
IV. Total > 60 Thrombus >60 <60 >180
fibrinolysis doesn’t
formed

General principles of DIC treatment are:

11. Heparin, fibrinogen are contraindicated in all stages of
thrombohemorrhagic syndrome.
12. Proteolytic enzymes inhibitors in the dose of 10 mg/kg/hour have been used
for inhibit excessive fibrinolysis and prevention of intracellular clotting.
13.Early and quick introduction of fresh frozen donor’s plasma. The main aim of
its usage is the restoration of haemostatic potential of blood (it contains all
soluble clotting factors, similar to whole blood). It has been used in all stages of
 thrombohemorrhagic syndrome. Initially the dose of intravenous introduction is 6-12
ml/kg. After it dose is 300-400 ml each 6-8 hours.
14. Stimulation of vascular-thrombocytes link of hemostasis (dicinone, etamsilat).
15. Transamacha acid usage – in the dose 500-750 mg on 0,9 % NaCl. This
medicine inhibits plasmine activity, stabilizes coagulate factors and fibrin, decreases
vascular permeability and gives permanent hemostatic action, which have been
prevented fibrinogen degradation.
Treatment of thrombhemorrhagic syndrome in obstetric hemorrhagic
shock in different stages
Stages Treatment
I.Hypercoagulation For normalization blood reology: Trental – 100mg on
100 ml 0,9 % NaCl, Curantill – 0,5 – 2, %
II.Hypocoagulation without Procoagulants: fresh frozen plasma 500,0, blood of 3-
generalizing fibrinolysis 5 days of conservation. Transamacha – antyplasmin
drug – 500-750 mg on 0, 9 % NaCl.
Fibrinolysis inhibitors: Contrical in the dose 10-
20.000 units/ daily dose 100-200.000 units; Trasilol –
40.000 units or Gordox – 100-200.000 units.
Cortycosteroids – Prednisolone – 10mg/kg/hour or
Hydrocortisone – 100 mg/kg.
III Hypocoagulation with Proteolytic enzymes inhibitors:Contrycal 40.000 units
generalizing fibrinolysis (daily dose 500.000 units)
Procoagulants – fresh frozen plasma, blood, albumin.
Cortycosteroids.Cryoprecipitate–200-400,0,
Transamcha – 500-700 mg.
IV. Total fibrinolysis The treatment should be started from the large doses
of proteolytic enzymes inhibitors – Contrical 100.000
units to 500.000 units. Blood, albumin, plasma,
cryoprecipitate, cortycosteroids.
 An estimated 5 % of women describe bleeding of some extent during pregnancy.
At times, the amount of bleeding is hardly more than "spotting," whereas at other
times profuse hemorrhage can lead to maternal death in a very short time. In most
cases, antepartum bleeding is minimal spotting, often following sexual intercourse,
and is thought to be related to trauma to the friable ectocervix.
The main causes of bleeding in the second half of pregnancy are:
Vulva
Varicose veins
Tears or lacerations
Vagina
Tears or lacerations
Cervix
Polyp
Glandular tissue (normal)
Cervicitis
Carcinoma Intrauterine
Placenta previa
Abruptio placentae
Vasa previa
A previous Pap test and examination of the lower genital tract should eliminate
the likelihood of lower genital tract neoplasms in most cases. At times, patients may
mistake bleeding from hemorrhoids or even hematuria for vaginal bleeding, but the
difference is easily distinguished by examination.
The two causes of hemorrhage in the second half of pregnancy that require
greatest attention, because of the associated maternal and fetal morbidity and
mortality rates, are placenta previa and abruptio placentae. Various characteristics of
these entities are compared in Table.
Differential characteristics between placenta previa and abruptio placentae
Characteristics Placenta previa Abruptio Placenta
Magnitude of blood loss Variable Variable
Duration Often ceases within 1-2 Usually continues
 hours
Abdominal discomfort None Can be severe
Absent Tachycardia, then
Fetal heart rate pattern
bradycardia; loss of
on electronic monitoring
variability; decelerations
frequently
present; intrauterine
demise not rare
Coagulation defects Rare Associated, but
infrequent; DIG often
severe when present
Cocaine use
Associated history None Abdominal trauma;
maternal hypertension;
multiple gestation;
polyhydramnios

PLACENTA PREVIA

Placenta previa refers to an abnormal location of the placenta over, or in close

proximity to, the internal cervical os. Placenta previa can be categorized as:
9. complete or total - if the entire cervical os is covered (Fig. 1);

10. partial - if the margin of the placenta extends across part but not all of the
internal os (Fig. 2);
11. marginal , if the edge of the placenta lies adjacent to the internal os;

12. low lying - if the placenta is located near but not directly adjacent to the internal
os.
Fig. 1 Total placenta previa
 Fig. 2 Partial placental previa

The etiology of placenta previa is not understood, but abnormal vascularization

has long been proposed as a mechanism for this abnormal placement of the placenta.
In some cases, such as in twin pregnancy or if it is hydropic, the placenta may extend
to the region of the internal cervical os because of its size alone. Increasing maternal
age, increasing parity, and previous cesarean delivery are factors commonly
associated with placenta previa, although recent evidence suggests that age alone is
not an important factor.

The incidence of placenta previa varies with gestational age, usually reported
overall as approximately 1 in 250 pregnancies. There is great variation in incidence,
however, with parity. The incidence in nulliparas is only 1 in 1000 to 1500, whereas
that in grandmultiparas is as high as 1 in 20. Women with the highest risk for
placenta previa are grandmultiparas, those who have had a previous placenta previa
(4% to 8%), and those who have had four or more cesarean sections. With common
use of ultrasonography examinations, it has been shown repeatedly that the placenta
may cover the internal cervical os in approximately 5% of pregnancies when
examined at midpregnancy, a finding seen even more frequently earlier in gestation.
Because of subsequent growth of both the upper and lower uterine segments, the
placenta appears to "migrate" away from the internal os in the majority of cases. The
likelihood of this apparent movement diminishes as the gestational age at first
detection increases.

Clinical findings and Diagnosis. The average gestational age at the time of the
first bleeding episode is 29 to 30 weeks. Although the bleeding may be substantial,
it almost always ceases spontaneously, unless digital examination or other trauma
occurs. The bleeding is caused by separation of part of the placenta from the lower
uterine segment and cervix, possibly in response to mild uterine contractions. The
blood that is lost is usually maternal in origin. The patient often describes a sudden
onset of bleeding without any apparent antecedent signs. There is no pain associ-
ated with placenta previa in most cases, unless coincident with labor or with an
abruptio placenta (approximately 5% to 10% of cases).
Frequently, bleeding from placenta previa has its onset without warning,
presenting without pain in a woman who has had an uneventful prenatal course.
Fortunately, the initial bleeding is rarely so profuse as to prove fatal. Usually it
ceases spontaneously, only to recur. In some cases, particularly those with a placenta
implanted near but not over the cervical os, bleeding does not appear until the onset
of labor, when it may vary from slight to profuse hemorrhage and may clinically
mimic placental abruption.

The cause of hemorrhage is reemphasized. When the placenta is located over the
internal os, the formation of the lower uterine segment and the dilatation of the
internal os result inevitably in tearing of placental attachments. The bleeding is
augmented by the inability of the myometrial fibers of the lower uterine segment to
contract and thereby constrict the torn vessels.
 Hemorrhage from the placental implantation site in the lower uterine segment
may continue after delivery of the placenta, because the lower uterine segment is
more prone to contract poorly than is the uterine body. Bleeding may also result from
lacerations in the friable cervix and lower uterine segment, especially following
manual removal of a somewhat adherent placenta.

Diagnosis

In women with uterine bleeding during the latter half of pregnancy, placenta
previa or abruptio placentae should always be suspected. The possibility of placenta
previa should not be dismissed until appropriate evaluation, including sonography,
has clearly proved its absence. The diagnosis of placenta previa can seldom be
established firmly by clinical examination unless a finger is passed through the cervix
and the placenta is palpated. Such examination of the cervix is never permissible
unless the woman is in an operating room with all the preparations for
immediate cesarean section, because even the gentlest examination of this sort
can cause torrential hemorrhage. Furthermore, such an examination should not be
made unless delivery is planned, for it may cause bleeding of such a degree that
immediate delivery becomes necessary even though the fetus is immature. Today,
however, such a “double set-up” examination is rarely necessary, as placental
location can almost always be obtained by careful sonography.

