UTERINE CONTRACTIONS ABNORMALITIES. DELIVERY AT BREECH PRESENTATIONS. MACROSOMIA IN OBSTETRICS, DELIVERY OF THE LARGE FETUS. PREGNANCY INTERRUPTING AND POSTTERM PREGNANCY. HYPERTENSIVE DISORDERS DURING PREGNANCY. PREECLAMPSIA, ECLAMPSIA.
prepared by N.Petrenko, MD, PhD
CLASSIFICATION OF ABNORMAL LABOR
BY CHERNUKHA, 1990.
1. False labor.
2. Uterine inertia (hypotonic dysfunction):
· inadequate voluntary expulsive forces .
3. Excessive uterine activity (hypertonic dysfunction).
4. Incoordinative uterine activity (hypertonic dysfunction):
· hyperactivity of lower uterine segment,
· circulative dystocia (contractile ring),
· uterine tetania.
Differentiating Contractions of True and False labor
(Braxton Hicks Contractions)
Regular intervals, gradually increasing
Irregular intervals and duration
Painless uterine contractions
Painful uterine contractions
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
Limits for abnormality
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
Impossibility to descend
< 1 cm / hour
< 2 cm / hour
< 1 cm /hour
< 2 cm / hour
Arrest of descend
> 1 hour
> 1/2 hour
< 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;
· 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
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.
Placenta of vase previa
Maternal medical problems
Abnormal/unstable fetal lie
Suspected fetal compromise
Presenting part above inlet
Prior classical uterine incision
Premature rupture of membranes
Prior uterine incision of unknown type
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.
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.
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 trong uterine and abdominal contractions, or, very rarely, from the absence of painful sensation and thus a lack of awareness of vigorous labor.
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.
PREGNANCY AND DELIVERY AT BREECH PRESENTATION. FETAL MALPRESENTATIONS .
Breech presentation is common remote from term. Most often, however, some time before the onset of labor the fetus turns spontaneously to a cephalic presentation so that breech presentation persists in only about 3 to 4 percent of singleton deliveries. For example, 3 percent of 58,334 singleton infants delivered from 1991 through 1994 at Parkland Hospital presented as breech.
As term approaches, the uterine cavity most often accommodates the fetus in a longitudinal lie with the vertex presenting. Factors other than gestational age that appear to predispose to breech presentation include uterine relaxation associated with great parity, multiple fetuses, hydramnios, oligohydramnios, hydrocephalus, anencephalus, previous breech delivery, uterine anomalies, and pelvic tumors.
Fianu and Vaclavinkova (1978) provided sonographic evidence of a much higher prevalence of placental implantation in the cornual–fundal region for breech presentations (73 percent) than for vertex presentations (5 percent). The frequency of breech presentation is also increased with placenta previa, but only a small minority of breech presentations are associated with a previa. No strong correlation has been shown between breech presentation and a contracted pelvis.
A live fetus is not required for a fetus to change presentations spontaneously. One woman admitted to Parkland Hospital at term had a fetus known to be dead, confirmed by real-time sonography. The presentation was cephalic during the first oxytocin induction. Three days later, at the time of the second attempt at labor induction, the fetus was in a breech presentation. Three days later, at the time of a third and successful induction, the fetus was again in a cephalic presentation!
In the persistent breech presentation, an increased frequency of the following complications can be anticipated:
(1) perinatal morbidity and mortality from difficult delivery;
(2) low birthweight from preterm delivery, growth restriction, or both;
(3) prolapsed cord;
(4) placenta previa;
(5) fetal, neonatal, and infant anomalies;
(6) uterine anomalies and tumors;
(7) multiple fetuses;
and (8) operative intervention, especially cesarean delivery.
The varying relations between the lower extremities and buttocks of breech presentations form the categories of frank, complete, and incomplete breech presentations. With a frank breech presentation, the lower extremities are flexed at the hips and extended at the knees, and thus the feet lie in close proximity to the head. A complete breech presentation differs in that one or both knees are flexed. With incomplete breech presentation, one or both hips are not flexed and one or both feet or knees lie below the breech, that is, a foot or knee is lowermost in the birth canal. The frank breech appears most commonly when the diagnosis is established radiologically near term.
Fig. 1 Longitudinal lie. Frank breech presentation.
Fig. 2 Longitudinal lie. Complete breech presentation.
Fig. 3 Longitudinal lie. Incomplete, or footing, breech presentation.
Typically, with the first Leopold maneuver, the hard, round, readily ballottable fetal head is found to occupy the fundus (Fig. 4). The second maneuver indicates the back to be on one side of the abdomen and the small parts on the other. On the third maneuver, if engagement has not occurred—that is, if the intertrochanteric diameter of the fetal pelvis has not passed through the pelvic inlet—the breech is movable above the pelvic inlet. After engagement, the fourth maneuver shows the firm breech to be beneath the symphysis. Fetal heart sounds are usually heard loudest slightly above the umbilicus, whereas with engagement of the fetal head the heart sounds are loudest below the umbilicus.
Fig. 4 Palpation in left sacroanterior position. A. First maneuver. B. Second maneuver. C. Third maneuver. D. Fourth maneuver.
