Medicine

Pregnancy interrupting

Pregnancy interrupting. Postterm pregnancy. Uterine contractions abnormalities.

Prepared by KordaI.

PRETERM AND POSTTERM LABOR

Definitions

With respect to gestational age, a fetus or infant may be preterm, term, or postterm. Preterm infant is the term used to define infants who are born between 22 and 37 weeks of gestation with the weight 500 – 2500 gram and length 24-25cm till 48 cm.

With respect to size, the fetus or infant may be normally grown or appropriate-for-gestational age, small in size or small-for-gestational age, or overgrown and consequently large-for-gestational age. The term small for gestational age have included fetal growth retardation or intrauterine growth retardation.

Causes of Preterm Birth

A wide spectrum of causes and demographic factors has been implicated in the birth of preterm infants.

Maternal infection

·        chronic tonsillitis

·        urinary tract infection

·        TORCH – infection

·        viral infection

·        chronic inflammatory diseases of the female sexual organs (vaginatis, bacterial vaginosis)

Amnionic Fluid Infection

·        Chorioamnionic infection caused by a variety of microorganisms has emerged as a possible explanation for many heretofore unexplained cases of ruptured membranes and/or preterm labor.

Bacterial Vaginosis

 Hillier and colleagues (1995) detected bacterial vaginosis in 16 percent of 10,397 pregnant women without risk factors for preterm birth who were screened between 23 and 26 weeks. Bacterial vaginosis was linked to poverty and to significantly increased preterm birth at 32 weeks or less but not to premature membrane rupture. Microbes most strongly associated with bacterial vaginosis included Gardnerella vaginalis, Bacteroides sp, and Mycoplasma hominis.

Hauth and co-workers (1995) studied 624 women at risk for preterm birth either because they had previously delivered preterm infants or because they weighed less than 50 kg before pregnancy. They were randomized to treatment with metronidazole, 250 mg three times a day for 7 days; erythromycin, 333 mg three times a day for 14 days; or placebo in a double-blind study. About 40 percent of women in each arm had bacterial vaginosis at 22 to 24 weeks. Delivery before 37 weeks in women with bacterial vaginosis was significantly decreased from 40 to 25 percent when metronidazole or erythromycin was given. In contrast, intravaginal topical treatment of bacterial vaginosis using clindamycin cream has been shown to be ineffective to prevent preterm birth (Joesoef and colleagues, 1995).

Trichomonas and Candida Vaginitis.    Other causes of vaginitis, including trichomoniasis and candidiasis infections, have been investigated. Meis and co-workers (1995a) examined 2929 women at 24 and 28 weeks using 10 percent potassium hydroxide wet mount preparations. Detection of Trichomonas vaginalis or Candida had no significant association with preterm birth.

Chlamydia.    Although Chlamydia trachomatis is the most common sexually transmitted bacteriasis pathogen in the United States (Webster and colleagues, 1993), the possible influence of cervical infection with this organism on preterm birth is unclear (McGregor and French, 1991). Ryan and associates (1990) used erythromycin to treat 1323 pregnant women with positive cervical cultures for chlamydia at enrollment for prenatal care. Pregnancy outcome in these women were compared with 1110 similar, but untreated women. Low birthweight and ruptured membranes more than 1 hour before labor were significantly decreased with erythromycin therapy. The effects on preterm birth, however, were not specified.

Identification of Women at Risk for Preterm Birth

Pathogenesis

Pathogenesis.    Schwarz and co-workers (1976) suggested that term labor is initiated by activation of phospholipase A2, which cleaves arachidonic acid from within fetal membranes, thereby making free arachidonic acid available for prostaglandin synthesis. Subsequently, Bejar and colleagues (1981) reported that many microorganisms produce phospholipase A2, and thus potentially may initiate preterm labor. Bennett and Elder (1992) have shown that common genital tract bacteria do not themselves produce the prostaglandins. Cox and associates (1989) provided data that bacterial endotoxin (lipopolysaccharide) introduced into the amnionic fluid stimulates decidual cells to produce cytokines and prostaglandins that may initiate labor. Romero and co-workers (1987, 1988) and Cox and associates (1988a) reported that endotoxin was present in the amnionic fluid.

It has now been established that endogenous host products secreted in response to infection are responsible for many of the effects of infection. In endotoxin shock, for example, bacterial endotoxins exert their deleterious effect through the release of endogenous cell mediators (cytokines) of the inflammatory response. Similarly, preterm parturition due to infection is thought to be initiated by secretory products resulting from monocyte (macrophage) activation (Fig.1). Cytokines, including interleukin-1, tumor necrosis factor, and interleukin-6, are such secretory products implicated in preterm labor. Narahara and Johnston (1993) have suggested that platelet-activating factor, which is found in the amnionic fluid, is synergistically involved in activating the cytokine network (Fig.1). Platelet activating factor is thought to be produced in the fetal lungs and kidneys. Thus, the fetus appears to play a synergistic role in the initiation of preterm birth due to bacterial infection. Teleologically, this could be advantageous to the fetus interested in extricating itself from an infected environment.

Gravett and colleagues (1994), in a remarkable experiment with rhesus monkeys, have provided the first direct evidence that infection incites preterm labor. Group B streptococci were injected into the amnionic fluid in preterm rhesus monkeys, and concentrations of cytokines and prostaglandins shown in Figure 1 were serially measured. Amnionic fluid cytokine concentrations increased about 9 hours after introduction of the bacteria, followed sequentially by production of the prostaglandins E2 and F2a and finally, uterine contractions. As observed in humans with preterm labor due to amnionic fluid infection, there was no clinical evidence of chorioamnionitis in these rhesus monkeys until after preterm labor ensued.

Although the pathway for bacteria to enter the amnionic fluid is obvious after membrane rupture, the route of access with intact membranes is unclear. Gyr and colleagues (1994) found that E coli can permeate living chorioamnionic membranes. Thus, intact fetal membranes at the cervix are not necessarily a barrier to ascending bacterial invasion of the amnionic fluid. Alternatively, the pathway for bacterial initiation of preterm labor described in Figure 1 may not require colonization of the amnionic fluid. For example, Cox and co-workers (1993) found that the cytokine network of cell-mediated immunity can be activated locally in decidual tissue that lines the forebag fetal membranes.

 

Fig. 1. Proposed schematic mechanism of action for bacteria to incite preterm labor. Examples of bacterial products include cell wall lipopolysacharide (endotoxin) – Compiled from Berry, 1995.

Maternal endocrine disorders:
·        ovarian hormonal insufficiency - patients with the late menarche, irregular menstrual cycle, genital infantilism, infertility;

·     adrenal impairment – hyperandrogeny

·     thyroid gland impairment - hypothoroidism

Organic cervical dilation (cervical incompetence), abnormal uterine development

 

Medical and Obstetrical Complications

·        placental abruption, placental previa

·        pregnancy induced hypertension

·        multiple pregnancy

·        polyhydramnios

Lifestyle Factors

·        cigarette smoking,

·        poor nutrition, and poor weight gain during pregnancy,

·        use of drugs such as cocaine or alcohol have been reported to play important roles in the incidence and outcome of low-birth weight infants;

·        low maternal age

·        poverty

·        short stature

·        occupational factors

·        psychological stress in the mother.

Incompetent Cervix

The term incompetent cervix is applied to a discrete obstetrical entity. It is characterized by painless cervical dilatation in the second trimester or perhaps early in the third trimester, with prolapse and ballooning of membranes into the vagina, followed by rupture of membranes and expulsion of an immature fetus. Unless effectively treated, this sequence tends to repeat in each pregnancy.

 Numerous methods have been described in nonpregnant women to make the diagnosis, usually by documenting a more widely dilated internal cervical os than is normal. Methods have included hysterography, pull-through techniques of inflated catheter balloons, and acceptance without resistance at the internal os of specifically sized cervical dilators (Ansari and Reynolds, 1987). During pregnancy, attempts have been made with moderate success to predict premature cervical dilation using ultrasonic techniques (Michaels and associates, 1989). Iams (1995) performed a cross-sectional study of cervical length measured by transvaginal ultrasonography in women with a prior preterm delivery, those with cervical incompetence, and normal controls delivered at term. Gestational age at the first preterm delivery was significantly correlated with cervical length in the pregnancy evaluated at each gestational age between 20 and 30 weeks. The diagnosis remains difficult and is a clinical one based upon carefully observed and recorded events which include painless cervical dilatation and spontaneously ruptured membranes.

 Although the cause of cervical incompetence is obscure, previous trauma to the cervix—especially in the course of dilatation and curettage, conization, cauterization, or amputation—appears to be a factor in many cases. In other instances, abnormal cervical development, including that following exposure to diethylstilbestrol in utero, plays a role/

The treatment of cervical incompetence is surgical, consisting of reinforcement of the weak cervix by some type of purse string suture. Bleeding, uterine contractions, or ruptured membranes are usually contraindications to surgery.

Preoperative Evaluation

Cerclage should generally be delayed until after 14 weeks so that early abortions due to other factors will be completed. There is no consensus as to how late in pregnancy the procedure should be performed. The more advanced the pregnancy, the more likely surgical intervention will stimulate preterm labor or membrane rupture. For these reasons, some prefer bed rest rather than cerclage some time after midpregnancy. We usually do not perform cerclage after 24 to 26 weeks. Aarts and associates (1995) have recently provided a review of late second-trimester cerclage, commonly known as an emergency cerclage. These authors concluded that emergency cerclage can be of benefit in some women, but that the incidence of complications, especially infection, is high. According to Schorr and Morales (1996), bulging membranes are associated with significantly increased failure rates.

Sonography to confirm a living fetus and to exclude major fetal anomalies is done prior to cerclage. Obvious cervical infection should be treated, and cultures for gonorrhea, chlamydia, and group B streptococci are recommended. For at least a week before and after surgery, there should be no sexual intercourse.

If there is a question as to whether cerclage should be performed, the woman is placed at decreased physical activity. Proscription of intercourse is essential, and frequent cervical examinations should be conducted to assess cervical effacement and dilation. Some recommend weekly ultrasonic surveillance of the lower uterine segment between 14 and 27 weeks (Michaels and associates, 1989). Unfortunately, rapid effacement and dilation develop even with such precautions (Witter, 1984).

Cerclage Procedures

Three types of operations are commonly used during pregnancy. One is a simple procedure recommended by McDonald (1963) and illustrated in Figure 2.

 

Fig. 2 Incompetent cervix treated with McDonald cerclage procedure. A. Somewhat dilated cervical canal and beginning prolapse of membranes (arrow). B. Start of the cerclage procedure with a suture of number 2 monofilament being placed superiorly in the body of the cervix very near the level of the internal os. C. Continuation of suture placement in the body of the cervix so as to encircle the os. D. Completion of encirclement. E. The suture is tightened around the cervical canal sufficiently to reduce the diameter of the canal to 5 to 10 mm. In the illustration the small dilator has been placed just through the level of ligation to maintain patency of the canal when the suture is tied. A second suture similarly placed but somewhat higher may be of value, especially if the first is not in close proximity to the internal os. F. The effect of the suture placement on the cervical canal is apparent.

 The second is the more complicated Shirodkar operation (1955). The third is the modified Shirodkar procedure shown in Figure 3 (Caspi and associates, 1990). There is less trauma and blood loss with both the McDonald and modified Shirodkar procedures than with the original Shirodkar procedure.

 

Fig. 3. Modified Shirodkar cerclage. A. After transverse cervical incision, bladder has been pushed cephalad. Double-needled ligature is passed anteriorly to posteriorly on each side of cervix. B. Ligature is tied posteriorly, usually around a 10-mm dilator. C. Cervical mucosa is run with chromic suture to bury the anterior purse-string suture.

 Success rates approaching 85 to 90 percent are achieved with both McDonald and modified Shirodkar techniques (Caspi and associates, 1990; Kuhn and Pepperell, 1977). Thus, there appears to be little reason for performing the more complicated original Shirodkar procedure. The modified Shirodkar procedure is often reserved for previous McDonald cerclage failures and structural cervical abnormalities. Success rates are higher when cervical dilatation was minimal and membrane prolapse was absent.

          Charles and Edward (1981) identified complications, especially infection, to be much less frequent when cerclage was performed by 18 weeks. When performed much after 20 weeks, there was a high incidence of membrane rupture, chorioamnionitis, and intrauterine infection. With clinical infection, the suture should be cut, and labor induced.