Ultrasonography has been of enormous benefit in localizing the placenta,

especially when the placenta is anterior or lateral. If the placenta lies in the posterior
portion of the lower uterine segment, its exact relation with the internal os may be
more difficult to ascertain. In most cases, though, ultrasonography examination can
accurately diagnose placenta previa or, by illustrating the placenta location away
from the cervix and lower uterine segment, exclude it as a cause for bleeding. In
some instances, transvaginal ultrasonography may be a useful adjunct to the
transabdominal approach, especially in the case of posterior placenta.
 Double setup examination can confirm the diagnosis of placenta previa. It
involves careful evaluation of the cervix in the operating room with full preparations
for rapid cesarean delivery.

Management

Includes initial hospitalization with hemodynamic stabilization, followed by

expectant management until fetal maturity has occurred. Ideal expectant
management would be continuous hospitalization with enforced bed rest and
immediate access to emergency care.

In the complete placenta previa – cesarean section in full term pregnancy. In the
case of low lying, marginal and partial placenta previa and full term pregnancy, when
blood loss is less than 250 ml – amniotomy with the following prescription of
contractile drugs. If blood loss is more than 250 ml – cesarean section.

The number of bleeding episodes is unrelated to the degree of placenta previa or

to the prognosis for fetal survival. Such expectant management combined with
appropriate use of blood transfusion and cesarean birth have resulted in the lowering
of the maternal mortality rate from !25%-30% to < 1% and the perinatal mortality
rate from 60%-70% to < 10%. If the fetus is thought to be mature by gestational
criteria or by amniocentesis for fetal lung maturity testing, there is little benefit to be
gained by a delay in delivery. The further from term that bleeding from placenta
previa occurs, the more important it is to delay delivery to allow for further fetal
growth and maturation. The degree of bleeding and the maturity of the fetus must be
constantly weighed in managing these patients. Fetal maturity is usually assessed at
approximately 36 weeks, with cesarean delivery performed once the fetus is deemed
mature.
In some cases, when the location of the placenta cannot be accurately determined
by ultrasound and delivery is required, the route of delivery is determined by a
double setup examination. This procedure involves careful evaluation of the cervix in
the oper-ating room with full preparations for rapid cesarean delivery.
 Localization by Sonography. The simplest, most precise, and safest method of
placental localization is provided by transabdominal sonography, which is used to
locate the placenta with considerable accuracy (Figs. 3, and 4 ).

Fig. 3 Partial anterior placenta previa at 36 weeks’ gestation. Placenta (P) extends
anteriorly and downward toward cervix (Cx). Fetus (F), amnionic fluid (AF), and
bladder (B) are seen. (Courtesy of Dr. R. Santos.)
 Fig. 4 Total placenta previa at 34 weeks’ gestation. Placenta (P) completely
overlies cervix (Cx). Bladder (B) and amnionic fluid (AF) are also visualized clearly.
(Courtesy of Dr. R. Santos.)
The average accuracy is about 95 percent, and rates as high as 98 percent have been
obtained. False-positive results are often a result of bladder distention. Therefore,
ultrasonic scans in apparently positive cases should be repeated after emptying the
bladder. Another source of error has been identification of abundant placenta implanted
in the uterine fundus but failure to appreciate that the placenta was large and extended
downward all the way to the internal os of the cervix. This, however is uncommon.
Farine and associates (1988) reported that the use of transvaginal ultrasonography
has substantively improved diagnostic accuracy of placenta previa. They were able to
visualize the internal cervical os in all cases with the transvaginal technique, in contrast
to only 70 percent using transabdominal equipment. An example is shown in Figure 5.
 Fig. 5 Transvaginal ultrasonic scan at 34 weeks’ gestation. Cervical canal is clearly
visible (CX) and distance from internal os to placental edge, measured between calipers
(X) is 0.75 cm. The patient was delivered by cesarean section 4 weeks later because
of vaginal bleeding. (P = placenta; B = bladder.) (Reproduced, with permission, from
Oppenheimer LW, Farine D, Ritchie JWK, Lewinsky RM, Telford J, Fairbanks LA.
What is a low-lying placenta? Am J Obstet Gynecol. 165:1035, 1991.)
Likewise, Leerentveld and colleagues (1990) studied 100 women suspected of
having placenta previa. They reported a 93 percent positive predictive value and 98
percent negative predictive value for transvaginal ultrasonography. Hertzberg and
associates (1992) demonstrated that transperineal sonography allowed visualization
of the internal os in all 164 cases examined because transabdominal sonography
disclosed a previa or was inconclusive. Placenta previa was correctly excluded in 154
women, and in 10 in whom it was diagnosed sonographically, nine had a previa
confirmed at delivery.
Magnetic Resonance Imaging.
Preliminary investigation using magnetic resonance imaging to visualize placental

abnormalities, including placenta previa, have been reported by several groups. Kay and
Spritzer (1991) discussed the many positive attributes of such technology (Fig. 6). It
is unlikely that this will replace ultrasonic scanning for routine evaluation in the near
future.

Fig. 6 A sagittal T2-weighted (2000/80 ms) image of a patient with a posterior

marginal placenta previa. The arrowhead points to the placental edge and the arrow
indicates the internal os. (F = fetal head; P = placenta; B = maternal bladder.) (From
Kay HH, Spritzer CE. Preliminary experience with magnetic resonance imaging in
patients with third-trimester bleeding. Obstet Gynecol. 78:424, 1991. Reprinted with
permission from the American College of Obstetricians and Gynecologists.)
Placental “Migration”
Since the report by King (1973), the apparent peripatetic nature of the placenta has
been well established. McClure and Dornal (1990) found a low-lying placenta in 25
percent of 1490 ultrasonic scans done at 18 weeks; however, at delivery, only 7 of these
385 low-lying placentas persisted. Sanderson and Milton (1991) found that only 12
percent of placentas were low lying in 4300 women surveyed ultrasonically at 18 to 20
weeks. Of those not covering the internal os, previa did not persist and hemorrhage was
not encountered. Conversely, of those covering the os at midpregnancy, about 40
percent persisted as a previa. Therefore, placentas that lie close to the internal
cervical os, but not over it, during the second trimester, or even early in the third
trimester, are very unlikely to persist as previas by term.
The low frequency with which placenta previa persists when it has been identified
sonographically before 30 weeks is shown in Table 32–4. It is apparent from these
data that in the absence of any other abnormality, sonography need not be frequently
repeated simply to follow placental position, and restriction of activity need not be
practiced unless the previa persists beyond 30 weeks, or becomes clinically apparent
before that time.
The mechanism of apparent placental movement is not completely understood.
The term migration is clearly a misnomer, however, as invasion of chorionic villi into
the decidua on either side of the cervical os will persist. The apparent movement of
the low-lying placenta relative to the internal os probably results from inability to
precisely define this relationship in a three-dimensional manner using two-
dimensional sonography in early pregnancy. This difficulty is coupled with
differential growth of lower and upper myometrial segments as pregnancy
progresses. Thus those placentas that “migrate” most likely never had actual
circumferential villus invasion that reached the internal cervical os in the first place.
If placental tissue is seen or palpated at the internal cervical os, prompt cesarean
delivery is performed. If the placental margin is away from the internal os, artificial
rupture of the membranes and oxytocin induction of labor may be performed in
anticipation of vaginal delivery. Before the widespread use of ultrasound, this
procedure was done more frequently than it is in modern obstetrics; nonetheless, it is
still an important tool in selected cases.
An attempt at vaginal delivery of a patient with placenta previa may be indicated if the
delivery can be accomplished with minimal blood loss and if the fetus is dead, has major
fetal malformations, or is clearly previable. If making such an attempt is appropriate,
ceasing the process and moving to cesarean delivery for a maternal indication must always
be considered. Placenta previa is associated with a nearly doubling of the rate of congenital
malformations, the most serious including major anomalies of the
central nervous system, gastrointestinal tract, cardiovascular system, and respiratory
tract. At the time of diagnosis of placenta previa, a detailed fetal survey should be
performed for anomalies.
Abnormal placental location can be further complicated by abnormal growth of the
placental mass into the substance of the uterus, a condition termed placenta previa
accreta. In placenta previa accreta, the poorly formed decidua of the lower uterine
segment offers little resistance to trophoblastic invasion. The incidence of this severe
complication is variously reported as 5% to 10% of placenta previas, although the inci-
dence is much higher in patients with multiple previous cesarean sections. At the time of
delivery, sustained and significant bleeding may ensue, often requiring hysterectomy.