With the frank breech presentation, both ischial tuberosities, the sacrum, and the anus are usually palpable, and after further descent, the external genitalia may be distinguished. Especially when labor is prolonged, the buttocks may become markedly swollen, rendering differentiation of face and breech very difficult; the anus may be mistaken for the mouth, and the ischial tuberosities for the malar eminences. Careful examination, however, should prevent this error, because the finger encounters muscular resistance with the anus, whereas the firmer, less yielding jaws are felt through the mouth. Furthermore, the finger, upon removal from the anus, is sometimes stained with meconium. The mouth and malar eminences form a triangular shape, while the ischial tuberosities and anus are in a straight line. The most accurate information, however, is based on the location of the sacrum and its spinous processes, which establishes the diagnosis of position and variety.
In complete breech presentations, the feet may be felt alongside the buttocks, and in footling presentations, one or both feet are inferior to the buttocks (Fig. 18). In footling presentations, the foot can readily be identified as right or left on the basis of the relation to the great toe. When the breech has descended farther into the pelvic cavity, the genitalia may be felt.
Fig. 5. Double-footling breech presentation in labor with membranes intact. Note possibility of umbilical cord accident at any instant, especially after rupture of membranes.
X-RAY, COMPUTED TOMOGRAPHY, AND ULTRASONIC EXAMINATIONS.
Sonography should ideally be used to confirm a clinically suspected breech presentation and to identify, if possible, any fetal anomalies. If cesarean delivery is planned, x-rays are not indicated. If, however, vaginal delivery is considered, the type of breech presentation is of considerable importance. Radiation exposure may be reduced considerably by using computed tomographic pelvimetry (Kopelman and associates, 1986). These imaging techniques can be used to provide information regarding the type of breech presentation, presence or absence of a flexed fetal head, and pelvic measurements.
The role of x-ray pelvimetry in deciding mode of delivery for breech presentation is controversial (Morrison and co-authors, 1995). Cheng and Hannah (1993) comprehensively surveyed the literature on breech delivery at term and reviewed 15 studies in which x-ray pelvimetry was used and 2 studies in which CT pelvimetry was used as one of the criteria for allowing vaginal delivery. They concluded that interpretation of the role of x-ray pelvimetry was complicated because pelvic dimensions for allowing labor varied among studies. Most authors, however, found no correlation between radiological pelvic measurements and the outcome of labor, while only one study (Ohlsén, 1975) demonstrated that the incidence of complicated labor rose with decreasing pelvic capacity.
BIOMECHANISM OF LABOR IN BREECH PRESENTATION
I moment – the internal breech rotation. The breech rotates and the fetal intertrochanteric diameter from one of oblique size of the pelvic inlet to anteteroposterior size of the pelvic outlet.
II moment – the lateral flexion of the body. The anterior hip is stemmed against the pubic arc. By lateral flexion of the fetal body the posterior hip is forced over the anterior margin of the perineum. Then anterior hip is born.
III moment – the internal shoulders rotation. After the birth of the breech, there is the slight external rotation as a result of the descends and rotations of the shoulders. The shoulders rotates on the pelvic floor and diameter biacromialis occupies anteroposterior diameter of the pelvic outlet.
IV moment – the lateral flexion the body in the thoraco-brachial part. The shoulders are born.
V moment – the internal rotation of the head. The rotation begins when the fetal head descends from the plane of greatest pelvic dimensions to the least pelvic dimensions (midpelvis). The rotation is complete when the head reaches the pelvic floor, the sagittal suture is in the anteroposterior diameter of the pelvic outlet and the small fontanel is under the symphysis.
VI moment – the flexion of the fetal head. The head fixes with its fossa suboccipitalis to the inferior margin of symphysis pubis and flexes. The face, forehead, vertex, and occiput are born.
THE MANUAL AIDS IN BREECH PRESENTATIONS
The manual aid by Tsovyanov I in frank breech presentations.
The aim of the manual aid: to prepare the maternal ways to the delivery of the head and shoulders and to keep the normal attitude of the fetus.
In the frank breech presentation the fetus extremities are flexed at the hips and extended at the knees and thus the feet lie in close proximity to the head. The circumference of the thorax with the crossing on it arms and legs is larger than circumference of the head and the after-coming head deliveries easily.
The technique. The aid begins after the delivery of the buttocks. The obstetrician’s hands are applied over the buttocks, the thumbs placed on the fetus sacrum and other fingers on the legs. The doctor gently supports the legs to avoid its flexion. If the normal attitude of the fetus is keeping the head deliveries easy.
The classic manual aid on the labor in complete and incomplete breech presentation.
The aim of the classic manual aid: to help of the shoulders and the head delivery.
The classic manual aid begins when the lower angular of the anterior scapula became visible. There are 4 moments of the classic manual aid.
I moment – the delivery of the posterior arm. The posterior shoulder must be delivered first. The feet are grasped in one hand and drawn upward over the groin of the mother toward which the ventral surface of the fetus is directed; in this manner, leverage is exerted upon the posterior shoulder, which slides out over the perineal margin, usually followed by the arm and hand.
