Medicine

Obstetric hemorrhages in the first term of pregnancy

Obstetric hemorrhages in the first term of pregnancy. Ectopic pregnancy. Obstetric hemorrhages in the second half of pregnancy, labor, and postpartum period. Intensive therapy and reanimation of obstetric hemorrhages.

Prepared by Korda I.

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 hours

Usually continues

Abdominal discomfort

None

Can be severe

Fetal heart rate pattern

on electronic monitoring

Absent

Tachycardia, then bradycardia; loss of

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 lyingif 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 associ­ated 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 oper­ating 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 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 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 consump­tive 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 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 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 stabiliza­tion 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

Hematocrit, %

Blood 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.

Algover’s index

Blood loss volume, % out of circulating 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

stage

Hypovolemia stage

Circulating blood volume deficiency

Blood loss,

ml

% from body weight

Hemodynamics data,

diuresis

I

Mild

10 %-20%

500 –

1000,0

1,0 – 1,5 %

Ps – 90-100 beats per min;

Arterial blood pressure (BP) - >100 mm Hg;

Central Venous pressure (CVP) – 80-100 mm Hg;

Diuresis – N.

II

Moderate

20%-30%

1000,0-

1500,0

1,5 -

2,0 %

Ps – 120 beats per min;

BP - <100 mm Hg;

CVP – < 60 mm Hg;

Diuresis – < 50 ml per hour (oligouria)

III

Severe

30%-40%

1500,0– 2000,0

2,0 –

2,5 %

Ps – 140 beats per min;

BP - < 70 mm Hg;

CVP – < 40 mm Hg;

Diuresis – < 30 ml per hour (anuria)

IV

Considerable

40% and >

2000,0 and >

>

2,5 %

Ps – 140 beats per min;

BP – < 50 mm Hg;

CVP – 0;

Diuresis– anuria

 

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 loss

Volume of infusion

Crysta-lloids

Refortan,

Gelofusin

Stabisol

Fresh-frozen plasma

Albumin

(10-20 %)

Erythro-massa

10-20 %

500-1000ml

 

2500 ml

10-15 ml/

kg

10 ml /kg

-

-

 

20-30 %

1000-

1500 ml

 

3000 ml

10 ml /kg

10 ml /kg

5 - 10 ml /kg

-

5 ml /kg

30-40 %

1500-

2000 ml

 

4000 ml

7 ml/kg

7 ml/kg

10 - 15 ml  /kg

200 ml

10 - 20 ml  /kg

40-and >

> 2000 ml

 

> 6000            ml

7 ml/kg

10 ml /kg

15 - 20 ml  /kg

 

200 ml

30 ml /kg

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

                                                   

Placenta praevia, placenta abruptio, uterine rupture

Uterine cervix rupture, deep vagival ruptures, traumatization of the soft birth canal tissues.

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

Bleeding stopping

 


Urgent cesarean section

Rupture suture

Manual uterine 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

 

 

Stages

The main laboratory data

Blood clotting time, minutes

Spontaneous thrombus lisis

Thrombin test

Throm-bocytes number, 10x9/l

Thrombin time,

seconds

I.Hypercoagulation

< 5 (N)

absent (N)

7-11 (N)

175-425 (N)

< 24

II.Hypocoagulation without generalizing fibrinolysis

 

5 -12

absent

7-11

< 120

>60

III Hypocoagu-lation with generalizing fibrinolysis

>12

quick

20-60

< 100

>100

IV. Total fibrinolysis

> 60

Thrombus doesn’t formed

>60

<60

>180

 

General principles of DIC treatment are:

1.     Heparin, fibrinogen are contraindicated in all stages of 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 generalizing fibrinolysis

 

Procoagulants: fresh frozen plasma 500,0, blood of 3-5 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 generalizing fibrinolysis

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.

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

Hematocrit, %

Blood 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.

Algover’s index

Blood loss volume, % out of circulating 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

stage

Hypovolemia stage

Circulating blood volume deficiency

Blood loss,

ml

% from body weight

Hemodynamics data,

diuresis

I

Mild

10 %-20%

500 –

1000,0

1,0 – 1,5 %

Ps – 90-100 beats per min;

Arterial blood pressure (BP) - >100 mm Hg;

Central Venous pressure (CVP) – 80-100 mm Hg;

Diuresis – N.