There is no evidence that prophylactic antibiotics prevent infection, or that progestational agents or b-mimetic drugs are of any adjunctive value (Thomason and co-workers, 1982). In the event that the operation fails and signs of imminent abortion or delivery develop, it is urgent that the suture be released at once; failure to do so may result in grave sequelae. Rupture of the uterus or cervix may be the consequence of vigorous uterine contractions with the ligature in place. Membrane rupture during suture placement or within the first 48 hours of surgery is considered by some to be an indication to remove the cerclage. Kuhn and Pepperell (1977) reported that when the membranes rupture in the absence of labor, the likelihood of serious fetal or maternal infection is increased appreciably if the suture is left in situ and delivery is delayed. Still, the range of management options spans from observation, to removal of the cerclage with observation, to removal of the cerclage and labor induction (Barth, 1995). There are insufficient data upon which to base any firm recommendation.

Following the Shirodkar operation, the suture can be left in place if it remains covered by mucosa, and cesarean delivery performed near term. Conversely, the Shirodkar suture may be released and vaginal delivery permitted.

Transabdominal cerclage placed at the level of the uterine isthmus has been recommended in some instances, especially in cases of anatomical defects of the cervix or failed transvaginal cerclage (Cammarano and colleagues, 1995; Gibb and Salaria, 1995; Herron and Parer, 1988). The procedure requires laparotomy for placement of the suture and another laparotomy for its removal, for delivery of the fetus, or both. The potential for trauma and other complications initially and subsequently is much greater with this procedure than with the vaginal procedures.

Preterm labor is classified according to clinic duration as:

·        Threatened preterm labor

·        Initial preterm labor

·        Inevitable preterm labor

Signs and Symptoms of Preterm Labor

Threatened preterm labor is characterized by:

-         symptoms of pelvic pressure, low back pain;

-         increase uterine tone;

-         absence of cervical effacement and dilation in vaginal examination.

Initial preterm labor is characterized by:

-         irregular cramp – like painful uterine contractions;

-         presence of cervical effacement and dilation of the cervix till 2-4 cm in vaginal examination;

-         amniotic fluid gush is present very often.

Inevitable preterm labor is characterized by:

-         regular uterine contractions;

-         cervical dilation more than 2-4 cm.

Because uterine contractions alone may be misleading, Herron and associates (1982) require the following criteria to document preterm labor: regular uterine contractions after 20 weeks or before 37 weeks, which are 5 to 8 minutes apart or less, and accompanied by one or more of the following: (1) progressive change in the cervix, (2) cervical dilatation of 2 cm or more, or (3) cervical effacement of 80 percent or more.

Peculiarities of Preterm labor duration:

1.     Preterm Ruptured Membranes

Known risk factors for preterm rupture of the membranes include:

-         preceding preterm labor;

-         occult amnionic fluid infection;

-         multiple fetuses;

-         abruptio placentae.

2.     Uterine contractions abnormalities: uterine inertia, uterine hyperactivity, discoordination.

3.     Precipitatous preterm labor as a result of cervical incompetence.

4.     Vaginal bleeding as a result of placental abruption or placenta previa is most common complication in labor.

5.     Fetal hypoxia is more common in labor

6.     Infectious complications are very common in labor (chorionamnionitis) and postpartum period (endometritis, phlebitis).

Diagnosis of preterm labor includes:

1.     To learn the cause of preterm labor and its elimination.

2.     To estimate gestational age of pregnancy and probable fetal weight, its lie, presentation, visus.

3.     To diagnose uterine activity (presence or absence regular uterine contractions).

4.     To perform vaginal examination for learning cervical effacement and dilation, preterm ruptured membranes and to put correct diagnose of the preterm labor stage.  

Early differentiation between true and false labor is difficult before there is demonstrable cervical effacement and dilatation. Uterine contractions alone can be misleading, however, because of Braxton Hicks contractions. These contractions, described as irregular, nonrhythmical, and either painful or painless, can cause considerable confusion in the diagnosis of preterm labor. Not infrequently, women who deliver before term have uterine activity that is attributed to Braxton Hicks contractions, prompting an incorrect diagnosis of false labor.

 Because uterine contractions alone may be misleading, Herron and associates (1982) require the following criteria to document preterm labor: regular uterine contractions after 20 weeks or before 37 weeks, which are 5 to 8 minutes apart or less, and accompanied by one or more of the following: (1) progressive change in the cervix, (2) cervical dilatation of 2 cm or more, or (3) cervical effacement of 80 percent or more.

Recently, sonographic measurement of cervical dilatation and effacement has been proposed as a means of avoiding some of the inherent subjectivity of digital examinations. For example, Iams and co-workers (1994b) used vaginal probe ultrasound transducers to measure cervical length in 60 women with preterm labor between 24 and 34 weeks compared with digital examinations to predict preterm birth before 36 weeks.  When the cervix was less than 3 cm in length as measured with sonography, then 100 percent of the women delivered preterm. In contrast, cervical dilatation of 2 cm or more, or effacement of 50 percent or more, were predictive of preterm birth in 62 percent and 83 percent, respectively. Conversely, absence of any of these sonographic or digital cervical changes was not superior in precluding subsequent preterm birth.

Richey and colleagues (1995) used transperineal sonography in 100 women with complaints consistent with imminent preterm birth, and compared sonographic measurements (Fig. 4) with those obtained with conventional cervical examinations.

Fig. 4 Transperineal ultrasound with measurements of cervical length (X  .  .  .  X) and dilatation (+  .  .  .  +). (From Richey SD, Ramin KS, Roberts SW, Ramin SM, Cox SM, Twickler DM. The correlation between transperineal sonography and digital examination in the evaluation of the third-trimester cervix. Obstet Gynecol. 85:745, 1995. Reprinted with permission from the American College of Obstetricians and Gynecologists.)

 

The investigators found significant correlation between the two methods. Transperineal cervical sonography, as opposed to transvaginal, has the advantage of avoiding vaginal instrumentation with preterm ruptured membranes or placenta previa.

In another attempt to assess cervical dilatation without using digital examination, Brown and colleagues (1993) assessed the validity of visual estimates during speculum examinations to diagnose ruptured membranes. If the fetus or membranes were visible, the cervix was usually 3 cm or more dilated. Similarly, visual estimates of 4 cm or more cervical dilatation were significantly correlated with actual cervical dilatation of 4 cm or more.

Management of preterm labor

1. Expectant Management - nonintervention or expectant management, in which nothing is done and spontaneous labor is simply awaited

2. Active Management - intervention that may include corticosteroids, given with or without tocolytic agents to arrest preterm labor in order that the corticosteroids have sufficient time to induce fetal maturation.

Indications for expectant management:

·        threatened and initial preterm labor;

·        intact membranes;

·        gestational age of pregnancy till 36 weeks of gestation;

·        satisfactory maternal and fetal conditions;

·        cervical dilation till 2-4 cm;

·        absence of infection, regular uterine contractions, serious obstetric and extragenital pathology. 

·        28-34 weeks of pregnancy with preterm ruptured membranes, absence of regular uterine contractions and infection.

·        28-24 weeks of gestation, intact membranes, 100 % cervical effacement and cervical dilation till 3-4 cm.

Expectant Management of Preterm labor in the case of Ruptured amniotic membranes:

Pregnancy complicated by preterm rupture of the membranes is managed as follows:

1.  One sterile speculum examination is performed to identify fluid coming from the cervix or pooled in the vagina. Demonstration of visible fluid or a positive Nitrazine test is indicative of ruptured membranes. Attempts are made to visualize the extent of cervical effacement and dilatation, but a digital examination is not performed. A cervicovaginal specimen is taken and culture sent for Neisseria gonorrhoeae.

2.  Ultrasound examination is performed to help confirm gestational age, identify the presenting part, and assess amniotic fluid volume.

3.  If the gestational age is 34 completed weeks or less and there are no other maternal or fetal indications for delivery, the woman is observed closely in Labor and Delivery, with continuous fetal heart rate monitoring to look for evidence of cord compression, especially if labor supervenes.

1.     If there is no evidence of fetal jeopardy, or if labor does not begin, the woman is transferred to the High Risk Pregnancy Unit for close observation for signs of labor, infection, or fetal jeopardy.

2.     General blood analysis – twice a day determination of leucocytes number, urine, vaginal smear, bacteriological examination  once a 5 days.

3.     If the gestational age is greater than 34 completed weeks and if labor has not begun spontaneously in 12 hours, a time period that provides for adequate evaluation, labor is induced with intravenous oxytocin. A breech presentation or transverse lie are contraindications for induction. If induction fails, cesarean delivery is performed.

4.     Inhibiting preterm labor drugs are prescribed - Spasmolytics, b-adrenergic inhibitors.

8. Accelerated Maturation of Pulmonary Function - Dexamethasone, 5 mg, is given intramuscularly every 12 hours for 4 doses for enhancement of fetal maturation. This dosage is repeated every 7 days.

9. Antimicrobial Therapy - ampicillin 2 g, is given intravenously every 6 hours prior to delivery for prevention of group B streptococcus infection in the neonate.

The greatest concern with prolonged membrane rupture is the risk of maternal or fetal infection. If chorioamnionitis is diagnosed, prompt efforts to effect delivery, preferably vaginally, are initiated.

Unfortunately, fever is the only reliable indicator for making this diagnosis; a temperature of 38°C or higher accompanying ruptured membranes implies infection. Maternal leukocytosis by itself has been found to be unreliable by most investigators, and this has also been our experience.

10. Labor and delivery are managed so as to minimize maternal hypotension and fetal hypoxia and acidosis, as well as infection.

Indications for active  management:

·        preterm ruptured membranes;

·        regular uterine contractions;

·        presence of infection;

·        fetal jeopardy, hypoxia;

·        severe maternal diseases;

·        birth defects of the fetus;

·        obstetric complications of pregnancy (severe pregnancy induced hypertension, polyhydramnios).

Vaginal delivery is indicated in cephalic presentations, cesarean section is performed in the case of breech presentation and transverse lie.

Preterm Labor with Intact Fetal Membranes

Antepartum management of women with signs and symptoms of preterm labor and intact membranes is much the same as already described for pregnancies with preterm ruptured membranes. That is, the cornerstone of treatment is to avoid delivery prior to 35 weeks if possible.

Expectant Management of Preterm labor in the case of Intact amniotic membranes:

1.     Diagnosis of the cause of preterm labor and its elimination.

2.  Methods Used to Inhibit Preterm Labor

1) Bed Rest

2) Hydration and Sedation

-         500 mL of lactated Ringer solution intravenously over 30 minutes and 8 to 12 mg of intramuscular morphine sulfate.

-         valeriannae, tazepam, seduksen, sibazone.

3) Spasmolytic agents - No-spani, Papaverini hydrochloridi, Baralgin

4) Beta-adrenergic Receptor Agonists

There are two classes of b-adrenergic receptors: b1-receptors, dominant in the heart and intestines; and b2-receptors, dominant in the myometrium, blood vessels, and bronchioles. A number of compounds generally similar in structure to epinephrine have been evaluated in the search for one that ideally would provide optimal stimulation of myometrial b2-receptors and thus inhibit uterine contractions while simultaneously causing few adverse effects from stimulation of receptors elsewhere.

1. Ritodrine – 1 g is dissolved in 250-400 ml isotonic solution and is prescribed invtravenously slowly during 4-12 hours.

2. Bricanil (Terbutaline)  0.5 mg is dissolved in 250-400 ml isotonic solution. Toxicity—especially maternal pulmonary edema and glucose intolerance—have been evident with its use (Angel and associates, 1988).

3. Partusistene (Fenoterol, Berotek)  - 0.5 mg is dissolved in 250-400 ml isotonic solution and prescribed slowly i/v.

Beta-adrenergic Receptor Agonists

Earlier in this century, epinephrine in low doses was demonstrated to exert a depressant effect on pregnant myometrium. Its tocolytic effects, however, proved to be rather weak, quite transient, and likely to be accompanied by troublesome cardiovascular effects. Several compounds capable of reacting predominantly with b-adrenergic receptors have subsequently been investigated. Some of these now are used in obstetrics, but only ritodrine hydrochloride has been approved (1980) by the Food and Drug Administration to treat preterm labor.