II and III moment – the external trunk rotation and the freeing the posterior arm. The aim of this moment is the reverse of the anterior shoulder to the sacrum and the delivery of second arm. The obstetrician applies his hand on the lateral sides of the fetus trunk and rotates it. The direction of the movement must be in this way: the occiput must go under the symphysis pubis. When the posterior shoulder and arm appears at the vulva the doctor put two fingers into the vagina, the fingers passed along the humorous until the elbow is reached. The fingers are now used to splint the arm, which is swept downward and delivered through the vulva.
IV moment – the freeing of the head. After the shoulder are born, the head usually occupies an oblique diameter of the pelvic with the occiput directed anteriorly. The fetal head may then be extracted by the method of Mauriceau-Levret. Employing the Mauriceau-Levre maneuver to help flex the head, the doctor’s middle finger of one hand are applied into the fetal mouth, while the fetal body rests upon the palm of the hand and fore arm, which is straddled the fetal legs. Two fingers of the operator’s other hand are then hooked over the fetal neck and grasping the shoulders, downward traction is applied until the suboccipital region appears under the symphysis. The body of the fetus is then elevated toward the mother abdomen, and the mouth, nose, brow and the occiput emerge over the perineum. Gentle traction should be exerted by the fingers over the shoulders.
The manual aid by Tsovyanov II in footling presentations.
The aim of the manual aid: To perform the footling presentation to the incomplete breech and to prepare the maternal ways to the delivery of the head and shoulders.
The doctor covers the area of the vulva with the sterile napkin and puts up resistance to the delivery of the feet. The feet are flexing and the footling presentation becomes incomplete breech presentation. Than the delivery manage as in incomplete breech presentation.
To try the minimize infant mortality and morbidity, cesarean section is now commonly used.
The indications to the cesarean section:
1. Breech presentation and a large fetus (the weight of the fetus estimated 3700 g and more).
2. Breech presentation and any degree of contraction or unfavorable shape of the pelvis.
3. Breech presentation and deflexed head.
4. Breech presentation and uterine dysfunction.
5. Breech presentation and previous perinatal death of children suffering from birth trauma.
6. Breech presentation and fetal hypoxia.
Prognosis. Both mother and fetus are at greater risk with breech presentation compared with cephalic presentation, but to nowhere near the same degree. In an analysis of 57,819 pregnancies in the Netherlands, Schutte and colleagues (1985) reported that even after correction for gestational age, congenital defects, and birthweight, perinatal mortality was higher in breech than in cephalic infants. They concluded that it may be possible that breech presentation is not coincidental but is a consequence of poor fetal quality. If this were true, then medical intervention may be unlikely to reduce perinatal mortality associated with breech presentation. This possibility had been suggested earlier by Hytten (1982) and by Susuki and Yamamuro (1985). This concept was strengthened by the report of Nelson and Ellenberg (1986), who observed that one third of children with cerebral palsy who were in a breech presentation at birth had major noncerebral malformations.
Because of the greater frequency of operative delivery, including cesarean delivery, there is a higher maternal morbidity and slightly higher mortality for pregnancies complicated by persistent breech presentation (Collea and co-authors, 1980). This risk is likely increased even more if an emergency operation is performed instead of an elective cesarean delivery (Bingham and Lilford, 1987). Labor is usually not prolonged; Hall and Kohl (1956) reported the median duration of labor to be 9.2 hours for nulliparas and 6.1 hours for multiparas.
The prognosis for the fetus in a cephalic presentation is considerably worse than when in a vertex presentation. The major contributors to perinatal loss are preterm delivery, congenital anomalies, and birth trauma. Brenner and associates (1974) provided a careful analysis of the characteristics and perils to the fetus from breech presentation. They determined the overall mortality rate for 1016 breech deliveries to be 25 percent compared with 2.6 percent for nonbreech deliveries at the University Hospitals of Cleveland. At every stage of gestation, they identified antepartum, intrapartum, and neonatal deaths to be significantly greater among breeches, and the average Apgar scores to be lower for those who survived. During the latter half of pregnancy, the birthweight at any gestational age was somewhat less for breech infants. Congenital abnormalities were identified in 6.3 percent of breech deliveries compared with 2.4 percent of nonbreech deliveries.
Tank and associates (1971) examined the character of serious traumatic vaginal delivery. At autopsy, the organs most frequently found to be injured were, in order of frequency, the brain, spinal cord, liver, adrenal glands, and spleen. It is of interest that, in retrospective analysis of cases of “idiopathic” adrenal calcification, breech delivery was very common. Other injuries from vaginal delivery included the brachial plexus; the pharynx, in the form of tears or pseudodiverticula from the obstetrician’s finger in the mouth as part of the Mauriceau maneuver; and the bladder, which might be ruptured if distended. Traction might injure the sternocleidomastoid muscle and, if not appropriately treated, lead to torticollis.
PROBLEMS WITH VAGINAL DELIVERY
Delivery of the breech draws the umbilicus and attached cord into the pelvis, which compresses the cord. Therefore, once the breech has passed beyond the vaginal introitus, the abdomen, thorax, arms, and head must be delivered promptly. This involves delivery of successively less readily compressible parts. With a term fetus, some degree of head molding may be essential for it to negotiate the birth canal successfully. In this unfortunate circumstance, the alternatives with vaginal delivery are both unsatisfactory: (1) delivery may be delayed many minutes while the aftercoming head accommodates to the maternal pelvis, but hypoxia and acidemia become severe; or (2) delivery may be forced, causing trauma from compression, traction, or both.