ABRUPTIO PLACENTAE

Whereas placenta previa refers to the abnormal location of the placenta, abruptio
placentae, often called placental abruption, refers to the premature separation of the
normally implanted placenta from the uterine wall.
Etiology. Placental abruption occurs when there is hemorrhage into the decidua
basalis, leading to premature placental separation and further bleeding. The cause for
this bleeding is not known.
Placental abruption is associated with maternal hypertension and sudden
decompression of the uterus in cases of rupture of membranes in a patient with
excessive amniotic fluid (hydramnios) or after delivery of the first of multiple fetuses.
A more recent and serious association involves cocaine use by the mother, which
leads to intense vasoconstriction and, in some cases, sudden separation of the
placenta from the uterine wall. Placental abruption can also occur following trauma,
even when the extent of injury is not considered serious. For example, pregnant
women involved in motor vehicle accidents can sustain placental abruption even
though lap belts and shoulder strap restraints are used. Moreover, direct trauma to the
abdomen is not required, because sudden force applied elsewhere to the body can
result in coup and countercoup injury.
 Fig. 7. Types of placental abruption
Clinical findings and Diagnosis
The signs and symptoms can vary considerable. External bleeding can be profuse
or there may be no external bleeding (concealed hemorrhage) but the placenta is
completely sheared off and the fetus dead. Besides, common findings are uterine
tenderness, back pain, fetal distress, uterine hypertonus or high-frequently
contractions, idiopathic preterm labor, and a dead fetus.
Because the separation of the placenta from the uterus interferes with oxygénation
of the fetus, a nonreassuring fetal status is quite common in cases of significant
placental abruption. Thus, in any patient in whom placental abruption is suspected,
electronic fetal monitoring should be included in the initial management.
Placental abruption may be total and partial.
.
 Fig. 8 Total placental abruption
Coagulation abnormalities may also be found, thereby compounding the patient's
already compromised status. Placental abruption is the most common cause of
consump-tive coagulopathy in pregnancy and is manifested by hypofibrinogenemia
as well as by increased levels of fibrin degradation products. The platelet count can
also be decreased, and prothrombin time and partial thromboplastin time can be
increased as well. Such coagulopathy is a result of intravascular and retroplacental
coagulation. The intravascular fibrinogen is converted to fibrin by way of the
extrinsic clotting cascade. Thus not only is serum fibrinogen decreased but platelets
and other clotting factors are thereby also depleted.
Ultrasound is of little benefit in diagnosing placental abruption, except to exclude
placenta previa as a cause for the hemorrhage. Relatively large retroplacental clots
may be detected on ultrasound examination, but the absence of ultrasonographically
identified retroplacental clots does not rule out the possibility of placental abruption,
and conversely, a retroplacental echogenic area can be seen in patients without
placental abruption. The diagnosis rests on the classic clinical presentation of vaginal
bleeding, a tender uterus, and frequent uterine contractions with some evidence of
fetal distress. The extravasation of blood into the uterine muscle causes contractions
such that the resting intrauterine pressure, when measured with an intrauterine pres-
sure catheter, is often elevated; this sign can be helpful in making the diagnosis. The
entire uterus has a purplish or bluish appearance, owing to such extravasation of
blood (Couvelaire uterus) – Fig. 9.

Fig. 9 Couvelaire uterus

Management of a patient with placental abruption when the fetus is mature is
hemodynamic stabilization and delivery. Appropriate facilities and staff for cesarean
section must be continuously available whenever placental abruption is suspected
Careful attention to blood component therapy is critical, and the coagulation status must
be followed closely. Unless there is evidence of fetal distress or hemodynamic
instability, vaginal delivery by oxytocin induction of labor is preferable to a cesarean
delivery, although the maternal or fetal status may require that abdominal delivery be
performed. When the fetus is not mature and the placental abruption is limited and not
associated with premature labor or fetal or maternal distress, observation with close
monitoring of both fetal and maternal well-being may be considered while awaiting fetal
maturity. In the case of Couvelaire uterus total hysterectomy is performed because of
danger of uterine hypotony and disseminated intravascular clotting syndrome.

AMNIOTOMY. Rupture of the membranes as early as possible has long been

championed in the management of placental abruption. The rationale for amniotomy
is that the escape of amnionic fluid might both decrease bleeding from the
implantation site and reduce the entry into the maternal circulation of thromboplastin
and perhaps activated coagulation factors from the retroplacental clot. There is no
evidence, however, that either is accomplished by amniotomy. If the fetus is
reasonably mature, rupture of the membranes may hasten delivery. If the fetus is
immature, the intact sac may be more efficient in promoting cervical dilatation than
will a small fetal part poorly applied to the cervix.

LABOR. With slight degrees of placental separation, uterine contractions are

usually of normal frequency, duration, and intensity. With extensive placental
abruption, the uterus will likely be persistently hypertonic. The baseline intra-
amnionic pressure may be 25 to 50 mm Hg or higher, with rhythmic increases up to
75 to 100 mm Hg. Because of persistent hypertonus, it may be difficult at times to
determine by palpation if the uterus is contracting and relaxing to any degree (Fig.
32–9 ).

OXYTOCIN. Although hypertonicity characterizes myometrial function in most

cases of severe placental abruption, if no rhythmic uterine contractions are
superimposed, then oxytocin is given in standard doses. Uterine stimulation to effect
vaginal delivery provides benefits that override the risks. The use of oxytocin has
been challenged on the basis that it might enhance the escape of thromboplastin into
the maternal circulation and thereby initiate or enhance consumptive coagulopathy or
amnionic fluid embolism syndrome. There is no evidence to support this fear (Clark
and colleagues, 1995; Pritchard and Brekken, 1967).

VASA PREVIA
 Although rarely encountered, vasa previa presents significant risk to the fetus. In
vasa previa (Fig. 10), the umbilical cord inserts into the membranes of the placenta
(rather than into the central mass of the placental tissue), and one such vessel lies
below the presenting fetal part in the vicinity of the internal os. If this vessel ruptures,
fetal bleeding occurs. Because of the low blood volume of the fetus, seemingly
insignificant amounts of blood may place the fetus in jeopardy. A small amount of
vaginal bleeding associated with fetal tachycardia may be the clinical presentation. A
test to distinguish fetal blood from maternal blood, such as the Kleihauer-Betke or the
Apt test, can be of value when such a condition is suspected. These tests distinguish
between maternal and fetal blood on the basis of the marked resistance to pH changes
in fetal red cells compared with the friable nature of adult red cells in the presence of
strong bases. Immediate cesarean section is the only way to save the fetus in vasa
previa.

Fig. 10 Sonogram showing placenta (P), succenturiate lobe (S), and leading fetal

vessels in vasa previa (arrow). (From Gianopoulas J, Carver T, Tomich PG, Karlman
 R, Gadwood K. Diagnosis of vasa previa with ultrasonography. Obstet Gynecol.
69:488, 1987).

APPROACH TO A PATIENT WITH VAGINAL BLEEDING IN THE

SECOND HALF OF GESTATION

In any woman with vaginal bleeding during the second half of pregnancy, fetal
and maternal status should be evaluated promptly. At the same time that a search is
undertaken for the cause of the bleeding, attention must be directed toward stabiliza-
tion of the maternal hemodynamic state. The approach is not unlike that for any
hemorrhaging patient and includes ready access for fluid replacement through one or
more large-bore intravenous catheters, serial complete blood counts, type and cross-
match of ample amounts of blood, and if the condition is unstable, intracardiac
monitoring. Attention to urinary output is a simple and important reflection of the
volume status of a patient. Because normal antepartum blood volume expansion is
substantial, pregnant women may lose considerable amounts of blood before vital
sign changes are apparent. In more than half of the cases of significant vaginal
bleeding in pregnancy, no specific cause can be discovered despite careful evaluation.
In general, patients with significant bleeding should remain hospitalized until
delivery, although in some cases minimal bleeding ceases, and the patient appears
normal in every way. Caution is advised, however, because patients with bleeding of
undetermined etiology can be at greater risk for preterm delivery, intrauterine growth
restriction, and fetal distress than patients with bleeding of known cause.
HEMORRHAGE IN THE THIRD STAGE OF LABOR AND EARLY
PUERPERAL PERIOD
Postpartum hemorrhage is defined as blood loss in excess of 400 mL at the
time of vaginal delivery.
Postpartum hemorrhage before delivery of the placenta is called third-stage
hemorrhage.
Postpartum hemorrhage after delivery of placenta during the first two hours is
called as hemorrhage in early puerperal stage.
Hemorrhage after placental separation is stopped thanks to:
 7. uterine contractions – caliberes of ruptured vessels decreases during
uterine contractions;
8. formation of thrombs, especially in the region of placental site;
9. torsion of thin septs in which vessels are situated.