The adrenergic receptors are located on the outer surface of the smooth muscle cell membrane, where specific agonists can couple with them. Adenyl cyclase in the cell membrane is activated by the receptor stimulation.  Adenyl cyclase enhances the conversion of ATP to cyclic AMP, which in turn initiates a number of reactions that reduce the intracellular concentration of ionized calcium and thereby prevent activation of contractile proteins. Flier and Underhill (1996) have comprehensively reviewed adrenergic receptors.

In the United States, b-agonist compounds employed in the United States to arrest preterm labor include ritodrine and terbutaline.

Ritodrine

In a multicenter United States study, infants whose mothers were treated with ritodrine for presumed preterm labor had a lower mortality rate, developed respiratory distress less often, and achieved a gestational age of 36 weeks or a birthweight of 2500 g more often than did infants whose mothers were not so treated (Merkatz and colleagues, 1980). Hesseldahl (1979), however, in a multicenter controlled study in Denmark, did not find any of several ritodrine regimens tested to be more efficacious than treatment with bed rest, glucose infusion, and placebo tablets.

Because of concerns for the efficacy and safety of ritodrine, we evaluated the drug on the obstetrical service at Parkland Hospital (Leveno and associates, 1986b). Preterm labor was carefully defined to include cervical dilatation plus regular uterine contractions, and 106 women between 24 and 33 weeks were randomly allocated to receive either intravenous ritodrine or no tocolysis. Although ritodrine treatment significantly delayed delivery for 24 hours or less, it did not significantly modify ultimate perinatal outcomes. Similar results in a randomized study involving 708 pregnancies were reported by the Canadian Preterm Labor Investigators Group (1992). A likely explanation for the transient uterine tocolytic effects of ritodrine and ultimate failure of such therapy may be the phenomenon of b-adrenergic receptor desensitization (Hausdorff and colleagues, 1990).

 The infusion of ritodrine, as well as the other b-adrenergic agonists, has resulted in frequent and at times serious side effects. Maternal tachycardia, hypotension, apprehension, chest tightness or pain, electrocardiographic S-T segment depression, pulmonary edema, and death have all been observed. Maternal metabolic effects include hyperglycemia, hyperinsulinemia (unless diabetic), hypokalemia, and lactic and ketoacidosis. Less serious but nonetheless troublesome side effects include emesis, headaches, tremulousness, fever, and hallucinations.

A single mechanism has not been identified to explain the development of pulmonary edema, but maternal infection appears to increase the risk (Hatjis and Swain, 1988). The cause of the pulmonary edema appears to be multifactorial. Beta-adrenergic agonists cause retention of sodium and water, and thus may lead to volume overload. The drugs have also been implicated as a cause of increased capillary permeability, disturbances of cardiac rhythm, and myocardial ischemia. Simultaneous administration of glucocorticoids to try to hasten fetal maturation may also contribute, although pulmonary edema has developed in their absence.

Only parenteral ritodrine is now available in the United States since the manufacturer discontinued distribution of tablets in 1995. The efficacy of oral ritodrine had been challenged on pharmacokinetic grounds (Schiff and colleagues, 1993).

Terbutaline

Terbutaline is commonly used to forestall preterm labor although, like ritodrine, toxicity—especially maternal pulmonary edema and glucose intolerance—have been evident with its use (Angel and associates, 1988).

Lam and colleagues (1988) described long-term subcutaneous administration of low-dose terbutaline using a portable pump in nine pregnancies. It was claimed that the lower dose of terbutaline used likely prevented b-adrenergic desensitization, resulting in less “breakthrough tocolysis.” The Tokos Corporation promptly marketed this approach, and between 1987 and 1993 had used these pumps in nearly 25,000 women with preterm labor (Perry and colleagues, 1995). The list price for terbutaline pump therapy in Dallas in 1996 was $484 per day. The only other reports concerning terbutaline pumps include a sudden maternal death (Hudgens and Conradi, 1993) and a description of newborn myocardial necrosis after the mother used the terbutaline pump for 12 weeks (Fletcher and colleagues, 1991). According to the American College of Obstetricians and Gynecologists (1995): “At present, there is no evidence to support the efficacy of this costly and complicated approach.”

Oral terbutaline therapy has also been reported as ineffective by several groups (How, 1995; Lewis, 1996; Parilla, 1993; and their associates).

Overview of Beta-Adrenergic Drugs to Inhibit Preterm Labor

Several meta-analyses of parenteral b-agonists given to prevent preterm birth have consistently confirmed that these agents delay delivery for no more than 48 hours. Moreover, this delay has not proven to be beneficial despite repeated attempts to revisit the data (Lamont, 1993). Finally, Macones and colleagues (1995) used meta-analysis to assess the available data on the efficacy of oral b-agonist therapy and found no benefits.

Thus, oral b-agonist therapy has convincingly been shown to be ineffective, and parenteral therapy can only delay delivery for a short time that has not been shown to be beneficial. Some authorities (Keirse, 1995), however, believe that the brief delay in delivery afforded may be useful to facilitate maternal transport to tertiary care centers, and also delay delivery sufficiently to effect fetal maturation with glucocorticoids (see p. 812).

5) Magnesium Sulfate

It has been recognized for some time that ionic magnesium in a sufficiently high concentration can alter myometrial contractility in vivo as well as in vitro. Its  role is presumably that of a calcium antagonist.

Steere and Petrie (1977) concluded that intravenously administered magnesium sulfate, 4 g given as a loading dose followed by a continuous infusion of 2 g/hr, will usually arrest labor. Elliott (1983), in a retrospective study, found tocolysis with magnesium sulfate to be successful, inexpensive, and relatively nontoxic.

Watt-Morse and associates (1995) studied the inhibitory effects of magnesium concentrations up to 8.3 mEq/L in preterm sheep with oxytocin-induced contractions. They concluded that magnesium sulfate in tolerable, nontoxic doses has no direct effect on uterine contractility.

There have been only two randomized controlled studies of the tocolytic properties of magnesium sulfate in humans. Cotton and associates (1984) compared magnesium sulfate with ritodrine as well as with a placebo, and they identified little difference in outcomes. Cox and associates (1990) randomized 156 women in preterm labor with intact membranes to infusions of magnesium sulfate or normal saline. Magnesium sulfate (20 percent solution) was begun using a 4-g loading dose followed by 2 g/hr intravenously. If contractions persisted after 1 hour, the infusion was increased to 3 g/hr. Their mean plasma magnesium concentration was 5.5 mEq/L. No benefits for such therapy were found, and this method of tocolysis was abandoned at Parkland Hospital. Similar results were recently reported in an evaluation of nonrandomized women in preterm labor and delivered of infants weighing less than 1000 g (Kimberlin and associates, 1996a).

Hollander and colleagues (1987) used an unprecedented infusion dose of magnesium sulfate that averaged 4.5 g/hr. They reported that such therapy was equivalent to ritodrine. Conversely, Semchyshyn and associates (1983) failed to stop labor in a woman who inadvertently was given 17.3 g of magnesium sulfate in 45 minutes! Women given high-dosage magnesium sulfate must be monitored very closely for evidence of hypermagnesemia that might prove toxic to them and their fetus-infants. The pharmacology and toxicology of parenterally administered magnesium are considered in more detail in Chapter 31.

6) Prostaglandin Inhibitors

Antiprostaglandin agents may act by inhibiting the synthesis of prostaglandins or by blocking the action of prostaglandins on target organs. Several drugs are known to block this system, including aspirin and other salicylates, indomethacin, naproxen, and sulindac.

Unfortunately, prostaglandin synthase inhibitors may adversely affect the fetus, and this has prevented widespread use of these agents for tocolysis. Complications include closure of the ductus arteriosus, necrotizing enterocolitis, and intracranial hemorrhage (Norton and co-workers, 1993).

Prostaglandin inhibitors have been the subject of considerable interest since it was appreciated that prostaglandins are intimately involved in myometrial contractions of normal labor. A group of enzymes collectively called prostaglandin synthase is responsible for the conversion of free arachidonic acid to prostaglandins.

Van der Heijden and colleagues (1994) linked long-term perinatal indomethacin to anemia, neonatal death, and cystic renal damage. Even the mother can be adversely affected by indomethacin therapy. Lunt and associates (1994) reported that indomethacin tocolysis causes profound changes in maternal bleeding time.

Sulindac, closely related to indomethacin in structure, has been reported to have fewer side effects when used for tocolysis (Rasanen and Jouppila, 1995). Preliminary trials, however, indicate that oral sulindac therapy may not be very useful in the prevention of preterm birth (Carlan and associates, 1995). Kramer and colleagues (1996) measured the effects of sulindac on fetal urine production and amnionic fluid volume and compared them with terbutaline in a randomized, double-blind study. Sulindac administration decreased fetal urine flow and amnionic fluid volume. Two fetuses also developed severe ductal constriction. Thus, sulindac shares many of the fetal side effects associated with indomethacin.

Panter and colleagues (1996) reviewed all randomized trials which have compared indomethacin with b-agonists for tocolysis. Indomethacin was found to be more effective in delaying delivery by 48 hours, and there were fewer maternal side effects compared with ritodrine. Indomethacin was, however, associated with increased neonatal morbidity. These investigators concluded that indomethacin needs to be further evaluated before it is used routinely for tocolysis.

7) Calcium Channel-blocking Drugs

Smooth muscle activity, including myometrium, is directly related to free calcium within the cytoplasm, and a reduction in calcium concentration inhibits contraction.  Nifedipine, izoptine is also used for this purpose.

Calcium ions reach the cytoplasm through specific membrane portals or channels, and calcium-channel blockers act to inhibit, by a variety of different mechanisms, the entry of calcium through the cell membrane channels. Calcium-entry blockers, because of their smooth muscle arteriolar relaxation effects, are currently being used for the treatment of coronary artery disease and hypertension.

The possibility that calcium channel-blocking drugs might have applications in the treatment of preterm labor has been the subject of research in both animals and humans since the late 1970s. Saade and colleagues (1994), using in vitro human myometrial strips, showed that nifedipine caused relaxation similar to ritodrine and more effectively than magnesium. The first clinical trial in which nifedipine was given for preterm labor was from Denmark by Ulmsten and colleagues (1980). Nifedipine treatment postponed delivery at least 3 days in 10 women with preterm labor at 33 weeks or less. No serious maternal or fetal side effects were noted. There have been several subsequent studies on nifedipine tocolysis, and these have been reviewed comprehensively by Childress and Katz (1994). In all the studies, nifedipine was as successful as or better than ritodrine in stopping preterm contractions without adverse fetal effects. Maternal side effects were much worse with ritodrine. Papatsonis and colleagues (1996) reported a randomized study of 181 women in preterm labor and treated with either nifedipine or ritodrine. They found that nifedipine was superior to ritodrine in efficacy and had fewer side effects. Unfortunately, there have been no studies measuring the efficacy of nifedipine against untreated controls.

As promising as calcium-channel blockers may appear for treatment of preterm labor, some investigators caution that more research is needed to clarify their potential maternal or fetal dangers. This is because smooth muscle relaxation by nifedipine is not limited to uterine muscle, but also includes the systemic and uterine vasculature. Nifedipine-induced decreased vascular resistance can lead to maternal hypotension and thus decrease uteroplacental perfusion. Parisi and colleagues (1986) reported that hypercapnia, acidosis, and possibly hypoxemia developed in fetuses of hypertensive ewes given nicardipine. Similarly, Lirette and colleagues (1987) observed a fall in uteroplacental blood flow in pregnant rabbits. Other investigators, however, have not found these adverse fetal effects (Childress and Katz, 1994).

 The combination of nifedipine and magnesium for tocolysis is potentially dangerous. Ben-Ami and colleagues (1994) and Kurtzman and associates (1993) have reported that nifedipine enhances the toxicity of magnesium to produce neuromuscular blockade that can interfere with both pulmonary and cardiac function.

8) Atosiban - a nonapeptide oxytocin analog. Atosiban has been shown to be a competitive oxytocin-vasopressin antagonist capable of inhibiting oxytocin-induced uterine contractions.