With a preterm fetus, the disparity between the size of the head and buttocks is even greater than with a larger fetus. At times, the buttocks and lower extremities of the preterm fetus will pass through the cervix and be delivered, and yet the cervix will not be dilated adequately for the head to escape without trauma (Bodmer and associates, 1986). In this circumstance, Dührssen incisions of the cervix may be attempted. Even so, trauma to the fetus and mother may be appreciable, and fetal hypoxia may prove harmful. Another mechanical problem with breech delivery is entrapment of the fetal arm behind the neck. A nuchal arm complicates up to 6 percent of vaginal breech deliveries and is associated with increased neonatal mortality (Cheng and Hannah, 1993).
The frequency of cord prolapse is increased when the fetus is small or when the breech is not frank. In the report by Collea and colleagues (1978), the incidence with frank breech presentation was about 0.5 percent, which is similar to the incidence (0.4 percent) reported for cephalic presentations (Barrett, 1991). In contrast, the incidence of cord prolapse with footling presentation was 15 percent, and it was 5 percent with complete breech presentation.
Soernes and Bakke (1986) confirmed earlier observations that the umbilical cord length is significantly shorter in breech compared with cephalic presentations. Moreover, multiple coils of cord entangling the fetus are more common in breech presentations (Spellacy and associates, 1966). These umbilical cord abnormalities likely play a role in the development of breech presentation as well as the relatively high incidence of a non-reassuring fetal heart rate pattern in labor. For example, Flanagan and co-workers (1987) selected 244 women with a variety of breech presentations (72 percent were frank breech) for a trial of labor, and there was a cord prolapse in 4 percent. Fetal distress not due to cord prolapse was diagnosed in another 5 percent of women selected for vaginal delivery. Overall, 10 percent of the women identified for vaginal birth underwent cesarean deliveries for fetal jeopardy in labor.
Apgar scores, especially at 1 minute, of vaginally delivered breech infants are generally lower than when elective cesarean delivery is performed (Flanagan and co-workers, 1987). Similarly, neonatal cord blood acid–base values are significantly different for vaginally delivered breech infants. Christian and Brady (1991) reported that umbilical artery blood pH was lower, PCO2 higher, and HCO3 lower compared with cephalic deliveries. Socol and colleagues (1988), however, concluded that cesarean delivery improved Apgar scores but not acid–base status. Flanagan and co-workers (1987) emphasized that ultimate infant outcome for breech birth was not worsened by these significant differences in Apgar scores or acid–base status at birth.
Unfavorable Pelvis. Because there is no time for molding of the aftercoming head, a moderately contracted pelvis that had not previously caused problems in delivery of an average-size cephalic fetus might prove dangerous with a breech. Rovinsky and colleagues (1973) urged not only accurate measurements of the pelvic dimensions but also precise evaluation of the pelvic architecture rather than reliance on pelvic indexes. Gynecoid (round) and anthropoid (elliptical) pelves are favorable configurations, but platypelloid (anteroposteriorly flat) and android (heart-shaped) pelves are not.
Fig. 6. Hyperextension of Fetal Head
In perhaps 5 percent of term breech presentations, the fetal head may be in extreme hyperextension (Fig. 19). In these, vaginal delivery may result in injury to the cervical spinal cord. In general, marked hyperextension after labor has begun is considered an indication for cesarean delivery (Svenningsen and associates, 1985).
Induction of labor in women with a breech presentation is defended by some and condemned by others. Brenner and associates (1974) found no significant differences in mortality rates and Apgar scores between cases with induced and those with spontaneous labor. In oxytocin-augmented labor, however, infant mortality rates were higher, and Apgar scores were lower. Gimovsky and Paul (1982) observed that augmentation of labor was followed by vaginal delivery in only 2 of 9 women, both multiparous. Moreover, one of the two deliveries resulted in entrapment of the aftercoming fetal head. The general policy at Parkland Hospital is to resort to cesarean delivery, rather than use oxytocin to induce or augment labor, unless the fetus is previable or has a severe anomaly.
The possibility of compression of a prolapsed cord or a cord entangled around the extremities as the breech fills the pelvis, if not before, is a threat to the fetus.
With a preterm fetus, the aftercoming head may be trapped by a cervix that is sufficiently effaced and dilated to allow passage of the thorax but not the less compressible head. The consequences of vaginal delivery in this circumstance all too often have been both hypoxia and physical trauma, both of which are especially deleterious to the preterm infant. Thus, delivery of the apparently healthy but very small fetus by cesarean is generally recommended.
Cheng and Hannah (1993) conducted a systemic search of the world literature regarding term breech delivery and found 82 reports published in English between 1966 and 1992. A total of 24 studies were selected for analysis because these compared planned vaginal delivery with planned cesarean section for the term, singleton breech fetus. The effects of planned vaginal delivery on perinatal mortality, corrected for lethal congenital anomalies and antepartum fetal death. The corrected perinatal mortality rate ranged from 0 to 48 per 1000 births and was higher among infants in the planned vaginal delivery groups.