Causes of Postpartum Hemorrhage:

9. uterine atony,
10.genital tract trauma,
11.bleeding from the placental site (retained placental tissue, low placental
implantation, placental adherence, uterine inversion)
12.coagulation disorders.

The main causes of third-stage bleeding are genital tract trauma

and bleeding from placental site.
The main causes of hemorrhage in early puerperal stage are all of the
above causes of Postpartum hemorrhage.
Predisposing factors and causes of immediate postpartum hemorrhage:
Uterine atony:
1. Overdistended uterus – multiple fetuses, Hydramnios, distention with
clots.
2. Anesthesia or analgesia – halogenated agents, conducted analgesia with
hypertension.
3. Exhausted myometrium – rapid labor, prolonged labor, oxytocin
or prostaglandin stimulation.
4. Chrionamnionitis.
4. Previous uterine atony.
Genital tract trauma:
1. Complicated vaginal delivery.
2. Cesarean section or hysterectomy, forceps or vacuum.
3. Uterine rupture; risk increased by: previously scarred uterus, high
parity, hyperstimulation, obstructed labor, intrauterine manipulation.
 4. Large episiotomy, including extensions.
5. Lacerations of the perineum, vagina or cervix.

Bleeding form placental implantation cite:

1. Retained placental tissue – avulsed cotyledon, succentuariate lobe
2.Abnormally adherent – accreta, increta, percreta.
Coagulation defects – intensifies other causes:
1. Placental abruption.
2. Prolonged retention of dead fetus.
3. Amnionic fluid embolism.
4. Saline-induced abortion.
5. Sepsis with endotoxemia.
6. Severe intravescular hemolysis.
7. Massive transfusions.
8. Severe preeclampsia or eclampsia.
9. Congenital coagulopathies.
Clinical findings and diagnosis
The two most common causes of immediate hemorrhage are hypotonic
myometrium (uterine atony) and lacerations of the vagina and cervix. Retention
of part or all of the placenta, a less common cause, may produce either immediate
or delayed hemorrhage (or both).
Uterine atony is called as total absence of uterine contractions into the
external irritation. Uterine hypotony is called as presence of inadequate uterine
contractions on the external irritation. In the pauses between uterine contractions a
uterus is soft. But blood form clots in the case of uterine hypo- or atony. These
clots are stored in the uterine cavity that’s why a uterus is enlarged in sizes.
The differentiation between bleeding from uterine atony and from lacerations
is tentatively based on the condition of the uterus. If bleeding persists despite a firm,
well-contracted uterus, the cause of the hemorrhage most probably lacerations.
Bright red blood also suggests lacerations. To ascertain the role of lacerations as a
cause of bleeding, careful inspection of the vagina, cervix, and uterus is essential.
 Placental accreta is any implantation of the placenta in which there is
abnormally firm adherence to the uterine wall. As a consequence of partial or
total absence of the decidua basalis and imperfect development of the
fibrinoid layer (Nitabush’s membrane):
9. the placental villi are attached into the basal layer - placenta adhaerens;
10. the placental villi are attached to the myometrium - placenta accreta (Fig.
11);
11. extensive growth of placental tissue into the uterine muscle itself – placenta
increta;
12. complete invasion through the sickness of the uterine muscle to the serosa or
beyond – placenta percreta (Fig. 12, 13 ).

Fig. 11 A fatal case of inverted uterus associated with placenta

accreta following delivery at home.
 Fig. 12 Placenta percreta in a woman at term with a known placenta previa.
The placenta had grown into the entire lower uterine segment. (Photograph
courtesy of Dr. Tom Dowd.)
 Fig. 13 Placenta percreta. On the left, the placenta is fungating through the
fundus above the old classical cesarean section scar. In the opened specimen on
the right, the variable penetration of the fundus by the placenta is evident.
(From Morison, 1978.)
Complete or total placenta accreta will not cause bleeding because the placenta
remains attached, but partial ( the abnormal adherence involves a few to several
cotyledons) or focal ( the abnormal adherence involves a single cotyledon) type
may cause profuse bleeding, as the normal part of the placenta separates and the
myometrium cannot contract sufficiently to occlude the placental site vessels.
The abnormal placental adherence is diagnosed by:
1. Absence of the signs of placental separation during
30 minutes. Signs of placental separation:
7. the uterus rises in the abdomen;
8. the shape of the uterus changes from discoid to globular
9. the umbilical cord lengthens.
 2. External bleeding – in the case of partial adherence, absence of the bleeding
– in the case of total placenta accreta.
3. Manual removal of the placenta confirms the diagnosis of different types
of abnormal placental adherence. In the case of partial placental adhaerence it
stops bleeding, but in the case of placenta accreta, increta and percrata it increases
bleeding. Attempts at manual removal are futile. That’s why in these cases
manual removal of the placenta should be stopped immediately and hysterectomy
should be performed.
Coagulation disorders are recognized thanks to coagulation
studies and inspection for clot formation.
MANAGEMENT OF THE PATIENTS IN THE THIRD-STAGE
BLEEDING
UTERINE ATONY
17. Catheterization of the urinary bladder.
18. Cold on the lower abdomen.
19. Manual massage of the uterine corpus: one hand gently massages the
uterus from the abdomen while the other is inserted so that the cervix is cradled in the
fingers and thumb to allow maximal compression and massage.
20. Prescription of the uterine contracting drugs: oxytocin – 5 units,
methylergonovine (Methergine) – 1mL intramuscularly or in intravenous infusion. If
the uterus remains atonic and the placental site bleeding continuos during the
oxytocin infusion, a rapid continuos intravenous infusion of dilute oxytocin (20 units
in 1L of normal saline) should be given to increase uterine tone. Analogues of
prostaglandin F2 alpha (Hemabate) in a dose 5 mg given intramuscularly or
intravenously are quite effective in controlling postpartum hemorrhage caused by
uterine atony. Large-bore intravenous catheters – 1 or 2 well functioning lines.
Mifipristone – 800 mkg per rectum, enzaprost – 5 mg into anterior abdominal wall.
21. Manual exploration of the uterine cavity under the general anesthesia,
bimanual uterine compression. (fig. 14)
22. A tampon with ether is inserted into the posterior fornix.
 23. Clemmas on the parametrium or into the cervix of the uterus are putted
on.
24. Aorta compression to the spinal column.
In a case if blood loss increase 800 mL and bleeding continuos - surgery
management should be perform:
1.Uterine artery ligation;
2. Hypogastric artery ligation;
3. Hysterectomy.

Fig.14 Bimanual compression of the uterus and massage with the

abdominal hand usually will effectively control hemorrhage from uterine atony.

GENITAL TRACT TRAUMA – ligation and suturing of all ruptures of the

vagina, cervix and perineum. In the case of uterine rupture – hysterectomy should
be performed.
BLEEDING FROM PLACENTAL IMPLANTATION CITE
1) placental separation signs are absent – manual separation and removal of
the placenta and exploration of the uterine cavity, uterine massage, uterine
contracting drugs are prescribed;
 2) complete and partial placenta adhaerens - manual separation and removal
of the placenta (Fig. 15);
3) placenta accreta, increta and percreta – hysterectomy. With more
extensive involvement, however, hemorrhage becomes profuse as manual
removal of the placenta is attempted.