9) Nitric Oxide Donor Drugs

Nitric oxide is a potent endogenous smooth-muscle relaxant in the vasculature, the gut, and the uterus. Nitroglycerin is an example of a nitric oxide donor drug. Lees and associates (1994) used nitroglycerin patches in 13 women with preterm labor and claimed that this drug was both effective and safe in preventing preterm birth. Clavin and colleagues (1996) randomized 34 women in preterm labor to tocolysis with intravenous nitroglycerin or magnesium sulfate. There was no difference in the tocolytic efficacy of these two drugs, but 3 of 15 women given nitroglycerin had severe hypotension.

Combined Therapy

10 ) Combined Therapy.  

The use of multiple drugs to inhibit preterm labor suggests that no single drug is completely satisfactory.

POTENTIAL COMPLICATIONS OF TOCOLYTIC AGENTS

                      Beta-adrenergic Agents 

                        Hyperglycemia   

                        Hypokalemia     

                        Hypotension      

                        Pulmonary edema        

                        Cardiac insufficiency   

                        Arrhythmias      

                        Myocardial ischemia   

                        Maternal death   

                      Magnesium Sulfate        

                        Pulmonary edema        

                        Respiratory depressiona       

                        Cardiac arresta   

                        Maternal tetanya

                        Profound muscular paralysisa                 

                        Profound hypotensiona        

                      Indomethacin       

                        Hepatitis

                        Renal failure

                        Gastrointestinal bleedingb    

                      Nifedipine   

                        Transient hypotension

3.     Accelerated Maturation of Pulmonary Function

A variety of clinical events— some well defined and others not—have been proposed to accelerate surfactant production sufficient to protect against respiratory distress. Gluck (1979) emphasized that surfactant production is likely to be accelerated remote from term in pregnancies complicated by the following conditions or stresses:

1.  Maternal: Chronic renal or cardiovascular disease, long-standing pregnancy-induced hypertension, sickle-cell disease, heroin addiction, or hyperthyroidism.

2.  Placenta and membranes: Placental infarction, chronic focal retroplacental hemorrhage, chorio-amnionitis, or preterm ruptured membranes.

3.  Fetal: The anemic member of parabiotic twins or the smaller member of nonparabiotic twins.

In contrast, Owen and associates (1990a) concluded that a “stressed” pregnancy (primarily pregnancy-associated hypertension) conferred a negligible fetal survival advantage. Similarly, Hallak and Bottoms (1993) reviewed 1395 pregnancies delivered between 24 and 35 weeks to determine if preterm ruptured membranes conferred advantages compared with preterm labor with intact membranes. Pulmonary maturation was not accelerated, and they concluded that the concept of accelerated maturation was a myth.

1. Glucocorticoid Therapy – is recommended till 34 weeks for gestation

The mechanism by which betamethasone or other corticosteroids are currently thought to reduce the frequency of respiratory distress involves induction of proteins that regulate biochemical systems within type II cells in the fetal lung that produce surfactant (Ballard and Ballard, 1995). The reported physiological effects of glucocorticoids on the developing lungs include increased alveolar surfactant, compliance, and maximal lung volume.

-         betamethasone (12 mg intramuscularly in two doses 24 hours apart) to prevent respiratory distress in the subsequently delivered preterm infant.

-         dexamethasone, 6 mg intramuscularly every 12 hours for four doses every 7 days, was introduced for selected women at risk for preterm birth between 24 and 34 weeks.

-         prednizolone in the dose 60 mg in a day during 2 days.

2. Thyrotropin-releasing Hormone for Fetal Maturation

Knight and colleagues (1994) from New Zealand reported that administration of thyrotropin-releasing hormone (400 mg given intravenously) in addition to betamethasone augmented fetal lung maturation compared with betamethasone used alone. This effect is based on experimental observations that tri-iodothyronine enhances surfactant synthesis.

3. Induction of prenatal lung stimulation by Lazolvan, Mucosolvan – 1000 mg a day during 3-5 days.

Thyrotropin-releasing Hormone for Fetal Maturation

Knight and colleagues (1994) from New Zealand reported that administration of thyrotropin-releasing hormone (400 mg given intravenously) in addition to betamethasone augmented fetal lung maturation compared with betamethasone used alone. This effect is based on experimental observations that tri-iodothyronine enhances surfactant synthesis. Crowther and co-workers (1995) and the Australian Collaborative Study Group randomized 1234 women to receive thyrotropin-releasing hormone in addition to corticosteroids or corticosteroids alone and were unable to reproduce these beneficial results. Indeed, the incidence of respiratory disease was increased in the thyrotropin-treated group! In this ACTOBAT study, the investigators also observed that 7 percent of the mothers became overtly hypertensive as a result of thyrotropin therapy. They concluded that thyrotropin-releasing hormone, given to augment fetal maturation “is associated with maternal and perinatal risks and cannot be recommended.”

Adverse Effects of Corticosteroids.

Studies initiated in the 1970s, which followed the development of children treated antenatally with corticosteroids up to the age of 12 years, showed no adverse outcomes in the areas of long-term neurodevelopment. These were measured by learning, behavioral, and motor or sensory disturbances (NIH Consensus Development Panel, 1995). There are, however, short-term maternal effects to include pulmonary edema, infection, and more difficult glucose control in diabetic women. No long-term adverse maternal effects have been reported.

Liggins and Howie (1972) based their use of corticosteroids to promote fetal lung maturation on experiments in sheep that indicated that such therapy not only affected lung maturation but also stimulated labor. Corticosteroids were reported to induce labor in humans more than 20 years ago (Jenssen and Wright, 1977; Mati and colleagues, 1973). Elliott and Radin (1995) recently confirmed that corticosteroids induce uterine contractions and preterm labor in humans.

Antenatal Phenobarbital and Vitamin K Therapy

As reviewed by Thorp and colleagues (1995), several studies have suggested that antenatal phenobarbital and vitamin K given to the mother may reduce the incidence of intracranial hemorrhage. They randomized 272 women at risk for preterm birth to placebo or treatment with phenobarbital and vitamin K and found that such therapy did not reduce the frequency or severity of neonatal intracranial hemorrhage.

Cerclage

Prophylactic cervical cerclage, which is typically recommended in the United States for women with recurrent midtrimester losses, has also been used in Europe to prevent preterm birth. Two randomized trials of cerclage included more than 700 women at risk for preterm delivery, and neither study showed a benefit for cervical sutures (Lazar and colleagues, 1984; Rush and associate, 1984). Prophylactic cerclage in twin pregnancies has also been shown to be of no benefit in a randomized trial (Dor and associates, 1982). More recently, the Medical Research Council of the Royal College of Obstetricians and Gynaecologists (1993) studied 1292 women from 12 countries with heterogenous and often unclear indications for cerclage to assess if this procedure prolonged pregnancy. Approximately 75 percent of women enrolled in this randomized study had previously delivered preterm infants. In 647 women, cervical sutures were placed at about 16 weeks and their outcomes compared with 645 women randomized to no cerclage. A small—from 17 to 13 percent—but significant decrease in births before 33 weeks was observed in women undergoing cerclage. Importantly, there was no difference in neonatal death between the two groups. The use of cerclage, however, was linked to increased interventions such as tocolysis and hospital admission. The investigators concluded that cervical sutures should be offered to women with a history of three or more pregnancies ending before 37 weeks.

Intrapartum Management

In general, the more immature the fetus, the greater the risks from labor and delivery.

Labor. Whether labor is induced or spontaneous, abnormalities of fetal heart rate and uterine contractions should be sought, preferably by continuous electronic monitoring.

Delivery.    In the absence of a relaxed vaginal outlet, a liberal episiotomy for delivery is advantageous once the fetal head reaches the perineum. Pudendal anesthesia for perineal muscles relaxation in performed obligatory by 0.25 % Novocaine in every side. Perineal protective maneuvers don’t apply.

Prevention of Neonatal Intracranial Hemorrhage

Following the report of Bejar and colleagues (1980) that preterm infants frequently had germinal matrix bleeding that might extend to more serious intraventricular hemorrhage, there was the idea that cesarean delivery to obviate trauma from labor and vaginal delivery might prevent these complications. These initial observations have not been validated by most subsequent studies. In the largest study, Malloy and colleagues (1991) analyzed 1765 infants with birthweights less than 1500 g and found that cesarean delivery did not lower the risk of mortality or intracranial hemorrhage. Anderson and colleagues (1988), however, made an interesting observation regarding the role of cesarean delivery in the prevention of neonatal intracranial hemorrhages. These hemorrhages were related to whether or not the fetus had been subjected to the active phase of labor, defined as the interval before 5 cm cervical dilatation. As emphasized by Anderson and colleagues (1988), avoidance of active-phase labor is impossible in most preterm births because the route of delivery cannot be decided until labor is firmly established.

Nelson and Grether (1995) reported that magnesium sulfate given to women delivered preterm for either tocolysis or preeclampsia was associated with a significantly reduced incidence of cerebral palsy when surviving infants with birthweights less than 1500 g were followed to 3 years of age. It was suggested that magnesium given to the fetus via the mother perhaps played a role in regulation of the vasculature supplying the germinal matrix of the fetal brain that is especially vulnerable to hemorrhage in the preterm infant. Murphy and colleagues (1995) from England, however, found that severe preeclampsia and delivery without labor were protective against cerebral palsy. They concluded that magnesium could not be the protective agent because this drug is not used for preeclampsia in England.

POSTDATE PREGNANCY

Definitions

 “Postterm”, “postdate” pregnancy is signify pregnancies that have exceeded a duration considered to be the upper limit of normal  - more than 42 completed weeks (294 days) with signs of Placental Dysfunction and delivery of the fetus with signs of postmaturity.

“Prolonged “ pregnancy is signify pregnancies that have exceeded a duration considered to be the upper limit of normal  - more than 42 completed weeks (294 days) with absence signs of Placental Dysfunction and delivery of the fetus without signs of postmaturity.

“Postmature” should be used to describe the infant with recognizable clinical features indicating a pathologically prolonged pregnancy.

Signs of Postmature Infant.

Clifford’s 1954 divided postmaturity into three stages: in stage 1 the amniotic fluid was clear, in stage 2 the skin was stained green, and in stage 3 the skin discoloration was yellow-green. Signs of infant’ postmaturity:

-         wrinkled, patchy peeling skin. Skin wrinkling can be particularly prominent on the palms and soles. The nails are typically quite long.

-         a long, thin body suggesting wasting,

-         open-eyed, unusually alert, old, and worried-looking.

Skin changes of postmaturity were due to loss of the protective effects of vernix caseosa. His second hypothesis that continues to influence contemporary concepts attributes postmaturity syndrome to placental senescence

The postterm fetus may continue to gain weight and thus be an unusually large infant at birth. That the fetus continues to grow serves to suggest that placental function is not compromised. Indeed, continued fetal growth, although at a slower rate, is characteristic between 38 and 42 weeks (Fig. 5). Nahum and colleagues (1995) have confirmed that fetal growth continues at least up until 42 weeks.

Fig. 5 Postmature infant delivered at 43 weeks’ gestation. Thick, viscous meconium coated the desquamating skin. Note the long, thin appearance and wrinkling of the palms of the hands.

Diagnosis of postdate pregnancy:

1. Taking female history.

2. Estimation of probable day of labor by all methods.

3. Clinical evaluation of the patient:

- decreasing of maternal weight

- decreasing of maternal skin tone

- decreasing of circumference of the maternal abdomen

- decreasing of fetal movement

4. Laboratory signs of fetal distress:

 - viscous meconium, decreased umbilical cord diameter  in ultrasonograophy and late decelerations in electronic monitoring.

- signs of oligohydramnios which is estimated by ultrasonography - the smaller the amnionic fluid pocket, the greater the likelihood that there was clinically significant oligohydramnios.

Oligohydramnios commonly develops as pregnancy advances beyond 42 weeks. It is also likely that fetal release of meconium  into an already reduced amnionic fluid volume is the reason for the thick, viscous meconium implicated in meconium aspiration syndrome. Diminished urine production was found to be associated with oligohydramnios was found by Trimmer and co-workers (1990). It was hypothesized, however, that decreased fetal urine flow was likely the result of preexisting oligohydramnios that limited fetal swallowing of amnionic fluid. Veille and co-workers (1993), using pulsed Doppler waveforms, reported that fetal renal blood flow is reduced in postterm pregnancies with oligohydramnios.