All but two deaths were in the groups of women allowed to labor and deliver vaginally. The main causes of death were head entrapment, cerebral injury and hemorrhage, cord prolapse, and severe asphyxia. Cheng and Hannah (1993) observed that the overall neonatal mortality and morbidity resulting from trauma were increased significantly in the planned vaginal delivery groups, with a typical odds ratio of 3.86. They suggested that until a well-designed randomized trial with sufficient statistical power is performed, planned cesarean delivery should be strongly considered for persistent breech presentation at term. Similarly, Gifford and co-workers (1995) performed a meta-analysis of outcomes after term breech delivery and observed that, given many methodological limitations of published studies, their analysis suggested an increased risk of injury or death after a trial of labor.
Only 2 of the 24 reports reviewed by Cheng and Hannah (1993) and Gifford and co-workers (1995) were randomized trials, and both were from the same institution. Collea and colleagues (1980) reported the results of 200 women with frank breech fetuses at term. Almost half of these women were excluded from further consideration because of possible fetopelvic disproportion based on x-ray pelvimetry. A total of 60 infants were eventually delivered vaginally, and all survived, although two sustained brachial plexus injuries. There were no perinatal deaths, but half of the 148 women who had cesarean deliveries experienced significant morbidity compared with only 7 percent of 60 women who were delivered vaginally. Gimovsky and colleagues (1983) later evaluated 105 nonfrank breech fetuses and reported similar findings. Although these two trials concluded that vaginal breech delivery was relatively safe, only 110 fetuses were actually allowed a trial of labor after careful selection. As emphasized by Eller and Van Dorsten (1995), this small number would not provide sufficient statistical power to demonstrate differences in uncommon adverse outcomes such as perinatal death and birth injury.
There are no randomized studies regarding delivery of the preterm breech fetus. Penn and colleagues (1996) attempted such a study in 26 hospitals in England and discontinued the trial after 17 months because only 13 patients could be recruited. Retrospective studies have yielded conflicting results. Bowes and colleagues (1979) and Main and co-workers (1983) found that infants born by cesarean section had a better prognosis. Others concluded that vaginal delivery did not significantly increase perinatal mortality (Olshan and co-workers, 1984; Rosen and Chik, 1984; Westgren and co-workers, 1985a, c). The National Institute of Child Health and Human Development Neonatal Research Network (Malloy and co-workers, 1991) collected data on 437 very-low-birthweight breech infants admitted to seven neonatal intensive care centers. After adjusting for several variables, the risk of intraventricular hemorrhage and neonatal death was not significantly affected by the mode of delivery for breech fetuses weighing less than 1500 g. A similar analysis was reported from the Netherlands (Gravenhorst and co-workers, 1993). Perinatal follow-up data were collected on 899 live-born singleton, nonanomalous infants with gestational age less than 32 weeks and birthweight less than 1500 g. Statistical analysis failed to conclusively resolve whether cesarean delivery was advantageous.
Eller and Van Dorsten (1995) recently surveyed the centers in the Maternal–Fetal Medicine Units Network to determine the feasibility of resolving the controversy regarding route of delivery by a randomized clinical trial. Virtually all participating obstetricians in the Network agreed that clear scientific evidence was needed to determine if mode of delivery of the breech affects outcome. Performing the needed investigation was judged to be not feasible, however, because the number of skilled operators with the ability to safely deliver breech fetuses continues to dwindle and medicolegal concerns make it difficult to train residents to perform such deliveries. Indeed, at least two other groups of investigators, who have attempted trials of breech delivery, concluded that such studies were likely impossible (Penn and Steer, 1990; Zlatnik, 1993).
What then is “standard of care” for delivery of term and preterm singleton breech presentations in the United States? Despite the inadequacy of scientific evidence as discussed, most breech presentations are delivered by cesarean section. Green and colleagues (1982) estimated that about 90 percent of breech presentations of all gestational ages undergo cesarean delivery. There are centers in the United States, however, in which perhaps half of breech presentations are safely delivered vaginally. For example, 44 percent of breeches weighing 1500 g or more and 60 percent of those less than 1500 g are safely delivered vaginally at the Chicago Lying-in Hospital (Brown and co-authors, 1994; Cibils and colleagues, 1994). At Parkland Hospital, the route of delivery is individualized to clinical circumstances by the attending faculty physician. Women with selected frank breech presentations of about 2000 g or more but less than about 3500 g are frequently offered planned vaginal delivery. Nonetheless, 85 percent of all singleton breech presentations in 1995 were delivered by cesarean section. We are of the view that individualized cesarean or vaginal delivery are both reasonable and acceptable in current obstetrical practice.
Media file 1: Footling breech presentation. Once the feet have delivered, one may be tempted to pull on the feet. However, a singleton gestation should not be pulled by the feet because this action may precipitate head entrapment in an incompletely dilated cervix or may precipitate nuchal arms. As long as the fetal heart rate is stable and no physical evidence of a prolapsed cord is evident, management may be expectant while awaiting full cervical dilation.
Media file 2: Assisted vaginal breech delivery. Thick meconium passage is common as the breech is squeezed through the birth canal. This is usually not associated with meconium aspiration because the meconium passes out of the vagina and does not mix with the amniotic fluid.