II

Moderate

20%-30%

1000,0-

1500,0

1,5 -

2,0 %

Ps – 120 beats per min;

BP - <100 mm Hg;

CVP – <60 mm Hg;

Diuresis – < 50 ml per hour (oligouria)

III

Severe

30%-40%

1500,0– 2000,0

2,0 –

2,5 %

Ps – 140 beats per min;

BP - <70 mm Hg;

CVP – <40 mm Hg;

Diuresis – < 30 ml per hour (anuria)

IV

Considerable

40% and >

2000,0 and >

2,5 %

Ps – 140 beats per min;

BP – <50 mm Hg;

CVP – 0;

Diuresis– anuria

 

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 loss

Volume of infusion

Crysta-lloids

Refortan,

Gelofusin

Stabisol

Fresh-frozen plasma

Albumin

(10-20 %)

Erythro-massa

10-20 %

500-1000ml

 

2500 ml

10-15 ml/

kg

10 ml /kg

-

-

 

20-30 %

1000-

1500 ml

 

3000 ml

10 ml /kg

10 ml /kg

5 - 10 ml /kg

-

5 ml /kg

30-40 %

1500-

2000 ml

 

4000 ml

7 ml/kg

7 ml/kg

10 - 15 ml /kg

200 ml

10 - 20 ml /kg

40-and >

> 2000 ml

 

> 6000 ml

7 ml/kg

10 ml /kg

15 - 20 ml /kg

 

200 ml

30 ml /kg

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

                                                   

Placenta praevia, placenta abruptio, uterine rupture

Uterine cervix rupture, deep vagival ruptures, traumatization of the soft birth canal tissues.

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

Bleeding stopping

 


Urgent cesarean section

Rupture suture

Manual uterine 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

 

 

Stages

The main laboratory data

Blood clotting time, minutes

Spontaneous thrombus lisis

Thrombin test

Throm-bocytes number, 10x9/l

Thrombin time,

seconds

I.Hypercoagulation

< 5 (N)

absent (N)

7-11 (N)

175-425 (N)

< 24

II.Hypocoagulation without generalizing fibrinolysis

 

5 -12

absent

7-11

< 120

>60

III Hypocoagu-lation with generalizing fibrinolysis

>12

quick

20-60

< 100

>100

IV. Total fibrinolysis

> 60

Thrombus doesn’t formed

>60

<60

>180

 

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 generalizing fibrinolysis

 

Procoagulants: fresh frozen plasma 500,0, blood of 3-5 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 generalizing fibrinolysis

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.

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.

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 hours

Usually continues

Abdominal discomfort

None

Can be severe

Fetal heart rate pattern

on electronic monitoring

Absent

Tachycardia, then bradycardia; loss of

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.

W03211

 

Fig. 1 Total placenta previa

W03212

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 associ­ated 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 oper­ating 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 ).

 

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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.)

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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.

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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.

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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.

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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.

.

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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 consump­tive 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.

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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.

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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 stabiliza­tion 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 ).

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Fig. 11 A fatal case of inverted uterus associated with placenta accreta following delivery at home.

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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.)

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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.

 

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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.

 

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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.

W03223

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.

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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.

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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

Hematocrit, %

Blood 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’sindex

Blood loss volume, % out of circulating 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

stage

Hypovolemia stage

Circulating blood volume deficiency

Blood loss,

ml

% from body weight

Hemodynamics data,

diuresis

I

Mild

10 %-20%

500 –

1000,0

1,0 – 1,5 %

Ps – 90-100 beats per min;

Arterial blood pressure (BP) - >100 mm Hg;

Central Venous pressure (CVP) – 80-100 mm Hg;

Diuresis – N.

II

Moderate

20%-30%

1000,0-

1500,0

1,5 -

2,0 %

Ps – 120 beats per min;

BP - <100 mm Hg;

CVP – <60 mm Hg;

Diuresis – < 50 ml per hour (oligouria)

III

Severe

30%-40%

1500,0– 2000,0

2,0 –

2,5 %

Ps – 140 beats per min;

BP - <70 mm Hg;

CVP – <40 mm Hg;

Diuresis – < 30 ml per hour (anuria)

IV

Considerable

40% and >

2000,0 and >

2,5 %

Ps – 140 beats per min;

BP – <50 mm Hg;

CVP – 0;

Diuresis– anuria

 

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 loss

Volume of infusion

Crysta-lloids

Refortan,

Gelofusin

Stabisol

Fresh-frozen plasma

Albumin

(10-20 %)

Erythro-massa

10-20 %

500-1000ml

 

2500 ml

10-15 ml/

kg

10 ml /kg

-

-

 

20-30 %

1000-

1500 ml

 

3000 ml

10 ml /kg

10 ml /kg

5 - 10 ml /kg

-

5 ml /kg

30-40 %

1500-

2000 ml

 

4000 ml

7 ml/kg

7 ml/kg

10 - 15 ml /kg

200 ml

10 - 20 ml /kg

40-and >

> 2000 ml

 

> 6000 ml

7 ml/kg

10 ml /kg

15 - 20 ml /kg

 

200 ml

30 ml /kg

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 praevia, placenta abruptio, uterine rupture

Uterine cervix rupture, deep vagival ruptures, traumatization of the soft birth canal tissues.