- placental Dysfunction   Clifford (1954) proposed that the skin changes of postmaturity were due to loss of the protective effects of vernix caseosa. His second hypothesis that continues to influence contemporary concepts attributes postmaturity syndrome to placental senescence. Clifford could not demonstrate placental degeneration histologically, and indeed, in the ensuing 40 years, no morphological or significant quantitative changes have been found (Larsen and co-workers, 1995; Rushton, 1991).

The postterm fetus may continue to gain weight and thus be an unusually large infant at birth. That the fetus continues to grow serves to suggest that placental function is not compromised. Indeed, continued fetal growth, although at a slower rate, is characteristic between 38 and 42 weeks (Fig. 35–4 ). Nahum and colleagues (1995) have confirmed that fetal growth continues at least up until 42 weeks.

MANAGEMENT OF POSRTERM PREGNANCY

Labor is a particularly dangerous time for the postterm fetus. Therefore, it is important that women whose pregnancies are known or suspected to be postterm come to the hospital as soon as they suspect they are in labor. Upon arrival, while being observed for possible labor, we recommend that fetal heart rate and uterine contractions be monitored electronically for variations consistent with fetal distress.

Fig. 6 Recommendations by American College of Obstetricians and Gynecologists (1995) for management of postdate pregnancy

Management of Postterm Pregnancy at Parkland Hospital.

In women with certain gestational age, labor is induced at the completion of 42 weeks (Fig. 5). Almost 90 percent of women are induced successfully, or enter labor within 2 days of induction. For those who do not deliver with the first induction, a second induction is performed within 3 days. Almost all women will be delivered by this plan of management, but in the unusual few who are not delivered, a cesarean section may be justified.

Women classified as having uncertain postterm pregnancies are followed on a weekly basis and without intervention unless fetal jeopardy is suspected. The latter is based upon clinical or sonographic perception of decreased amnionic fluid volume. Equally worrisome is diminished fetal motion reported by the mother. If fetal jeopardy is suspected by either method, labor induction is carried out as described previously for the woman with certain postterm gestation. Other details of management are summarized in Figure 7.  This protocol has been used successfully for more than 15 years.

Fig. 7. Parkland Hospital protocol for management of prolonged pregnancies.

When a cervix is not favorable, intravaginal prostaglandin E2 gel (dinoprostone; Prepidil gel) has been used to ripen the cervix, and indeed, labor often ensues without the need of oxytocin stimulation. A dose of 0.5 mg of prostaglandin gel is inserted next to the cervix every 4 to 6 hours. The main concern in the use of prostaglandin is uterine hyperstimulation, which in turn may cause uteroplacental insufficiency and, rarely, uterine rupture. Prostaglandin gel is relatively contraindicated in patients with concurrent asthma. Another method to ripen the cervix is insertion of laminaria.

   In the case of postdate pregnancy at 42 weeks or more induction is recommended unless the cervix is unfavorable, in which case cervical ripening agents or fetal surveillance are acceptable options.

Induction of labor is usually carried out with several ways:

·        intravenous administrated 5 units (1 ml) oxytocin in 500 ml 0,9 % isotonic solution NaCl (dilute intravenous solution) with the initiated dose 6-8 drops per minute to 40 drops per minute;

·        intravenous administrated 5 mg (1 ml) prostaglandin F2a in 500 ml   0,9 % isotonic solution NaCl with the initiated dose 6-8 drops per minute to 25-30 drops per minute;

·        combine intravenous administration of 2,5 units of oxytocin and 2,5 mg of prostaglandin F2a in 500 ml 0,9 % isotonic solution NaCl with the initiated dose 6-8 drops per minute to 40 drops per minute.

The mother should never be left alone while the oxytocin infusion is running.  Uterine contractions must be evaluated continually and oxytocin shut off immediately if contractions exceed 1 minute in duration or if the fetal heart rate decelerate significantly. When either occurs, immediate discontinuation of the oxytocin nearly always correct the disturbances, preventing harm to mother and fetus. The oxytocin concentration in plasma rapidly falls, since the mean half-loaf of oxytocin is approximately 5 minutes.

Caution: oxytocin has potent antidiuretic action. Whenever 20 mV per min or more of oxytocin is infused, water intoxication may lead to convulsion, coma, and even death.

In the case of prolonged pregnancies have included use of prostaglandin E2 for cervical ripening with the follow induction of labor.

In the case of oligohydramnios amniotomy is precede induction of labor.  When to perform amniotomy is problematic. Further reduction in fluid volume following amniotomy can certainly enhance the possibility of cord compression. On the other hand, amniotomy will aid diagnosis of thick meconium, which may be dangerous to the fetus if aspirated. Moreover, once the membranes are ruptured, a scalp electrode and intrauterine pressure catheter can be placed, which usually provide more precise data concerning fetal heart rate and uterine contractions.

Identification of thick meconium in the amnionic fluid is particularly worrisome. The viscosity probably signifies the lack of liquid and thus oligohydramnios. Aspiration of thick meconium may cause severe pulmonary dysfunction and neonatal death This may be minimized but not eliminated by effective suctioning of the pharynx as soon as the head is delivered but before the thorax is delivered. If meconium is identified, the trachea should be aspirated as soon as possible after delivery. Immediately thereafter, the infant should be ventilated as needed. The likelihood of successful vaginal delivery is reduced appreciably for the nulliparous woman who is in early labor with thick meconium-stained amnionic fluid. Therefore, when the woman is remote from delivery, strong consideration should be given to prompt cesarean section, especially when cephalopelvic disproportion is suspected or either hypotonic or hypertonic dysfunctional labor is evident. Some choose to avoid oxytocin use in these cases.

At times, the continued growth of the fetus postterm will result in a large-for-gestational-age infant, and shoulder dystocia may develop. Therefore, an obstetrician experienced in managing this complication should be available to effect delivery.

Intrapartum Management

 Labor is a particularly dangerous time for the postterm fetus. Therefore, it is important that women whose pregnancies are known or suspected to be postterm come to the hospital as soon as they suspect they are in labor. Upon arrival, while being observed for possible labor, we recommend that fetal heart rate and uterine contractions be monitored electronically for variations consistent with fetal distress (American College of Obstetricians and Gynecologists, 1995a).

When to perform amniotomy is problematic. Further reduction in fluid volume following amniotomy can certainly enhance the possibility of cord compression. On the other hand, amniotomy will aid diagnosis of thick meconium, which may be dangerous to the fetus if aspirated. Moreover, once the membranes are ruptured, a scalp electrode and intrauterine pressure catheter can be placed, which usually provide more precise data concerning fetal heart rate and uterine contractions.

Identification of thick meconium in the amnionic fluid is particularly worrisome. The viscosity probably signifies the lack of liquid and thus oligohydramnios. Aspiration of thick meconium may cause severe pulmonary dysfunction and neonatal death. This may be minimized but not eliminated by effective suctioning of the pharynx as soon as the head is delivered but before the thorax is delivered. If meconium is identified, the trachea should be aspirated as soon as possible after delivery. Immediately thereafter, the infant should be ventilated as needed. The likelihood of successful vaginal delivery is reduced appreciably for the nulliparous woman who is in early labor with thick meconium-stained amnionic fluid. Therefore, when the woman is remote from delivery, strong consideration should be given to prompt cesarean section, especially when cephalopelvic disproportion is suspected or either hypotonic or hypertonic dysfunctional labor is evident. Some choose to avoid oxytocin use in these cases.

At times, the continued growth of the fetus postterm will result in a large-for-gestational-age infant, and shoulder dystocia may develop. Therefore, an obstetrician experienced in managing this complication should be available to effect delivery.

UTERINE CONTRACTIONS ABNORMALITIES

CLASSIFICATION OF ABNORMAL LABOR

 BY CHERNUKHA, 1990.

1. False labor.

2. Uterine inertia (hypotonic dysfunction):

·        primary,

·        secondary,

·        inadequate voluntary expulsive forces .

3. Excessive uterine activity (hypertonic dysfunction).

4. Incoordinative uterine activity (hypertonic dysfunction):

·        dyscoordination,

·        hyperactivity of lower uterine segment,

·        circulative dystocia (contractile ring),

·        uterine tetania.

 

Differentiating Contractions of True and False labor

 (Braxton Hicks Contractions)

True Labor

False Labor

Regular intervals, gradually increasing

Irregular intervals and duration

Painless uterine contractions

Painful uterine contractions

Intensity increasing

Intensity unchanged

Normal uterine tone

Increased uterine tone

Cervical dilation occurs

No cervical dilation

Back and abdominal discomfort

Lower abdominal discomfort

No relief from sedation

Relief from sedation

Uterine contractions increased with physical activity

Uterine contractions don’t increased with physical activity

It lasts for 6-8 hours

It lasts for 7-24-48 hours

 

 

Etiology of  uterine contractions abnormalities:

·        excess maternal nervous sickness and emotions (maternal exhaustion);

·        impairment of nervous mechanisms of labor regulation as a result of previous acute and chronic infectious diseases, nervous system disorders:

·        pathological changes of uterine cervix and uterus;

·    Cephalopelvic disproportion” -  is a disparity between the size or shape of the maternal pelvis and the fetal head, preventing vaginal delivery, and is similar to arrest disorder. This may be caused by the size or shape of the pelvis and/or the fetal head, or a relative disparity as a result of malpresentation of the fetal head.

·        hydramnion, multiple pregnancy, oligohydramnion;

·        postdate pregnancy;

·        administration of excess anesthesia;

·        inadequate usage of uterotonic drugs

Treatment of false labor.  Central regulation of uterine contractions is the leading point in the treatment of false labor.

1. Prescription of sedative drugs: Diazepam in the dose of 10-40 mg intramuscularly or intravenously (10-20 mg into 20 ml of 0.9 % NA CL slowly). General dose is 40 mg. 

2. Prescription of Prostaglandines’ synthesis inhibitors: Indometacine in the daily dose 200-250 mg should prescribed during 3-5 days. Its initial dose is 125 mg     (25 mg – per os, 100 mg – per rectum).

3. Prescription of b-adrenomimetic drugs:

·        0,5 mg Partusisten in 500 mg 5 % of Glucose solution or 0,09 % NaCl – during 5 hours. Then 5 mg 6 times a day per os should prescribe; Finoptine in the dose of 40 mg twice a day is indicated in the case of tachycardia;

·        Bricanil, Alupent in the dose 0,5 mg should be used for this purpose also.

Contraindications to b-adrenomimetic drugs prescriptions are: hypertensive disorders during pregnancy, Diabetes Mellitus type I, chorionamnionitis, dead fetus syndrome, heart failure, thyroid gland hyperfunction.

4. Therapeutic rest is very effective in the case of false labor. For this purpose such drugs have bee used as: Promedol – 40 mg, Pipolphen – 50 mg, Diazepam – 20 mg.

5. Calcium antagonists should be prescribed also: Niphedipine in the dose 10 mg every 15 minutes. Its general dose is 30 mg.  

 

ABNORMAL LABOR, or dystocia (literally, “difficult labor or childbirth”) results when anatomic or functional abnormalities of the fetus, the maternal bony pelvis, the uterus and cervix, and/or a combination of these interfere with the normal course of labor and delivery. The diagnosis and management of dystocia is a major health care issue, because more than one fourth of all cesarean sections are performed for this indication. Because the goal of modern obstetrics is a safe, healthy delivery for both mother and fetus, minimizing the morbidity and mortality of the labor process continues to be a primary focus of clinical attention.

Functional dystocia has been associated with two different types of abnormal contraction patterns.

A hypertonic pattern (incoordinative) typically has an elevated resting pressure and contractions of increased frequency but decreased coordination. It is seen more  often with fetal malpresentation and uterine overdistension. Some researchers have theorized multiple pacemakers sites or asynchronous spread of contractile impulses as the cause of this dysfunctional pattern. Oxytocin generally has not been recommended..

 A second type of abnormal contraction pattern, called hypotonic dysfunction, is more common and frequently responds to oxytocin. The contractions are synchronous but weak or infrequent. With primary dysfunction, it is hypothesized that contractions were never normally established; with secondary dysfunction, it is suggested that contractions were once adequate and became weaker as labor progressed, usually after 4 cm of dilation.