Media file 3: Assisted vaginal breech delivery. The Ritgen maneuver is applied to take pressure off the perineum during vaginal delivery. Episiotomies are often performed for assisted vaginal breech deliveries, even in multiparous women, to prevent soft tissue dystocia.
Media file 4: Assisted vaginal breech delivery. No downward or outward traction is applied to the fetus until the umbilicus has been reached.
Media file 5: Assisted vaginal breech delivery. With a towel wrapped around the fetal hips, gentle downward and outward traction is applied in conjunction with maternal expulsive efforts until the scapula is reached. An assistant should be applying gentle fundal pressure to keep the fetal head flexed.
Media file 6: Assisted vaginal breech delivery. After the scapula is reached, the fetus should be rotated 90° in order to deliver the anterior arm.
Media file 7: Assisted vaginal breech delivery. The anterior arm is followed to the elbow, and the arm is swept out of the vagina.
Media file 8: Assisted vaginal breech delivery. The fetus is rotated 180°, and the contralateral arm is delivered in a similar manner as the first. The infant is then rotated 90° to the backup position in preparation for delivery of the head.
Media file 9: Assisted vaginal breech delivery. The fetal head is maintained in a flexed position by using the Mauriceau maneuver, which is performed by placing the index and middle fingers over the maxillary prominence on either side of the nose. The fetal body is supported in a neutral position, with care to not overextend the neck.
Media file 10: Piper forceps application. Piper forceps are specialized forceps used only for the after-coming head of a breech presentation. They are used to keep the fetal head flexed during extraction of the head. An assistant is needed to hold the infant while the operator gets on one knee to apply the forceps from below.
Media file 11: Assisted vaginal breech delivery. Low 1-minute Apgar scores are not uncommon after a vaginal breech delivery. A pediatrician should be present for the delivery in the event that neonatal resuscitation is needed.
Media file 12: Assisted vaginal breech delivery. The neonate after birth.
Media file 13: Ultrasound demonstrating a fetus in breech presentation with a hyperextended head (ie, "star gazing").
EXTERNAL CEPHALIC VERSION
Whenever a breech presentation is recognized during the third trimester, an attempt may be made to substitute a cephalic presentation by external version. This procedure, well known to our obstetrical predecessors, has received renewed interest in the past two decades coincidental with the availability of ultrasound, electronic fetal monitoring, and effective tocolytic agents. It is likely that these developments have improved the maternal and fetal safety of external version compared with prior obstetrical eras.
Van Dorsten and co-workers (1981) rekindled interest in this procedure in the United States. They used ultrasound, fetal monitoring, and a b-agonist for uterine relaxation in 25 pregnancies randomized to receive external version between 37 and 39 weeks and compared outcomes with 23 similar pregnancies managed without version. Almost 70 percent of versions were successful, resulting in a 30 percent cesarean delivery rate compared with 75 percent when version was not attempted. It is estimated that an active program of breech version could reduce the expected 3 to 4 percent breech presentation rate at delivery by about half (Laros and colleagues, 1995).
Fig. 7 Hypothetical results of a trial of external cephalic version for breech presentation derived from 1339 published patients. (From Zhang J, Bowes WA, Fortney JA. Efficacy of external cephalic version: A review. Obstet Gynecol. 82:306, 1993. Modified with permission from the American College of Obstetricians and Gynecologists.
Zhang and co-authors (1993) reviewed 25 selected reports on external cephalic version published between 1980 and 1991. Shown in Figure 20, and based on data derived from their review, are hypothetical results if all women with otherwise normal pregnancies and with singleton breech presentations had attempted external cephalic version at 35 to 37 weeks. Several points are noteworthy: (1) external cephalic version is successful in 65 percent of cases; (2) if version succeeds, almost all fetuses stay in the cephalic presentation, and vice-versa; and (3) ultimately, and despite version attempts, 37 percent of women identified to have late pregnancy breech presentations will require cesarean delivery. Zhang and co-workers (1993) estimated that universal application of external cephalic version could reduce the overall cesarean rate by no more than 2 percent.
Prepare for the possibility of cesarean delivery. Obtain a type as well as an anesthesia consult. The patient should have nothing by mouth for at least 8 hours prior to the procedure. Perform an ultrasound to confirm breech, check growth and amniotic fluid volume, and rule out anomalies associated with breech.
Perform a nonstress test (biophysical profile as backup) prior to ECV to confirm fetal well-being.
Perform ECV in or near a delivery suite in the unlikely event of fetal compromise during or following the procedure, which may require emergent delivery.
ECV can be performed with 1 or 2 operators. An assistant may help turn the fetus, elevate the breech out of the pelvis, or monitor the ultrasound position of the baby.
ECV is accomplished by judicious manipulation of the fetal head toward the pelvis while the breech is brought up toward the fundus. Attempt a forward roll first and then a backward roll if the initial attempts are unsuccessful. No consensus has been reached regarding how many ECV attempts are appropriate at one time.
Following an ECV attempt, whether successful or not, repeat the nonstress test (biophysical profile if needed) prior to discharge. Also, administer Rh immune globulin to women who are Rh-negative. Some physicians induce labor following successful ECV. However, as virtually all of these recently converted fetuses are unengaged, many practitioners will discharge the patient and wait for spontaneous labor to ensue, thereby avoiding the risk of a failed induction of labor.