Fig. 15 Technique of manual removal of the placenta

Technique of Manual Removal. Adequate analgesia or anesthesia is
mandatory. Aseptic surgical technique should be employed. After grasping the
fundus through the abdominal wall with one hand, the other hand is introduced into
the vagina and passed into the uterus, along the umbilical cord. As soon as the
placenta is reached, its margin is located and the ulnar border of the hand insinuated
between it and the uterine wall. Then with the back of the hand in contact with the
uterus, the placenta is peeled off its uterine attachment by a motion similar to that
employed in separating the leaves of a book. After its complete separation, the
placenta should be grasped with the entire hand, which is then gradually withdrawn.
Membranes are removed at the same time by carefully teasing them from the
decidua, using ring forceps to grasp them as necessary. Some prefer to wipe out the
uterine cavity with a sponge. If this is done, it is imperative that a sponge not be left
in the uterus or vagina.
Placenta Accreta, Increta, and Percreta
In most instances, the placenta separates spontaneously from its implantation
site during the first few minutes after delivery of the infant. The precise reason for
delay in detachment beyond this time is not obvious always, but quite often it seems
to be due to inadequate uterine contraction. Very infrequently, the placenta is
unusually adherent to the implantation site, with scanty or absent decidua, so that
the physiological line of cleavage through the decidual spongy layer is lacking. As a
consequence, one or more cotyledons are firmly bound to the defective decidua
basalis or even to the myometrium. When the placenta is densely anchored in this
fashion, the condition is called placenta accreta.
The term placenta accreta is used to describe any placental implantation in
which there is abnormally firm adherence to the uterine wall. As the consequence of
partial or total absence of the decidua basalis and imperfect development of the
fibrinoid layer (Nitabuch layer), placental villi are attached to the myometrium in
placenta accreta, actually invade the myometrium in placenta increta, or penetrate
through the myometrium in placenta percreta. The abnormal adherence may involve
all of the cotyledons (total placenta accreta), a few to several cotyledons (partial
placenta accreta), or a single cotyledon (focal placenta accreta).
Significance
An abnormally adherent placenta, although an uncommon condition, assumes
considerable significance clinically because of morbidity and, at times, mortality from
severe hemorrhage, uterine perforation, and infection. The true frequencies of
placenta accreta, increta, and percreta are unknown. Breen and associates (1977)
reviewed reports published since 1891. The incidence varied from 1 in 540 deliveries
to 1 in 70,000 deliveries, with an average incidence of about 1 in 7000. Read and co-
workers (1980) reported an incidence of about 1 per 2500 deliveries and concluded
that today there is a higher reported incidence, lower parity, and greater incidence of
associated placenta previa, as well as decreasing maternal and perinatal mortality.

Abnormal placental adherence is found most often in circumstances where

decidual formation was likely to have been defective. Associated conditions include
implantation in the lower uterine segment, over a previous cesarean section scar or
other previous uterine incisions, or after uterine curettage. In his review of 622
reported cases of placenta accreta collected between 1945 and 1969, Fox (1972)
noted the following characteristics: (1) placenta previa was identified in a third of
affected pregnancies, (2) one fourth of the women had been previously delivered by
cesarean section, (3) nearly one fourth had previously undergone curettage, and (4)
one fourth were gravida 6 or more. Read and co-workers (1980) reported similar
findings for women studied in the 1970s; however, the overall incidence and parity
had decreased. In a preliminary investigation, Hardardottir and colleagues (1996)
found that almost half of placentas in women with a prior cesarean section had
adherent myometrial fibers detected microscopically.
Antepartum hemorrhage is common, but in the great majority of cases, bleeding
before delivery is the consequence of coexisting placenta previa. Myometrial
invasion by placental villi at the site of a previous cesarean section scar may lead to
uterine rupture during labor or even before (Berchuck and Sokol, 1983). Archer and
Furlong (1987) described a woman who presented with an acute abdomen from
massive hemoperitoneum caused by placenta percreta at 21 weeks’ gestation. In
women whose pregnancies go to term, however, labor will most likely be normal in
the absence of an associated placenta previa or an involved uterine scar.
The problems associated with delivery of the placenta and subsequent
developments vary appreciably, depending upon the site of implantation, depth of
myometrial penetration, and number of cotyledons involved. It is very likely that
focal placenta accreta with implantation in the upper uterine segment develops much
more often than is recognized. The involved cotyledon is either pulled off the
myometrium with perhaps somewhat excessive bleeding, or the cotyledon is torn
from the placenta and adheres to the implantation site with increased bleeding,
immediately or later.
 With more extensive involvement, hemorrhage becomes profuse as delivery of
the placenta is attempted. Successful treatment depends upon immediate blood
replacement therapy, and nearly always prompt hysterectomy.
With total placenta accreta, there may be very little or no bleeding, at least until
manual placental removal is attempted. At times, traction on the umbilical cord will
invert the uterus, as will be described in the next section. Moreover, usual attempts at
manual removal will not succeed, because a cleavage plane between the maternal
placental surface and the uterine wall cannot be developed. The safest treatment in
this circumstance is prompt hysterectomy.
In the 622 cases reviewed by Fox (1972), the most common form of
“conservative” management was manual removal of as much placenta as possible and
then packing of the uterus. One fourth of the women died, which was four times as
many as when treatment consisted of immediate hysterectomy. So-called
“conservative” treatment in at least four instances was followed by an apparently
normal pregnancy.
The possibility exists that placenta increta might be diagnosed antepartum. Cox
and associates (1988) described a case of placenta previa in which they also were
able to identify placenta increta ultrasonically from the lack of the usual subplacental
sonolucent space. They hypothesize that the presence of this normal subplacental
sonolucent area represents the decidual basalis and the underlying myometrial tissue.
The absence of this sonolucent area is consistent with the presence of a placenta
increta. Pasto and associates (1983) confirmed that the absence of a subplacental
sonolucent or “hypoechoic retroplacental zone” is consistent with placenta increta.
Inversion of the Uterus
Complete uterine inversion after delivery of the infant is almost always the
consequence of strong traction on an umbilical cord attached to a placenta implanted
in the fundus (Fig. 16).
Most likely site of placental implantation in cases of uterine inversion. With
traction on the cord and the placenta still attached, the likelihood of inversion is
obvious.
 Fig. 16 Contributing to uterine inversion is a tough cord that does not readily
break away from the placenta, combined with fundal pressure and a relaxed uterus,
including the lower segment and cervix.
Placenta accreta may be implicated although uterine inversion can occur
without the placenta being so firmly adherent. At times, the inversion may be
incomplete (Fig. 11).
Shah-Hosseini and Evrard (1989) reported an incidence of about 1 in 6400
deliveries at the Women and Infants Hospital of Rhode Island. Of the 11 inversions
identified, most were in primiparous women and immediate vaginal replacement of
the inverted uterus was successful in nine instances. Platt and Druzin (1981) reported
28 cases in over 60,000 deliveries, for an incidence of about 1 in 2100. These same
investigators suggested that parenteral magnesium sulfate, which was administered to
women with pregnancy-induced hypertension, might have played a role in the
etiology of this complication.
Uterine inversion is most often associated with immediate life-threatening
hemorrhage, and without prompt treatment it may be fatal (Fig. 11).
 In the past it was stated that shock tends to be disproportionate to blood loss.
Careful evaluation of the effects from transfusion of large volumes of blood in such
cases does not support this concept, but instead makes it very apparent that blood loss
in such circumstances was often massive but greatly underestimated (Watson and
associates, 1980).
Treatment
Delay in treatments increases the mortality rate appreciably. It is imperative that
a number of steps be taken immediately and simultaneously:
1. Assistance, including an anesthesiologist, is summoned immediately.
2. The freshly inverted uterus with placenta already separated from it may often
be replaced simply by immediately pushing up on the fundus with the palm of the
hand and fingers in the direction of the long axis of the vagina.
3. Preferably two intravenous infusion systems are made operational, and
lactated Ringer solution and whole blood are given to reverse hypovolemia.
4. If attached, the placenta is not removed until the infusion systems are
operational, fluids are being given, and anesthesia, preferably halothane or enflurane,
has been administered. Tocolytic drugs have also been used successfully for this
purpose. Terbutaline, ritodrine, or magnesium sulfate have been used for uterine
relaxation and repositioning (Catanzarite and associates, 1986; Kovacs and DeVore,
1984; Thiery and Delbeke, 1985). To remove the placenta before this time increases
hemorrhage. In the meantime, the inverted uterus, if prolapsed beyond the vagina, is
replaced within the vagina.
5. After removing the placenta, the palm of the hand is placed on the center of
the fundus with the fingers extended to identify the margins of the cervix. Pressure is
then applied with the hand so as to push the fundus upward through the cervix.
6. Oxytocin is not given until after the uterus is restored to its normal
configuration.
As soon as the uterus is restored to its normal configuration, the agent used to
provide relaxation is stopped and simultaneously oxytocin is started to contract the
uterus while the operator maintains the fundus in normal relationship. Initially,
bimanual compression will aid in the control of further hemorrhage until uterine tone
is recovered.