Garfield described the cellular and molecular bases of functional dystocia. It involves the disturbance of any factor that promotes uterine contractility, including a lack of stimulation, strong inhibition, or both. Effective treatment depends on identification of the defect. Alterations in myogenic control could be caused by inadequate depolarization with impaired ionic milei, hormonal or receptor deficiencies, insufficient gap junction formation, inadequate muscle development, or lack of energy. Hormonal control could be defective with inadequate steroid ratios or failure of synthesis of hormonal receptors.

Abnormal labor describes complications of the normal labor process:

·        slower – than – normal progress (protraction, prolonged disorders) or

·        a cessation of progress ( arrest disorders).

The patterns of abnormal labor are summarized in the table.

Abnormal Labor Patterns (according to labor stages) by A. Friedman

Phase of labor

Labor

pattern

Limits for abnormality

Nulliparous labor

Multiparous

labor

Latent phase of cervical stage

Prolonged labor phase (no progress from latent to active phase of labor)

> 21 hour

> 14 hours

Active phase of cervical stage

Prolonged active phase of labor

< 1.2 cm / hour

< 1.5 cm / hour

Secondary arrest ( no change for “cervical dilatation )

> 2 hours

> 2 hours

Prolonged deceleration phase

> 3 hours

> 1 hour

Pelvic stage

Impossibility to descend

< 1 cm / hour

< 2 cm /  hour

Protracted descend

< 1 cm /hour

< 2 cm / hour

Arrest of descend

> 1 hour

> 1/2 hour

All stages

Precipitous labor

< 4 hours

< 2 hours

 

Graphic documentation of progressive cervical dilatation and effacement facilitates assessing a patient’s progress in labor and identifying any type of abnormal labor pattern that may develop.

Less specific terms have also been applied to abnormal labor patterns and remain in common usage and are wide spread in our country. 

 

UTERINE INERTIA  (“Failure to progress”, hypotonic uterine dysfunction) describes lack of progressive cervical dilatation and/or descent of the fetus and is similar to the arrest disorders.  It is such condition in which uterine contractions strength, duration and frequency are inadequate, that’s why cervical effacement, dilation and fetal descending is slowly than in normal labor (in the case if cephalopelvic disproportion is absent). Its frequency is 10 %.   

Primary and secondary types of uterine inertia have been distinguished.

Primary uterine inertia occurs from the early onset of labor and lasts during the its second stage until the end of labor.

  Primary uterine inertia is characterized by such signs as:

·        Inadequate uterine activity;

·        Lack of the progressive cervical effacement and dilation;

·                        Station of presenting part in the pelvic inlet (- 3 station) for a long period of time and slowly descent of the fetus in the case of “cephalopelvic disproportion” absence;

·        Increased duration of labor;

·        Maternal exhaustion and impairment of fetal well-being .  

Diagnosis of primary uterine inertia is made during dynamic monitoring for woman during 2-3 hours. Important clinical evaluation of labor duration is the rate of cervical dilation. If, the cervical dilation to 6 cm is absent if from the onset of labor in nulliparous women have been passed 12 hours and in multiparous women have been passed 6 hours, the diagnosis of primary uterine inertia has been made.

Secondary uterine inertia occurs after adequate uterine contractions and manifests by decreasing of uterine contractions strength, duration and frequency  later.

Secondary uterine inertia as a rule is presented in the end of the cervical stage of labor and in the pelvic stage. Its frequency is 2,4 % to all number of labor. The causes of secondary uterine inertia are the same, as primary uterine inertia has had. But, as a rule, secondary uterine inertia is more common as a result of:

·      “cephalopelvic disproportion” in clinic contracted pelvis, hydrocephalia, fetal malpresentations, transversus and oblique fetal lies, tumors in true pelvis;

·        “unripe” uterine cervix, its scar’s changes;

·        vaginal stenosis;

·        breech presentation;

·        expressed pain in uterine contractions;

·        inadequate usage of  amniotomy;

·        endometritis;

·        administration of excess and inadequate anesthesia, uterotonic and spasmolytics drugs.  

It is very important to differentiate secondary uterine inertia with “cephalopelvic” disproportion for preventing obstetric complications. Arrest of descent over a 2 hour-period is suggestive of either “cephalopelvic” disproportion or ineffective uterine contractions.

Management of abnormal labor in the case of uterine inertia

Uterine inertia, as a rule,  accompanies by female sickness and tiredness. That’s why for successful induction or augmentation of labor therapeutic rest should be prescribed obligatory.

In the case of maternal exhaustion therapeutic rest should be indicated. Obstetrics anesthesia is prescribed by combination of such drugs as: Sol. Promedoli 1% - 1,0, Sol. Dimedroli – 2% -2, 0,  Sol. Atropini Sulfatis 0,1 % - 1,0. For this purpose Droperidoli 0,25 % - 1 ml or Natrii Oxybuturatis 20 % should be prescribed also.

Induction of labor is the stimulation of uterine contractions before the spontaneous onset of labor, with the goal of achieving delivery.

Augmentation of labor is the stimulation of uterine contractions that began spontaneously but are either too infrequent or too weak, or both. 

Stimulation of labor is usually carried out with several ways:

·        intravenous administrated 5 units (1 ml) oxytocin in 500 ml 0,9 % isotonic solution NaCl (dilute intravenous solution) with the initiated dose 6-8 drops per minute to 40 drops per minute;

·        intravenous administrated 5 mg (1 ml) prostaglandin F2a in 500 ml        0,9 % isotonic solution NaCl with the initiated dose 6-8 drops per minute to 25-30 drops per minute;

·        combine intravenous administration of 2,5 units of oxytocin and 2,5 mg of prostaglandin F2a in 500 ml 0,9 % isotonic solution NaCl with the initiated dose 6-8 drops per minute to 40 drops per minute.

The mother should never be left alone while the oxytocin infusion is running.  Uterine contractions must be evaluated continually and oxytocin shut off immediately if contractions exceed 1 minute in duration or if the fetal heart rate decelerate significantly. When either occurs, immediate discontinuation of the oxytocin nearly always correct the disturbances, preventing harm to mother and fetus. The oxytocin concentration in plasma rapidly falls, since the mean half-loaf of oxytocin is approximately 5 minutes.

Caution: oxytocin has potent antidiuretic action. Whenever 20 mV per min or more of oxytocin is infused, water intoxication may lead to convulsion, coma, and even death.

The following precautions should be observed when using oxytocin to treat hypotonic dysfunction:

1. The patient must be in true labor, nor false or prodromal labor. labor must have progressed to 3-5 cm of dilatation. One of the most common mistakes in obstetrics is to try to stimulate labor in women who have not been in active labor.

2. There must be no other discernible evidence of mechanical obstruction to save delivery.

3. Do not use oxytocin in cases involving abnormal presentations of the fetus and marked uterine overdistention such as gross hydramnios, a large singleton fetus, or multiple fetuses.

4. In general, women of high parity (more than five deliveries) should not be given oxytocin because their uteri rupture more readily than those of women of lower parity.

5. The condition of the fetus must be good, as evidence by a normal heart rate and lack of heavy contamination of the amniotic fluid with meconium.

6. The frequency, intensity, and duration of contractions – and uterine tone between contractions, must not exceed those of normal spontaneous labor.

7. Continuous electronic monitoring of the fetal heart and uterine activity should be maintained

Spasmolytic agents are indicated in the case of augmentation after cervical dilation to 3-4 cm. The incidence of prolongation of the first stage of labor can be minimized by avoiding unnecessary intervention.

 Labor should not be induced when the cervix is not well prepared, or “ripe” (softened, anteriorly rotated, partially effaced). The degree of cervical ripening or readiness for labor is estimated by digital examination of the cervix. The Bishop score has been used to try to quantify this determination, and although not especially precise, it provides an excellent schema for cervical evaluation and a rough approximation of the likelihood of successful induction of labor and transvaginal delivery.

The Bishop Score for cervical status

 

0

1

2

3

Dilation

Closed

1-2 cm

3-4 cm

5 cm

Effacement

0-30 %

40-50 %

60-70 %

80 %

Station

-3

-2, -1

0

+1, +2

Consistency

Firm

Medium

Soft

 

Position

Posterior

Mid

Anterior

 

A score of 0 to 4 points associated with the highest likelihood of failed induction; of 9 to 13 points is associated with the highest likelihood of successful induction.

Induction of labor is indicated if the anticipated benefits of delivery exceed the risks of allowing the pregnancy to continue. Therefore, careful evaluation of both mother and fetus is needed to make this decision. Currently, “elective” induction solely for convenience is controversial. Table  summarizes commonly cited indications and contraindications to labor induction.

INDICATIONS

CONTRAINDICATIONS

Post-term pregnancy

Placenta of vase previa

Maternal medical problems

Cord presentation

Fetal demise

Abnormal/unstable fetal lie

Suspected fetal compromise

Presenting part above inlet

Pregnancy-induced hypertension

Prior classical uterine incision

Premature rupture of membranes

Prior uterine incision of unknown type

Chorionamnionitis

Active genital gerpes

 

When a cervix is not favourable, intravaginal prostaglandin E2 gel (dinoprostone; Prepidil gel) has been used to ripen the cervix, and indeed, labor often ensues without the need of oxytocin stimulation. A dose of 0.5 mg of prostaglandin gel is inserted next to the cervix every 4 to 6 hours. The main concern in the use of prostaglandin is uterine hyperstimulation, which in turn may cause uteroplacental insufficiency and, rarely, uterine rupture. Prostaglandin gel is relatively contraindicated in patients with concurrent asthma.

Another method to ripen the cervix is insertion of laminaria. Laminaria can be made from the stems of the seaweed Laminaria japonica or be of artificial origin. They are hydroscopic rods that are inserted into the internal os. As the rods absorb moisture and expand, the cervix is slowly dilated. The risks associated with laminaria use include failure to dilate the cervix, cervical lacerations, inadvertent rupture of the membranes, and infection.

During the active phase of labor, mechanical factors such as fetal malprosition and malpresentation as well as fetopelvic disproportion must be considered before augmentation of uterine contractions with oxytocin. In cases in which the fetus fails to descend in the face of adequate contractions, disproportion is likely and cesarean section warranted. If no disproportion is present, oxytocin can be used if uterine contractions are judged to be inadequate. In cases of maternal exhaustion resulting in secondary arrest of dilatation, rest followed by augmentation with oxytocin is often effective. If not already ruptured, artificial rupture of the membranes is also recommended.

Amniotomy, or artificial rupture of membranes, is also advocated for patients with prolonged latent phase. It is believed that after amniotomy the fetal head will provide a better dilating force than would the intact bag of waters. In addition, there may be a release of prostaglandins, which could aid in augmenting the force of contractions. Before amniotomy is performed, the  presenting part should be firmly applied to the cervix so as t minimize the risk of causing an umbilical cord prolapse. Amniotomy is usually performed with as “amnihook”, a thin, plastic rod with a sharp hook on the end. The end is guided to the open cervical os with examiner’s fingers, and the hook is used to snag and tear the amniotic sac. The fetal heart rate should be  evaluated both before and immediately after rupture of the membranes.

Should fetal or maternal distress occur, prompt intervention is warranted. If this happens during the second stage of labor with vertex low in the pelvis, forceps or vacuum can be used to effect a vaginal delivery. In all other cases, cesarean section may have to be carried out. Distress of either mother or fetus in the first stage of labor usually mandates cesarean delivery.

Inadequate voluntary expulsive forces is characterized by insufficiency of abdominal prelum muscles or woman’ sickness. It manifests by elongation of pelvic stage of labor. bearing down efforts become frequent, low strength, weak. Arrest of presenting part is common. Elongation of cervical stage of labor leads to female external genitalia edema, signs of adjacent organs compression should be presented, endometritis in labor should developed. A fetus may be die from asphyxia.

With full cervical dilatation, women usually feel the urge to “bear down” or “push” each time the uterus contracts. Typically, the laboring woman inhales deeply, closes her repetitively to increase intraabdominal pressure throughout of the uterus and the abdominal musculature propel the fetus down the vagina and through the vaginal outlet.

Causes of inadequate expulsive forces – conduction analgesia is likely to reduce the reflex urge for the woman to “push” and at the same time may impair her ability to increase intra-abdominal pressure. Loss of consciousness associated with general anesthesia certainly imposes these adverse effects, as does heavy sedation.