In those with an unsuccessful ECV, the practitioner has the option of sending the patient home or proceeding with a cesarean delivery. Expectant management allows for the possibility of spontaneous version. Alternatively, cesarean delivery may be performed at the time of the failed ECV, especially if regional anesthesia is used (see Regional anesthesia). This would minimize the risk of a second regional analgesia. However, be aware of the small risk for iatrogenic respiratory distress syndrome, especially when delivery is prior to 37 weeks' gestation.
Success rates vary widely but range from 35-86% (average, 58%). Improved success rates occur with multiparity, with earlier gestational age, with frank breech presentation, with a transverse lie, and in African American patients. Opinions differ regarding the influence of maternal weight, placental position, and amniotic fluid volume, but these factors may also influence success rates. Be prepared for an unsuccessful ECV; version failure is not necessarily a reflection of the skill of the practitioner.
Zhang reviewed 25 studies of ECV in the United States, Europe, Africa, and Israel. The average success rate in the United States was 65%. Of successful ECVs, 2.5% reverted to breech presentation (other estimates range from 3-5%, while 2% of unsuccessful ECVs had spontaneous version to cephalic presentation (other estimates range from 12-26%) prior to labor. Spontaneous version rates depend on the gestational age when the breech is discovered, with earlier breeches more likely to have spontaneous version.
The performance of an ECV decreases the cesarean delivery rate for breech by approximately 50%. Because breech presentations complicate only 3-5% of all deliveries, decreasing the cesarean delivery rate for breeches by 50% will have only a marginal impact on the overall cesarean delivery rate.
Hofmeyr and Kulier reviewed 5 randomized clinical trials of ECV versus no ECV at term. ECV was associated with a significant reduction in noncephalic births (relative risk [RR], 0.38; 95% confidence interval [CI], 0.18-0.8) and a reduction in cesarean delivery for breech (RR, 0.55; 95% CI, 0.33-0.91).
While most studies of ECV have been performed in university hospitals, Cook showed that ECV has also been effective in the private practice setting. Of 65 patients with term breeches, 60 were offered ECV. ECV was successful in 32 (53%) of the 60 patients, with vaginal delivery in 23 (72%) of the 32 patients. Of the remaining breech fetuses believed to be candidates for vaginal delivery, 8 (80%) had successful vaginal delivery. The overall vaginal delivery rate was 48% (31 of 65 patients), with no significant morbidity.
In 1995, Gifford et al performed a cost analysis of 4 options for breech presentations at term: (1) ECV attempt on all breeches, with attempted vaginal breech delivery for selected persistent breeches; (2) ECV on all breeches, with cesarean delivery for persistent breeches; (3) trial of labor for selected breeches, with scheduled cesarean delivery for all others; and (4) scheduled cesarean delivery for all breeches prior to labor.
ECV attempt on all breeches with attempted vaginal breech delivery on selected persistent breeches was associated with the lowest cesarean delivery rate and was the most cost-effective approach. The second most cost-effective approach was ECV attempt on all breeches, with cesarean delivery for persistent breeches.
Uncommon risks of ECV include fractured fetal bones, precipitation of labor or premature rupture of membranes, abruptio placentae, fetomaternal hemorrhage (0-5%), and cord entanglement ( <1.5%). A more common risk of ECV is transient slowing of the fetal heart rate (in as many as 40% of cases). This risk is believed to be a vagal response to head compression with ECV. It usually resolves within a few minutes after cessation of the ECV attempt and is not usually associated with adverse sequelae for the fetus.
Women with breech presentation, reassuring fetal heart rate tracings, and no contraindications to vaginal delivery at 36 weeks' gestation and beyond are usually candidates for ECV (see Contraindications below).
ECV is usually not performed on preterm breeches because they are more likely to undergo spontaneous version to cephalic presentation and are more likely to revert to breech after successful ECV (approximately 50%). Studies of preterm ECV did not show a difference in the rates of breech presentations at term or overall rates of cesarean delivery. Additionally, if complications of ECV were to arise that warranted emergent delivery, it would result in a preterm neonate with its inherent risks.
Absolute contraindications for ECV include multiple gestations with a breech presenting fetus, contraindications to vaginal delivery (eg, herpes simplex virus infection, placenta previa), and nonreassuring fetal heart rate tracing.
Relative contraindications include polyhydramnios or oligohydramnios, fetal growth restriction, uterine malformation, and fetal anomaly.
Women with prior uterine incisions may be candidates for ECV, but data are scant. In 1991, Flamm et al attempted ECV on 56 women with one or more prior low transverse cesarean deliveries. The success rate of ECV was 82%, with successful vaginal births in 65% of patients with successful ECVs. No uterine ruptures occurred during attempted ECV or subsequent labor, and no significant fetal complications occurred.
Another controversial area is performing ECV on a woman in active labor. In 1985, Ferguson and Dyson reported on 15 women in labor with term breeches and intact membranes. Four patients were dilated greater than 5 cm (2 women were dilated 8 cm). Ritodrine was used for acute tocolysis, and intrapartum ECV was attempted. ECV was successful in 11 of 15 patients, with successful vaginal births in 10 patients. No adverse effects were noted. Further studies are needed to evaluate the safety and efficacy of intrapartum ECV.