Fig.17 Uterine replacement

After the uterus is well contracted, the operator continues to monitor the uterus
transvaginally for any evidence of subsequent inversion.
Surgical Intervention. Most often, the inverted uterus can be restored to its
normal position by the techniques described. If the uterus cannot be reinverted by
vaginal manipulation because of a dense constriction ring (Fig. 18), laparotomy is
imperative.
 Fig. 18 Completely inverted uterus viewed from above.
The fundus then may be simultaneously pushed upward from below and pulled
from above. A traction suture well placed in the inverted fundus may be of aid. If the
constriction ring still prohibits reposition, it is carefully incised posteriorly to expose
the fundus. A graphic outline of this surgical technique was described by Van Vugt
and associates (1981). After replacement of the fundus, the anesthetic agent used to
relax the myometrium is stopped, oxytocin infusion is begun, and the uterine incision
repaired. Following restoration of the uterus, the adjacent viscera are carefully
examined for trauma.
Attention ! Irrespective of the apparent cause, whenever there is any suggestion at
the delivery or postpartum of excessive blood loss from the genital tract,
immediate steps must be taken to identify the presence of uterine atony, retained
placental fragments, and trauma.
5. At least one or, in the presence of frank hemorrhage, two
intravenous infusion systems of large caliber must be established right
away to permit rapid administration of aqueous electrolyte solutions and
blood as nedded
 6. An operating room and a surgical team, including
an anesthesiologist, must be immediate available.
COAGULATION DEFECTS
The treatment of coagulation defects is aimed at correcting the
coagulation defects and include infusion of:
3. platelet concentrate – increases platelet count by about 20 000 to 25 000;
7. cryoprecipitate – supplies fibrinogen, factor VIII, and factor XIII (3 to
10 times more concentrated than the equivalent volume of fresh plasma);
8. fresh-frozen plasma – supplies all factors except platelets (1 g of fibrinogen);
9. packed red blood cells – raises hematocrit 3 % to 4 %.

OBSTETRIC SHOCK. TERMINAL STATES IN OBSTETRICS

Shock encompasses various pathophysiological aberrations that lead to
inadequate tissue perfusion and impaired cellular metabolism. Although hypotension
often is the most obvious clinical sign in shock of any cause, such blood pressure
changes are the final common manifestation of a number of distinct pathologic
processes. The successful clinical management of patients in shock depends on the
proper definition of the underlying pathophysiology as well as an under of the unique
effects of pregnancy on such conditions.
Uterine bleeding (hemorrhage) during labor and early puerperal stage play an
important role among different kinds of severe obstetrics pathology, such as
hemorrhagic shock, disseminated intravascular coagulopathy, sepsis and other.
Uterine bleeding is the leading cause of maternal death.
Uterine bleeding frequency is 8,0 – 11, 0 %.
The main causes of uterine bleeding are:
During pregnancy: placenta praevia, placenta abruptio.
During labor: placenta praevia, placenta abruptio, uterine rupture, traumatization
of the soft birth canal tissues.
In the third period of labor and early puerperal stage: uterine hypo- and atony;
uterine rupture and traumatization of the soft birth canal tissues; placenta accreta,
increta, and percreta; retention of some parts of afterbirth in the uterine cavity;
thrombohemorrhagic bleeding.
Methods of blood loss determination
10. Libov’s method.
After surgical intervention the napkins, which are filling by blood, should be
weighted.
Blood loss volume = Weight x 15 % ( if blood loss is < 1000 ml);
2
Blood loss volume = Weight x 30 % ( if blood loss is > 1000 ml).
2
11. By hematocrit
Hematocr Blood
it, % loss
volume,
ml
44–40 500
38–32 1000
30–22 1500
< 22 >
1500
12. Algover’s index
Shock’ index = Heart rate
Systolic arterial blood pressure
In normal Algover’s index is < 1.
Algov
Blood loss
er’s index volume, %
out of
circulating
blood volume
0,8 10 %
and <
 0,9 – 20 %
1,2

1,3 – 30 %
1,4
1,5 40 %
and >

HEMORRHAGIC (HYPOVOLEMIC) SHOCK

Hemorrhagic shock is a very serious complication in the case of pathological
hemorrhage.
Physiological blood loss during labor is 0, 5 % out of puerperant’ weight.
Physiological blood loss is 350, 0 – 400, 0 ml.in the puerperant with 70-75 kg of
weight. If blood loss predominate physiological one, hemorrhagic shock have been
occurred.
There are 4 stages of hemorrhagic shock according to Baker classification.
Evaluation of hemorrhagic shock stage severity is presented in the table.
Evaluation of hemorrhagic shock stage severity
Shock Hypovolemia Circulating Blood loss, % from body weight Hemodynamic
stage stage blood ml diuresis
volume
deficiency
I Mild 10 %-20% 500 – 1,0 – 1,5 % Ps – 90-100 be
1000,0 Arterial blood
Central Venou
Diuresis – N.
II Moderate 20%-30% 1000,0- 1,5 - Ps – 120 beats
1500,0 2,0 % BP - <100 mm
CVP – < 60 m
Diuresis – < 5
III Severe 30%-40% 1500,0– 2,0 – Ps – 140 beats
2000,0 2,5 % BP - < 70 mm
 CVP – < 40 m
Diuresis – < 3
IV Considerable 40% and > 2000,0 and > > Ps – 140 beats
2,5 % BP – < 50 mm
CVP – 0;
Diuresis– anur

The main principles of obstetrics hemorrhage and hemorrhagic shock

treatment:
31. Hemorrhage stopping.
32. Determination of blood loss stage.
33. Restoration of the circulating blood volume.
34. Normalization of vascular tone.
35. Blood reology, its structural, biochemical, and electrolytes compounds
correction.
36. Detoxication therapy.
37.Desensibilizing therapy.
38.Correction of clotting, antyclotting, fibrinolitic systems functions.
39.Regulation of the main human organs functions.
40. Prevention of infectious complications.
INTERM restoration of the circulating blood volume – is the main step in the
treatment of acute blood loss. Human organism should be survived in the case of 2/3-
erythrocytes volume loss, but it doesn’t survive in the case of 1/3 plasma volume
loss. That’s why it should be remembered that in considerable blood loss the first step
is the transfusion not only blood, but also кровозамінники, which eliminate
hypovolemia very quickly.
Transfusion therapy in obstetrics hemorrhages

Blood Volume Crysta- Refortan, Fresh- Albumin Erythro-

loss of infusion lloids Gelofusin frozen (10-20 massa
Stabisol plasma %)
 10-20 10-15 10 ml /kg - -
% 2500 ml/
500- ml kg
1000ml

20-30 10 ml 10 ml /kg 5-10 - 5 ml /kg

% 3000 /kg ml /kg
1000- ml
1500
ml

30-40 7 ml/kg 7 ml/kg 10 - 200 ml 10-20

% 4000 15 ml /kg ml /kg
1500- ml
2000
ml

40- 7 ml/kg 10 ml /kg 15 - 200 ml 30 ml

and > > 6000 20 ml /kg /kg
> ml
2000 ml
The volume of infusion therapy in hemorrhagic shock should be predominated in
1,5-2,5 times its real blood loss.
Glucose transfusion doesn’t administrated in blood loss, because it very quickly
enter intracellular space and doesn’t increase circulating blood volume, it caused
metabolic acidosis.
Attention! Erythrocyte transfusion has value only after hemodynamics and
peripheral blood circulation normalization. Only in these conditions erythrocytes
should be taken oxygen.
Attention ! In all stages of hemorrhagic shock 2-4 veins should be catheterized
in one moment (one or two of them are central, such as v. subclavia).
Infusion speed depends on blood loss volume and patient state. In the case of
hemorrhagic shock and low arterial blood pressure it should be reach 200 ml per
minute. The infusion speed gradually decreased to 150-100-50 ml-per minute in the
case of increasing arterial blood pressure to 80-90 mm Hg.
The main prescription of infusion therapy in the case of acute blood lose is the
stabilization of central hemodynamics which lead to cerebral and coronary blood
circulation stabilization.
Vascular tone normalization.
In the first stage of hemorrhagic shock because of vascular spasm presence
spasmolitics drugs are used, such as Nospani, Papaverini hydrochloridi. On the II-III-
IV stages because of vascular dilation glucocorticoids are prescribed. They are:
Prednisoloni, Hydrocortisone – in the dose 1,5-2 g/ daily, Dexametazoni.
If intravenous insertion 800-1000 ml any solution with the speed of 50-100
ml/per minute doesn’t change (increase) arterial blood pressure – vasopressors agents
should be prescribed, such as Remestip – in the dose 0,2-1,0 mg; Dopamine –
5mkg/kg/minute or glucocrticoids.
In considerable infusion therapy after circulating blood volume normalization
diuresis stimulation is recommended. For this purpose Euphillini in the dose 3 mh per
kg, lazix – 2-4 mg/kg or furosemidi in the dose 6-8 mg/kg have been used.
Structural, biochemical, electrolytes compounds correction of blood,
detoxycation, desensibilizing therapy and normalization of clotting, antyclotting,
fibrinolytic systems functions and functions of the main human organs is obligatory
in the treatment of hemorrhagic shock.
Introduction of cardiologic drugs is possible only after blood loss restoration.
For this purpose such agents have been used as Corgliconi –0, 6 % - 0,5 –1 ml;
Cocarboxylase – 50 mg twice a day.
Prevention of infectious complications by prescription of wide spectrum
antibiotics (cefalosporines, aminoglycozides) in the daily dose is recommended also.