Management. Careful selection of analgesic agents and the timing of their administration are important to prevent compromise of voluntary expulsive efforts. With rare exceptions, intrathecal analgesia or general anesthesia should not be administered until all conditions for a safe forceps delivery or vacuum extraction  have been met.

EXCESSIVE UTERINE ACTIVITY (UTERINE HYPERACTIVITY) is characterized by high strength of uterine contractions and increasing of their frequency. Uterine tone is increased also. The frequency of its pathology is 0,8 %.

The main cause of this disorder is hyperexcitability of nervous system in woman. Impairment of fetoplacental circulation, placental abruptio, deep cervical and vaginal ruptures should be  presented in uterine hyperactivity. Fetal molding is absent in labor, that’s why intracranial hemorrhages and fetal trauma in labor are common.

 

 

Management of abnormal labor in the case of  uterine hyperactivity

For elimination of excessive uterine forces tocolysis by b-adrenomimetics (Partusisten, Bricanil, Ritodrine.) is very effective. 0.5 mg Partusisten in 250 ml of 0.9 % NaCl is prescribed intravenously with the rate 6-8 drops in one minute. Anesthesia with Phtorotan is indicated in such cases also. Pudendal anesthesia should be recommended in the second stage of labor.

 

Fig. 8. Registration of  Excessive uterine activity

 

 

INCOORDINATIVE UTERINE ACTIVITY is characterized by absence adequate coordinate  uterine contractions between different uterine parts: right and left its sides, upper and lower uterine parts, different its regions. Its frequency is         1-3 %.

The main causes of incoordinate uterine contractions are:

·        uterine abnormality;

·        uterine cervix dystocia;

·        flat amniotic sac;

·        impairment of uterine innervating;

·        damaging of uterine regions as a result of inflammatory, degenerative and neoplastic changes. 

Incoordinative uterine activity is characterized by painful, irregular and  frequent uterine contractions. “Unripe” cervix and slow its dilation, preterm rupture of amniotic fluid, flat amniotic sac is common. Presenting part is movable or fixated to the pelvic inlet for a long period of time. Woman in labor  has been tired later and the arrest of presenting part is presented..

It is very important to differentiate incoordinative uterine activity with uterine inertia, “cephalopelvic” disproportion for different ways of these disorders management.

Fig. 9. Incoordinate uterine contractions (clinically contracted pelvis)

Management of abnormal labor in incoordinative uterine activity

Amniotomy gives good results. Uterotonic drugs are contraindicated for incoordinative uterine activity treatment.

The b-mimetics, calcium chammel blockers, magnesium sulfate, and antiprostaglandins and sedative drugs have been used to inhibit labor. Ethanol has a direct depressant effect on smooth muscle and inhibits oxytocin release. Atropine and scopolamine relax the lower uterine segment and decrease the frequency of contractions

In the case of presence maternal exhaustion, therapeutic rest is indicated. In the case of “cephalopelvic” disproportion cesarean section is performed.

 

PRECIPITATE LABOR AND DELIVERY

Precipitate – ie, extremely rapid – labor and delivery mat result from abnormally low resistance of the soft parts of the birth canal, from abnormally strong uterine and abdominal contractions, or, very rarely, from the absence of painful sensation and thus a lack of awareness of vigorous labor.

 

Fig. 9. Abnormally strong uterine and abdominal contractions

 

Precipitate labor combined with a long, firm, cervix and a vagina, vulva, or perineum that resists stretch may lead to rupture of the uterus or extensive lacerations of the cervix, vagina, vulva, or perineum. The uterus that contracts with unusual vigor before delivery is likely to be hypotonic after delivery, with hemorrhage from the placental implantation site as the consequence. 

Perinatal mortality and morbidity from precipitate labor may be increased considerably for several reasons. First, the tumultuous uterine contractions often prevent appropriate uterine blood flow and oxygenation of the fetal blood. Second, resistance of the birth canal to expulsion of the head may cause intracranial trauma. Morover, Erb-Duchenne palsy is associated with such labors in a third of cases. Third, during an unattended birth, the infant may fall to the floor and be injured or may need resuscitation that is not immediately available.

Management. Any oxytocic agents being administrated should be stopped immediately. Tocolytic agents such as Ritodrine and parenteral Magnesium sulfate may prove effect.

 

 

Normal labor is defined as uterine contractions that result in progressive dilation and effacement of the cervix. By following thousands of labors resulting in uncomplicated vaginal deliveries, time limits and progress milestones have been identified that define normal labor. Failure to meet these milestones defines abnormal labor, which suggests an increased risk of an unfavorable outcome. Thus, abnormal labor alerts the obstetrician to consider alternative methods for a successful delivery that minimize risks to both the mother and the infant.

 

Dystocia of labor is defined as difficult labor or abnormally slow progress of labor. Other terms that are often used interchangeably with dystocia are dysfunctional labor, failure to progress (lack of progressive cervical dilatation or lack of descent), and cephalopelvic disproportion (CPD).

 

Friedman's original research in 1955 defined the following 3 stages of labor[1] :

The first stage starts with uterine contractions leading to complete cervical dilation and is divided into latent and active phases. In the latent phase, irregular uterine contractions occur with slow and gradual cervical effacement and dilation. The active phase is demonstrated by an increased rate of cervical dilation and fetal descent. The active phase usually starts at 3-4 cm cervical dilation and is subdivided into the acceleration, maximum slope, and deceleration phases.

The second stage of labor is defined as complete dilation of the cervix to the delivery of the infant.

The third stage of labor involves delivery of the placenta.

 

See images below for the normal labor curves of both nulliparas and multiparas. The following table shows abnormal labor indicators.

 

 

 

Abnormal labor constitutes any findings that fall outside the accepted normal labor curve. However, the authors hesitate to apply the diagnosis of abnormal labor during the latent phase because it is easy to confuse prodromal contractions for latent labor. In addition, the original labor curve, as defined by Friedman, may not be completely applicable today.

 

Contemporary practice with supporting data suggest that the duration of labor appears longer today than in the past. For both nulliparous and multiparous women, labor may take longer than 6 hours to progress from 4 cm to 5 cm and longer than 3 hours to progress from 5 cm to 6 cm of dilation. Cervical dilation of 6 cm appears to be a better landmark for the start of the active phase. The 95th percentile for duration of the second stage in a nulliparous woman with conduction anesthesia is closer to 4 hours

 

 

Average labor curves by parity in singleton term pregnancies with spontaneous onset of labor. Average labor curves by parity in singleton term pregnancies with spontaneous onset of labor.

 

 

First stage of labor

Definitions for prolonged latent phase are outlined in the Table above. Diagnosis of abnormal labor during the latent phase is uncommon and likely an incorrect diagnosis.

 

Around the time uterine contractions cause the cervix to become 3-4 cm dilated, the patient usually enters the active phase of the first stage of labor. Abnormalities of cervical dilation (protracted dilation and arrest of dilation) as well as descent abnormalities (protracted descent and arrest of descent) are outlined in the Table above.

 

Both American College of Obstetrics and Gynecology (ACOG) and the Consortium on Safe Labor have proposed extending the minimum period before diagnosing active-phase arrest. The Consortium on Safe Labor defines 6 hours as the 95th percentile of time to go from 4 cm to 5 cm dilation, with the active phase defined as beginning at 6 cm (instead of 4 cm.  The ACOG has also stated that extending the time from 2 to 4 hours with oxytocin augmentation appears effective. Irrespective of the duration, maternal and fetal well-being status must be confirmed.

 

The maternal risk of a first stage greater than the 95th percentile (>30 h) is associated with a higher cesarean delivery rate (adjusted odds ratio [aOR]: 2.28) and chorioamnionitis (aOR: 1.58). The neonatal risk is associated with a higher incidence of neonatal ICU admissions in the absence of any other of the major morbidities (aOR: 1.53).

 

Second stage of labor

 

The Consortium on Safe Labor also addressed the 95th percentile for the second stage for nulliparous women; it was 2.8 hours (168 min) without regional anesthesia and 3.6 hours (216 min) with regional anesthesia. For multiparous women, the 95th percentiles for second-stage duration with and without regional anesthesia remained around 2 hours and 1 hour, respectively.[6, 7] However, other studies demonstrate the risks of both maternal and perinatal adverse outcomes rising with increased duration of the second stage, particularly for durations longer than 3 hours in nulliparous women and 2 hours in multiparous women.[8] Thus, careful clinical assessment of fetal and maternal well-being must be confirmed when extending the duration of the first and second stages of labor.

In general, abnormal labor is the result of problems with one of the 3 P' s.

Pelvis or passage (size, shape, and adequacy of the pelvis)

Power (uterine contractility)

A prolonged latent phase may result from oversedation or from entering labor early with a thickened or uneffaced cervix. It may be misdiagnosed in the face of frequent prodromal contractions. Protraction of active labor is more easily diagnosed and is dependent upon the 3 P' s.

 

The first P, the passenger, may produce abnormal labor because of the infant's size (eg, macrosomia) or from malpresentation.

 

The second P, the pelvis, can cause abnormal labor because its contours may be too small or narrow to allow passage of the infant. Both the passenger and pelvis cause abnormal labor by a mechanical obstruction, referred to as mechanical dystocia.

 

With the third P, the power component, the frequency of uterine contraction may be adequate, but the intensity may be inadequate. Disruption of communication between adjacent segments of the uterus may also exist, resulting from surgical scarring, fibroids, or other conduction disruption. Whatever the cause, the contraction pattern fails to result in cervical effacement and dilation. This is called functional dystocia. Uterine contractile force can be quantified by the use of an intra-uterine pressure catheter. Use of this device allows for direct measurement and calculation of uterine contractility per each contraction and is reported in Montevideo units (MVUs). For uterine contractile force to be considered adequate, the force produced must exceed 200 MVUs during a 10-minute contraction period. Arrest disorders cannot be properly diagnosed until the patient is in the active phase and had no cervical change for 2 or more hours with the contraction pattern exceeding 200 MVUs. Uterine contractions must be considered adequate to correctly diagnose arrest of dilation.

Evaluate every pregnant patient who presents with contractions in the labor and delivery unit. Any patient in labor is at risk for abnormal labor regardless of the number of previous pregnancies or the seemingly adequate dimensions of the pelvis. Plot the progress of any patient in labor, and evaluate it on a labor curve (see images below).

 

 

Physical

Upon admission to the labor and delivery unit, determine and document clinical findings.

 

Clinical pelvimetry, which is best performed at the first prenatal care visit, is important in order to assess the pelvic type (eg, android, gynecoid, platypelloid, anthropoid). Evaluate the position of the fetal head in early labor because caput and moulding complicate correct assessment as labor progresses. Establish and document an estimated fetal weight. Monitor fetal heart rate and uterine contraction patterns to assess fetal well-being and adequacy of labor. Perform a cervical examination to determine whether the patient is in the latent or active phase of labor.

Addressing these issues allows for an assessment of the current phase of labor and anticipation of whether abnormal labor from any of the 3 P' s may be encountered.

 

Causes

Prolonged latent phase

The latent phase of labor is defined as the period of time starting with the onset of regular uterine contractions and ending with the onset of the active phase (usually 3-4 cm cervical dilation).

 

A prolonged latent phase is defined as exceeding 20 hours in patients who are nulliparas or 14 hours in patients who are multiparas.

 

The most common reason for prolonged latent phase is entering labor without substantial cervical effacement.

Power

 

Power is defined as uterine contractility multiplied by the frequency of contractions.

 

Montevideo units (MVUs) refer to the strength of contractions in millimeters of mercury multiplied by the frequency per 10 minutes as measured by intrauterine pressure transducer.

 

The uterine contraction pattern should repeat every 2-3 minutes.

 

The uterine contractile force produced must exceed 200 MVUs/10 min for active labor to be considered adequate. For example, 3 contractions in 10 minutes that each reach a peak of 60 mm Hg are 60 X 3 = 180 MVUs.

 

An arrest disorder of labor cannot be diagnosed until the patient is in the active phase and the contraction pattern exceeds 200 MVUs for 2 or more hours with no cervical change. Extending the minimum period of oxytocin augmentation for active-phase arrest from 2 up to 4 hours may be considered as long as fetal reassurance is noted with fetal heart rate monitoring.

Pelvis or the size of the passageway inhibiting delivery

 

The shape of the bony pelvis (eg, anthropoid or platypelloid) can result in abnormal labor.