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

Bleeding stopping

 


Urgent cesarean section

Rupture suture

Manual uterine 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

 

 

Stages

The main laboratory data

Blood clotting time, minutes

Spontaneous thrombus lisis

Thrombin test

Throm-bocytes number, 10x9/l

Thrombin time,

seconds

I.Hypercoagulation

< 5 (N)

absent (N)

7-11 (N)

175-425 (N)

< 24

II.Hypocoagulation without generalizing fibrinolysis

 

5 -12

absent

7-11

< 120

>60

III Hypocoagu-lation with generalizing fibrinolysis

>12

quick

20-60

< 100

>100

IV. Total fibrinolysis

> 60

Thrombus doesn’t formed

>60

<60

>180

 

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 generalizing fibrinolysis

 

Procoagulants: fresh frozen plasma 500,0, blood of 3-5 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 generalizing fibrinolysis

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.

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 hours

Usually continues

Abdominal discomfort

None

Can be severe

Fetal heart rate pattern

on electronic monitoring

Absent

Tachycardia, then bradycardia; loss of

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 lyingif 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 associ­ated 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 oper­ating 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 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 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 consump­tive 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 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 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 stabiliza­tion 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

Hematocrit, %

Blood 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.

Algover’s index

Blood loss volume, % out of circulating 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

stage

Hypovolemia stage

Circulating blood volume deficiency

Blood loss,

ml

% from body weight

Hemodynamics data,

diuresis

I

Mild

10 %-20%

500 –

1000,0

1,0 – 1,5 %

Ps – 90-100 beats per min;

Arterial blood pressure (BP) - >100 mm Hg;

Central Venous pressure (CVP) – 80-100 mm Hg;

Diuresis – N.

II

Moderate

20%-30%

1000,0-

1500,0

1,5 -

2,0 %

Ps – 120 beats per min;

BP - <100 mm Hg;

CVP – < 60 mm Hg;

Diuresis – < 50 ml per hour (oligouria)

III

Severe

30%-40%

1500,0– 2000,0

2,0 –

2,5 %

Ps – 140 beats per min;

BP - < 70 mm Hg;

CVP – < 40 mm Hg;

Diuresis – < 30 ml per hour (anuria)

IV

Considerable

40% and >

2000,0 and >

>

2,5 %

Ps – 140 beats per min;

BP – < 50 mm Hg;

CVP – 0;

Diuresis– anuria

 

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 loss

Volume of infusion

Crysta-lloids

Refortan,

Gelofusin

Stabisol

Fresh-frozen plasma

Albumin

(10-20 %)

Erythro-massa

10-20 %

500-1000ml

 

2500 ml

10-15 ml/

kg

10 ml /kg

-

-

 

20-30 %

1000-

1500 ml

 

3000 ml

10 ml /kg

10 ml /kg

5 - 10 ml /kg

-

5 ml /kg

30-40 %

1500-

2000 ml

 

4000 ml

7 ml/kg

7 ml/kg

10 - 15 ml  /kg

200 ml

10 - 20 ml  /kg

40-and >

> 2000 ml

 

> 6000            ml

7 ml/kg

10 ml /kg

15 - 20 ml  /kg

 

200 ml

30 ml /kg

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

                                                   

Placenta praevia, placenta abruptio, uterine rupture

Uterine cervix rupture, deep vagival ruptures, traumatization of the soft birth canal tissues.

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

Bleeding stopping

 


Urgent cesarean section

Rupture suture

Manual uterine 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

 

 

Stages

The main laboratory data

Blood clotting time, minutes

Spontaneous thrombus lisis

Thrombin test

Throm-bocytes number, 10x9/l

Thrombin time,

seconds

I.Hypercoagulation

< 5 (N)

absent (N)

7-11 (N)

175-425 (N)

< 24

II.Hypocoagulation without generalizing fibrinolysis

 

5 -12

absent

7-11

< 120

>60

III Hypocoagu-lation with generalizing fibrinolysis

>12

quick

20-60

< 100

>100

IV. Total fibrinolysis

> 60

Thrombus doesn’t formed

>60

<60

>180

 

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 generalizing fibrinolysis

 

Procoagulants: fresh frozen plasma 500,0, blood of 3-5 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 generalizing fibrinolysis

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.

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.