Main steps of urgent medical care in the obstetrics bleeding

during pregnancy, labor, and puerperal stage
10. Blood loss is 0, 8 – 1, 0 % of body weight
1. To determine the cause of hemorrhage
 Pla Uterine Uterine
centa cervix hypo- and
praevia, rupture, deep atony; uterine
placenta vagival rupture and
abruptio, ruptures, traumatization
uterine traumatization of the soft
rupture of the soft birth canal
birth canal tissues;
tissues. placenta
accreta,
increta, and
percreta;
retention of
some parts of
afterbirth in
the uterine
cavity

Bleeding stopping

Urgent Rupture Manual

cesarean suture uterine
section revision

2. To start intravenous infusion: crystalloids (0,9 % NaCl + 10

Units of oxytocin), colloids – Refortan, Stabisol, Poliglucin.

11. Blood loss is 1, 0 %– 1, 5 % of body weight.

1. Injection of 250 – 1000 mkg Prostin F2a intramuscularly or 0,4 mg Remestip
+ 10 ml 0,9 % NaCl into uterine cervix.
 2. Catheterization of two veins (one of them is v. subclavia), intravenous
transfusion of autoblood, plasma, erythrocyte massa, Refortan, Stabisol.

Attention! Surgical intervention should be performed in continuing

bleeding! (if blood loss is more than 1, 0 % - 800 ml of body weight ).

12. Blood loss is > 1, 5 % of body weight.

1. Laparotomy. Total hysterectomy without adnexa (adnexa are removed
if inflammatory, degenerative changes are presented).

2. Restoration of the blood circulating volume: autoblood, donor’s blood – 100

% from blood loss, cryoprecipitate, albumin.
DISSEMINATED INTRAVASCULAR COAGULOPATHY (DIC)
DIC is not a distinct clinical entity; rather, it represents a manifestation of
various disease processes that have in common activation of intravascular clotting
and fibrinolysis, resulting in excess consumption of solutable coagulation
components. In obstetrics, secondary fibrinogenolysis commonly dominates the
clotting aberration and results in the circulation of fibrin and fibrinolytic split
products, which further accentuates the clinical presentation of henorrhage. In
addition, sometimes a dilutional coagulopathy is encountered in pregnancy. This
condition obtains when massive hemorrhage is teplaced only by red blood cells and
crystalloids solution, resulting in a dilutional depletion of platelets and soluble
clotting factors.. In practice, the hemorrhage associated with dilutional coagulopathy
often results in hypotension and shock. The tissue hypoxia that accompanies shock of
any cause is well known to potentially activate the coagulation-fibrinolysis cycle
associated with DIC.
DIC is the pathological complex, which is characterized by blood clotting that
has been leading to microcirculation blockade by fibrin in the main human organs
(lungs, kidneys, liver). Dysfunction of these organs is the result of their damage. In
the end of this process thrombohemorrhagic disorders have been developed.
 The main causes of DIC in the obstetrics are:
40.All kinds of shock (hemorrhagic, septic, anaphylactic);
41.Placenta abruption;
42. Embolic fluid embolism;
43. OPH – hestosis;
44. Hypotonic bleeding;
45. Uterine ruptures;
46. Excessive labor induction;
47. Cesarean section;
48.Extragenital pathology;
49.Septic abortion;
50.Puerperal endometritis;
51.Intensive uterine massage;
52.dead fetus syndrome
Classification of thrombohemorrhagic syndrome
7. By clinical duration:
1. Acute;
2. Subacute;
3. Chronic.
8. By stages:
I stage – hypercoagulation;
II stage – hypocoagulation without generalizing fibrinolysis
activation; III stage – hypocoagulation with generalizing
fibrinolysis activation; IV stage – total fibronolysis.
Clinical manifestatiuon.
Clinical manifestation of DIC is connected with ischemic and hemorrhagic
changes in human organs and tissues. They are:
16. Hemorrhages into skin and mucous membranes;
17. Hemorrhages from the places of injections, incisions, uterus.
18. Necrosis of some areas of skin and mucous membranes;
19. Central nervous system impairment;
 20. Acute renal, liver, lung insufficiency.

Laboratory diagnosis of DIC

The main laboratory data

Blood Spontaneous Thrombin Throm- Thrombin
Stages clotting thrombus test bocytes time,
time, lisis number, seconds
minutes 10x9/l
I.Hypercoagulation <5(N) absent (N) 7-11 (N) 175-425 < 24
(N)
II.Hypocoagulation 5 -12 absent 7-11 < 120 >60
without
generalizing
fibrinolysis

III Hypocoagu- >12 quick 20-60 < 100 >100

lation with
generalizing
fibrinolysis
IV. Total > 60 Thrombus >60 <60 >180
fibrinolysis doesn’t
formed

General principles of DIC treatment are:

16. Heparin, fibrinogen are contraindicated in all stages of
thrombohemorrhagic syndrome.
17. Proteolytic enzymes inhibitors in the dose of 10 mg/kg/hour have been used
for inhibit excessive fibrinolysis and prevention of intracellular clotting.
18.Early and quick introduction of fresh frozen donor’s plasma. The main aim of
its usage is the restoration of haemostatic potential of blood (it contains all
soluble clotting factors, similar to whole blood). It has been used in all stages of
 thrombohemorrhagic syndrome. Initially the dose of intravenous introduction is 6-12
ml/kg. After it dose is 300-400 ml each 6-8 hours.
19. Stimulation of vascular-thrombocytes link of hemostasis (dicinone, etamsilat).
20. Transamacha acid usage – in the dose 500-750 mg on 0,9 % NaCl. This
medicine inhibits plasmine activity, stabilizes coagulate factors and fibrin, decreases
vascular permeability and gives permanent hemostatic action, which have been
prevented fibrinogen degradation.
Treatment of thrombhemorrhagic syndrome in obstetric hemorrhagic
shock in different stages
Stages Treatment
I.Hypercoagulation For normalization blood reology: Trental – 100mg on
100 ml 0,9 % NaCl, Curantill – 0,5 – 2, %
II.Hypocoagulation without Procoagulants: fresh frozen plasma 500,0, blood of 3-
generalizing fibrinolysis 5 days of conservation. Transamacha – antyplasmin
drug – 500-750 mg on 0, 9 % NaCl.
Fibrinolysis inhibitors: Contrical in the dose 10-
20.000 units/ daily dose 100-200.000 units; Trasilol –
40.000 units or Gordox – 100-200.000 units.
Cortycosteroids – Prednisolone – 10mg/kg/hour or
Hydrocortisone – 100 mg/kg.
III Hypocoagulation with Proteolytic enzymes inhibitors: Contrycal 40.000 units
generalizing fibrinolysis (daily dose 500.000 units)
Procoagulants – fresh frozen plasma, blood, albumin.
Cortycosteroids.Cryoprecipitate–200-400,0,
Transamcha – 500-700 mg.
IV. Total fibrinolysis The treatment should be started from the large doses
of proteolytic enzymes inhibitors – Contrical 100.000
units to 500.000 units. Blood, albumin, plasma,
cryoprecipitate, cortycosteroids.

AMNIOTIC FLUID EMBOLISM (AFE)

 Amniotic fluid embolism is a rare, sudden, and often fatal obstetric
complication caused by entry of amniotic fluid into the maternal venous circulation.
The initial physiological disturbances involve profound alterations in
hemodynamics and oxygenation, often followed by the development of a
consumptive coagulopathy.
The main pathogenetical factors that have been predisposing to amniotic fluid
embolism are predomination of amniotic pressure over venous and traumatization of
venous uterine vessels.
Predomination of amniotic pressure over venous is presented in excessive labor
contractions, breach presentation, postdate pregnancy, multiple pregnancy, uterine
cervix dystocia, hypovolemia of different etiology.
Traumatization of venous uterine vessels is presented in placenta abruption,
cesarean section, manual removal of placenta, puerperal hypotonic hemorrhage.