 

A patient who is extremely short or obese, or who has had prior severe trauma to the bony pelvis, may also be at increased risk of abnormal labor.

Size and/or presentation of the infant

 

Abnormal labor could also be secondary to the passenger, the size of the infant, and/or the presentation of the infant. In addition to problems caused by the differential in size between the fetal head and the maternal bony pelvis, the fetal presentation may include asynclitism or head extension. Asynclitism is malposition of the fetal head within the pelvis, which compromises the narrowest diameter through the pelvis. Fetal macrosomia and other anomalies (including hydrocephalus, encephalocele, fetal goiter, cystic hygroma, hydrops, or any other abnormality that increases the size of the infant) are likely to cause deviation from the normal labor curve.

Other factors

Other factors include either a low-dose epidural or combined spinal-epidural anesthetics that minimize motor block and may contribute to a prolonged second stage. These have also been associated with an increase in oxytocin use and operative vaginal delivery. However, use of epidural for analgesia during labor does not result in a statistically significant increase in cesarean delivery. Intravenous oversedation has also been implicated as prolonging labor in both the latent and active phases.

An 11-year review by Zuo et al found significant correlation of reactive, infectious, atypical, and dysplastic cytologic changes during pregnancy with abnormal placental findings; all but dysplastic cytologic changes had significant association with preterm birth. The study also found that the presence of high-risk human papillomavirus (HPV) DNA was associated with placental abnormalities and preterm birth. This suggests that cervical infection of HPV is a risk factor for preterm birth; thus, cervical cytology is an effective tool for screening women.

Differential Diagnoses

Abruptio Placentae

Amnionitis

Malpresentation

Obstruction (eg, myomas, cervical stenosis)

Uterine anomaly (eg, müllerian, bands)

Other Tests

 

The simplest test used to evaluate abnormal labor is to plot the patient's labor progress (cervical dilation vs duration in hours) on a labor curve.

A second test used to address adequate labor is the review of the uterine contraction pattern by determining adequacy of contractions with use of an intrauterine pressure catheter.

Most importantly, the fetal heart tracing must be reassuring throughout the labor course.

 

Procedures

Clinical pelvimetry, at a minimum, must address the angles of the spinous processes (convergent, divergent, straight), the bi-ischial diameter (>8 cm), the distance to the sacral promontory from the symphysis pubis (>12 cm), and the relation of the bony pelvis to the fetal head.

 

Clinical pelvimetry requires experience and deliberate attention to the question of pelvic adequacy. It cannot account for fetal size or strength/frequency of contractions, but, in experienced hands, it may reliably identify a pelvis as adequate, borderline, or contracted.

 

An estimate of the fetal weight must be documented in the hospital chart early in the labor course. If concern for macrosomia exists, this must be addressed with the patient and the labor/delivery team in order to anticipate and prepare for labor dystocia.

A prolonged latent phase (see Table in Background) is not indicative of dystocia in itself because this diagnosis cannot be made in the latent phase. Gabbe and colleagues state the following:[12]

 

For those in the latent phase, the treatment of choice is rest for several hours. During this interval, uterine activity, fetal status, and cervical effacement must be evaluated to determine if progress to the active phase has occurred. Approximately 85% of patients so treated progress to the active phase. Approximately 10% will cease to have contractions, and the diagnosis of false labor may be made. For the approximately 5% of patients in whom therapeutic rest fails and in patients for whom expeditious delivery is indicated, oxytocin infusion may be used.

 

Use of oxytocin for active management of labor is described in the Medication section.

Limited studies have shown improvement in dysfunctional labor with use of a beta-blocker. In cases of dysfunctional labor resulting from functional dystocia or an abnormal uterine contractility pattern and in which oxytocin implementation has not improved the outcome, a beta-blocker may be considered. Low-dose administration of intravenous propranolol in abnormal labor augmented with oxytocin reduced the need for cesarean delivery, particularly among patients with inadequate uterine contractility.

Anecdotal reports have stated that simply repositioning the patient frequently relieves a seemingly obstructed labor. Although not studied rigorously, there appears to be little harm in this maneuver. In theory, it may unseat an asynclitic or malrotated presenting part and allow it to engage in the pelvis more effectively.

 

Induction of labor

In a large cohort of nulliparous women who delivered singleton live births at 39-42 weeks, Cheng et al observed that induction of labor was not associated with an increased risk of cesarean delivery compared with delivery at a later gestational age. Additionally, the risk of labor dystocia for women who were induced at 39 weeks (5.93%) was lower than for those expectantly managed and delivered later (6.71%; aOR, 0.88). Labor dystocia was also less likely for women who had induction at 40 weeks compared with delivery later. Additionally, no difference in risk of operative vaginal delivery, including forceps or vacuum-assisted vaginal delivery, was reported.

While these data support that induction may provide improved perinatal outcomes, without impacting labor dystocia or increasing cesarean delivery rate, the authors caution generalized implementation and recommend future large prospective, randomized, clinical trials to further assess the potential benefit in low-risk populations.

 

Surgical Care

Amniotomy is often used and has become an accepted practice once the patient has reached the active phase of labor, although it has not been shown to result in shorter labor. This practice is not recommended in the latent phase of labor because it may only serve to increase the risk of intrauterine infection or cord prolapse.

 

If one of the arrest or protraction disorders is identified and fails to respond to conservative measures, or if the fetal heart pattern is nonreassuring, expedient delivery is justified; this includes operative vaginal delivery (if appropriate) or cesarean delivery as indicated. Operative delivery with use of forceps or vacuum must be performed by an experienced provider. One should be aware of the increased associations for shoulder dystocia and neonatal injury with operative vaginal delivery in the setting of abnormal labor.

 

Diet

Most institutions have standing orders that patients in labor have nothing by mouth as a precaution should the need for an emergent cesarean delivery arise.

Some institutions permit ice chips, and others permit a clear liquid diet.

If patients have been carefully selected as low risk for labor obstruction, a regular diet may be ordered.

Pregnant women have delayed gastric emptying, and aspiration is a very serious concern in the event of an anesthetic induction.

For patients in labor, remaining active and mobile while in the latent and early active phase is best. However, once rupture of membranes has occurred or signs of fetal nonreassurance exist, then bed rest and continuous fetal monitoring is appropriate.

 

Some clinicians allow ambulation throughout labor as long as the fetal head is well applied (minimizing risk of cord prolapse) and evidence of fetal well-being exists (monitoring for 20 min/h without signs of fetal compromise).

A protocol called active management of labor can be applied to nulliparous women with singleton cephalic presentations at term. This method involves the use of high-dose oxytocin, with a starting rate of 6 mU/min and increasing by 6 mU/min every 15 min to a maximum of 40 mU/min. The goal is no more than 7 uterine contractions per 15 min. Under this protocol, cesarean delivery is performed if vaginal delivery has not occurred or is not imminent 12 hours after admission or for fetal compromise. Initially, cesarean delivery rates were quoted at 4.8%, but it has since doubled, which is attributed to widespread use of epidural anesthesia. Other studies using the active management protocol describe cesarean delivery rates similar to that of the low-dose protocol. Randomized clinical trials have shown that the high-dose oxytocin regimens result in shorter labors than low-dose regimens without adverse effects for the fetus.

 

Dinoprostone and misoprostol are prostaglandin analogs used to stimulate cervical dilation and uterine contractions; they are pharmacologic alternatives to using laminaria or placing a Foley bulb in the cervix. Using prostaglandin analogs with a scarred uterus (eg, from prior cesarean or myomectomy) for labor induction is absolutely contraindicated due to the significant risk for uterine rupture.

 

A randomized clinical trial testing the safety and efficacy of prostaglandin E2 (PgE2) as a treatment for dystocia in spontaneous labor revealed that a single 1-mg dose of PgE2 vaginal gel is more effective than placebo in resolving dystocia without increasing uterine hyperstimulation, but it may be associated with an increase in the incidence of second stage cesarean delivery

Oxytocics

Oxytocin is the only US Food and Drug Administration (FDA)–approved medication recommended for labor augmentation. Other options include dinoprostone and misoprostol.

View full drug information

Oxytocin (Pitocin)

Produces rhythmic uterine contractions and can stimulate the gravid uterus. Has vasopressive and antidiuretic effects. Can also control postpartum bleeding or hemorrhage. Has a half-life of 3-5 min, and reaches steady state in approximately 40 min.

Beta-adrenergic blocking agents

 

Another option for abnormal labor secondary to inadequate uterine contractility is a beta-blocker.

View full drug information

Propranolol (Inderal)

Nonselective beta-adrenergic receptor blocker.

Beta-adrenergic blocking agents

Class Summary

Another option for abnormal labor secondary to inadequate uterine contractility is a beta-blocker.

View full drug information

Propranolol (Inderal)

 Nonselective beta-adrenergic receptor blocker.

 

Complications

Maternal infection is a risk, especially when rupture of membranes occurs for more than 18 hours. Administer antibiotics for signs and symptoms of chorioamnionitis.

Fetal compromise can occur from the inability to tolerate labor (eg, uterine hyperstimulation) or infection, and it must be closely evaluated. Fetal heart monitoring often reveals signs of compromise with decelerations, and fetal scalp pH is an option when indicated.

Probably the most common complication of the medical induction of labor is hyperstimulation of the uterus. If unrecognized and untreated, excessive stimulation of the uterus can result in fetal compromise, cord compression, and uteroplacental insufficiency. Uterine rupture, postpartum uterine atony, and postpartum hemorrhage may occur and can be life-threatening complications requiring emergent action.

Allen et al found that increased duration of the second stage of labor—in particular, duration longer than 3 hours in nulliparous women and longer than 2 hours in multiparous women—increases the risk of both maternal and perinatal adverse outcomes. In their population-based cohort study in 121,517 women (52% nulliparous), women with a prolonged second stage were at increased risk for obstetric trauma, postpartum hemorrhage, puerperal febrile morbidity, and composite maternal morbidity, while their infants were at increased risk for low 5-minute Apgar score (see the Apgar Score calculator), birth depression, admission to the neonatal intensive care unit, and composite perinatal morbidity. Method of delivery modified the effect of duration of second stage among nulliparous women only.

Nerve injury is more common in nulliparous women and is associated with long labor, fetal macrosomia, and certain positions that women assume during labor. Peripheral nerve injuries typically manifest as weakness or numbness in the distribution of the affected nerve(s), and most authors describe an uncomplicated resolution of the neuropathy within approximately 6 months. The development of a complex regional pain syndrome has also been described.

 

Prognosis

The prognosis of subsequent pregnancies depends on the cause for abnormal labor. For example, if abnormal labor occurs from macrosomia, the next infant may not be macrosomic. However, if the abnormal labor was secondary to a contracted pelvis with a normal-sized or small infant, then the likelihood for a recurrence of abnormal labor is high.

In an attempt to determine whether increasing maternal age is more commonly associated with dystocia, a study by Treacy et al demonstrated that the incidences of oxytocin augmentation, prolonged labor, instrument delivery, and intrapartum cesarean delivery (including cesarean for dystocia) all increased significantly and progressively with increasing maternal age.[22] This study used an established active management protocol, and oxytocin augmentation proved a generally effective intervention in all age categories. These findings have implications for the analysis of intervention rates by health care providers, particularly in developed countries where the proportion of older nulliparas is increasing.

A study by Zhu et al revealed that, with increasing interpregnancy intervals, the risk for labor dystocia increases. Both functional and mechanical dystocia were more prevalent in first births than in subsequent births. In singleton births to multiparous mothers, labor dystocia was associated with the interpregnancy interval in a dose-response fashion. Compared with an interpregnancy interval of less than 2 years, the adjusted odds ratios that was associated with interpregnancy intervals of 2-3, 4-5, 6-7, 8-9, and 10+ years were 1.06, 1.15, 1.25, 1.31, and 1.50, respectively, when controlled for other reproductive risk factors. Functional dystocia was associated more strongly with interpregnancy interval than mechanical dystocia.

 

Patient Education

The patient must be aware of all risks involved with labor, including the potential for emergent cesarean delivery if the fetus appears compromised. Furthermore, she should be kept informed of her status throughout the labor course, especially if a change in management is anticipated. Counsel patients early in pregnancy that maternal weight gain correlates with fetal weight gain, and excessive gain and prepregnancy obesity are risk factors for abnormal labor.