Clinical manifestation
The condition results in severe cardiorespiratory collapse and usually a
coagulopathy.
Cardiorespiratory collapse is the result of entry large amount of amniotic fluid
into the maternal circulation and characterized by severe pain in the chest, cough,
feeling of the death. The most common presentation is that of sudden dyspnea and
hypotension commonly followed within minutes by cardiorespiratory arrest. Heart
fibrillation and sudden death are the results of this disorder. In 10 % to 20 % of cases,
these initial events accompanied by seizure activity. In 70 % of cases, a chest
radiography reveals some degree of pulmonary edema. One half of the patients with
AFE die within 1 hour after the onset of symptoms; in survivors, neurologic damage
or brain death secondary to the initial severe hypoxia is not uncommon..
In the case of entering of small number of amniotic fluid into the maternal
circulation disseminated intravascular coagulopathy is common.
The definitive diagnosis of AFE has classically been made at autopsy with the
demonstration of fetal squamosus cells, mucin, hair, or vernix in the pulmonary
artery vasculature.
 Treatment is directed toward total support of the cardiovascular and
coagulation systems and include:
I. 1. Assisted pulmonary ventilation, oxygen therapy, closed chest massage.
Intravenous 10 % 10,0 ml Calcii chloridi and intracardiac 0.1 % - 0,5 ml adrenalin
hydrochloridi are indicated.
2. Sedative drugs: Droperidol – 4-5 ml intravenous, 20 % - 20, 0 ml
Natrii oxybuturate, 2, 0 ml Diazepame.
3. Spasmolytic agents are prescribed: Euphyllini – 2,4 % 10, 0 ml
intravenous, Nospani – 2 % - 4 ml, Papaverini hydrochloridi – 2 % - 4 ml.
4. Cardiovascular drugs: Corglyconi 0, 06 % - 0,5 ml or Strophantini – 0,05 %
- 0, 5 ml intravenous on 20 ml 10 % glucose.
5. Drugs that have been increasing arterial pressure and vascular tone:
hydrocortizone 250 mg, dopamine infusion.
6. Elimination of acute hypovolemia and metabolic acidosis, initial optimization of
cardiac preload: polyglucin 400 ml, Natrii hydrocarbonatis 200 ml intravenous.
7. Disseminated intravascular coagulopathy treatment.
II. Immediate delivery: by cesarean section or by forceps.

SEPTIC SHOCK
Septic shock is the result of entering of infective agents into the maternal
circulation in different obstetrics and gynecologic conditions. It is a serious
complication that requires aggressive management. Pregnancy is classically thought
to be a factor that predisposes a patient to septic shock. In obstetrics, septic abortion,
chorionamnionitis, pyelonephritis, and endometritis are the most common conditions
associated with septic shock.
Pathogenesis. Septic shock in obstetrics most commonly is associated with
infection caused by endotoxin-releasing gram-negative aerobic coliform organisms.
Endotoxin, a complex cell wall-associated lipopolysaccharide, is released into the
circulation at the time of bacterial death, resulting in multiple hemodynamic effects.
Early septic shock is a classic example of distributive shock, related to a
systemic maldistribution of relatively normal or even increased output. Clinical
findings include hypotension, fever, and chills. Initial hemodynamic findings include
decreased systemic vascular resistance and high normal or elevated cardiac output
The continued maldistribution of cardiac output leads to local tissue hypoxia and the
development of lactic acidosis and end-organ dysfunction. This decrease in systemic
vascular resistance is caused by the release of vasoactive substances as well as by
vascular endothelial cell injury, which promotes capillary plugging secondary to
complement induced leukocyte aggregation. These factors lead to increased
arteriovenous shunting.

These patients are acutely ill, with fevers of up to 39,5 0 C, general weakness,
tachycardia, severe pelvic and abdominal pain, and nausea and vomiting.
On physical examination patients may exhibit muscular guarding, and or
rebound tenderness. A purulent cervical discharge is often seen and uterus or adnexa
are usually moderately to exquisitely tender.
Such phases of septic shock have been distinguished as:
7. hyperdynamic or “warm” phase (systolic arterial blood pressure is
decreased to 80-90 mm. Hg durinh 1-2 hours);
8. hypodynamic or “cold” phase (continuous decreasing of arterial blood
pressure; shock’ index is more than 1,5; chest, abdominal, back pain;
oliguria, consciousness impairment, dyspnea; mulberry rash; skin
necrosis);
9. irreversible shock (anuria, respiratory and heart insufficiency, coma).
The treatment of septic shock in this early phase involves optimizing preload by
restoring relative intravascular volume with crystalloid infusion as well as aggressive
treating the underlying infection. If the offending organism is known, single-agent
antibiotic therapy may be used. More commonly in obstetrics, the infection is
polymicrobial, and broad-spectrum coverage for gram-negative and gram-positive
aerobic and anaerobic organisms is most appropriate.. If an abscess is involved,
prompt surgical drainage after initial resuscitation is mandatory.
If the process should continue, the patient may enter a second hemodynamic
phase of septic shock. Of primary importance in this late phase is the development
and progression of myocardial dysfunction leading to ventricular failure.
 Patients who recover from the initial hemodynamic instability of septic shock
may suffer prolonged morbidity secondary to endotoxin-mediated pulmonary
capillary injury and noncardiogenic pulmonary capillary edema. Such lung failure is
a major cause of death in patients with septic shock. Similarly, pregnant patients
whose hypotension was prolonged may experience acute tubular necrosis. Endotoxin-
mediated endothelial cell injury and associated tyhromboplastin-like activity as well
as prolonged shock from any cause may also lead to activation of the coagulation
cascade and a clinical picture of disseminated intravascular coagulation. Although the
use of high-dose corticosteroids has been advocated in the acute management of
septic shock, reports have failed to demonstrate a benefit from such therapy.
Aggressive therapy for patients with septic shock should be tailored the site of
infection and the individual patient. Hospitalized patients require high dose
intravenous antibiotic therapy with an antimicrobial spectrum that covers aerobic and
anaerobic organisms (Tienam – 1000 mg 4 times a day intravenous each 6 hours. Its
daily dose is 4 gram. Cyprinol – intravenous administration 400 mg twice a day).
Surgical intervention - hysterectomy should be performed immediately. Pulmonary
ventilation, disseminated intravascular coagulopathy elimination, normalization of
vascular tone, immunocorrection, detoxycation therapy have been prescribed.

ANAPHYLACTIC SHOCK
Anaphylactic shock is a allergic reaction of human organism as result of
bounding of different origin antigens with antibodies which are fixed on the cell
membranes. It is leading to cell’ membranes destruction and excessive entering into
the blood such substances as histamine, serotonin, acetylcholine, and some
substances of anaphylaxia. The last ones effect into the vessels and provoke arterial
blood pressure decreasing and , as result, development of hypovolemia and tissual
hypoxia. Human reaction should be general and local. Local reaction is characterized
by edema in the site of drug’ injection, its chills, and hyperemia (allergic
manifestation after drug’s administration). General reaction is manifested by
respiratory, cardiovascular disorders.
 Such forms of anaphylactic shock have been distinguished as typical,
hemodynamics, asphyxial, cerebral, and abdominal.
The management of the patients with anaphylactic shock consists of medicines
that have been eliminated cardiovascular, respiratory, epileptic disorders, antyallergic
drugs.
The urgent care in the case of anaphylactic shock include:
1. Intravenous administration of adrenalini hydrochloridu 0.1 % - 1, 0.
In cardiac arrest – this drug is injected intracardiac.
2. Injection in the place of allergen’ entering adrenalini hydrtochloridi also.
3. The place above the allergic drug injection should be pressed obligatory.
3. For elimination respiratory disorders (asphyxia) intravenous (or
intramuscular) administration of Cordiamine 4 ml, Coffeini benzoate Natrii – 10 %
- 10. 0 ml, Euphylline – 2,4 % - 10, 0 ml have been prescribed.
4. Cortycosteroids are very effective for allergic manifestations elimination.
Prednizolone in the dose 0,005 g/kg intravenous, Dexamatazone – 0,02 g
intravenous, Hydrocortizone – 0,5 g into 0,9 % Nacl have been prescribed.
4. Antyhistaminic drugs are indicated also – Diphynylhydramine hydrochloride
– 1, 0 % - 5 ml, Suprastin – 2-6 ml 2 % intravenous or intramuscular.
5. Epileptic state is eliminated by intravenous administration of Aminazine – 2,5
% - 2 ml or Sibazone – 0,5 % - 2-4 ml.
Introduction of detoxycative, hypoallergenic, dehydrative drugs and
glucocorticoids is prescribed during 8-10 days after anaphylactic reaction.