Data regarding the benefit of intravenous or subcutaneous beta-mimetics in improving ECV rates are conflicting.
In 1996, Marquette et al performed a prospective, randomized, double-blinded study on 283 subjects with breech presentations between 36 and 41 weeks' gestation. Subjects received either intravenous ritodrine or a placebo. The success rate of ECV was 52% in the ritodrine group versus 42% in the placebo group (P = .35). When only nulliparous subjects were analyzed, significant differences were observed in the success of ECV (43% vs 25%, P <.03). ECV success rates were significantly higher in parous versus nulliparous subjects (61% vs 34%, P <.0001), with no additional improvement with ritodrine.
In 2004, Hofmeyr reviewed 6 trials of tocolysis prior to ECV and concluded that routine tocolysis resulted in fewer failures of ECV (RR, 0.74; 95% CI, 0.64-0.87). Sublingual nitroglycerine was not found to be useful.
Whether tocolysis should be used routinely or selectively is still unclear.
Regional analgesia, either epidural or spinal, may be used to facilitate ECV success. When analgesia levels similar to that for cesarean delivery are given, it allows relaxation of the anterior abdominal wall, making palpation and manipulation of the fetal head easier. Epidural or spinal analgesia also eliminates maternal pain that may cause bearing down and tensing of the abdominal muscles. If ECV is successful, patients can be induced with the epidural in place or the epidural can be removed and the patient sent home to await spontaneous labor. If ECV is unsuccessful, a patient can proceed to cesarean delivery under her current anesthesia.
The main disadvantage is the inherent risk of regional analgesia, which is considered small. Additionally, lack of maternal pain could potentially result in excessive force being applied to the fetus without the knowledge of the operator.
In 1994, Carlan et al retrospectively analyzed 61 women who were at more than 36 weeks' gestation and had ECV with or without epidural. The success rate of ECV was 59% in the epidural group and 24% in the nonepidural group (P <.05). In 7 of 8 women with unsuccessful ECV without epidural, a repeat ECV attempt after epidural was successful. Of the epidural group, 86% had obstetrical intervention (induction or cesarean delivery) immediately after the ECV. No effects on maternal or perinatal morbidity or mortality occurred.
In 1997, Schorr et al randomized 69 subjects who were at least 37 weeks' gestation to either epidural or control groups prior to attempted ECV. Those in whom ECV failed underwent cesarean delivery. The success rate of ECV was 69% in the epidural group and 32% in the control group (RR, 2.12; 95% CI, 1.24-3.62). The cesarean delivery rate was 79% in the control group and 34% in the epidural group (P = .001). No complications of epidural anesthesia and no adverse fetal effects occurred.
In 1999, Dugoff et al randomized 102 breech subjects who were at more than 36 weeks' gestation with breech presentations to either spinal anesthesia or a control group. All subjects received 0.25 mg terbutaline subcutaneously. The success rate of ECV was 44% in the spinal group and 42% in the nonspinal group, which was not statistically significant.
It would hence appear that epidural analgesia, though not spinal, is associated with a higher success rate of ECV. Further studies are needed to confirm these initial findings.
Johnson and Elliott performed a randomized, blinded crossover trial on 23 subjects to compare acoustic stimulation prior to ECV with a control group when the fetal spine was in the midline (directly back up or back down). Of those who received acoustic stimulation, 12 of 12 fetuses shifted to a spine-lateral position after acoustic stimulation, and 11 (91%) underwent successful ECV. In the control group, 0 of 11 shifts and 1 (9%) successful ECV (P <.0001) occurred. After crossover to the alternate modality, all 10 fetuses in the control group in whom ECV initially failed shifted to a spine-lateral position following acoustic stimulation and 8 of these had successful ECV, compared with 0 of 1 ECV successes in the acoustic stimulation group that crossed over to the control group.
VAGINAL DELIVERY RATES AFTER SUCCESSFUL VERSION
The rate of cesarean delivery ranges from 0-31% after successful ECV.
In 1994, a retrospective study by Egge et al of 76 successful ECVs matched with cephalic controls by delivery date, parity, and gestational age failed to note any significant difference in the cesarean delivery rate (8% in ECV group, 6% in control group).
In 1997, Lau et al compared 154 successful ECVs to 308 spontaneously occurring cephalic controls (matched for age, parity, and type of labor onset) with regard to the cesarean delivery rate. Cesarean delivery rates were higher after ECV (16.9% vs 7.5%, P <.005) because of higher rates of cephalopelvic disproportion and nonreassuring fetal heart rate tracings. This may be related to an increased frequency of compound presentations after ECV.
Immediate induction of labor after successful ECV may also contribute to an increase in the cesarean delivery rate due to failed induction in women with unripe cervices and unengaged fetal heads.
Vaginal breech delivery requires an experienced obstetrician and careful counseling for the parent(s). Although studies on the delivery of the preterm breech are limited, the recent multicenter term breech trial found an increased rate of perinatal mortality and serious immediate perinatal morbidity.
Parents must be informed about potential risks and benefits to the mother and neonate for both vaginal breech delivery and cesarean delivery. The likelihood is high that the trend will continue toward 100% cesarean delivery for term breeches and that vaginal breech deliveries will no longer be performed.
ECV is a safe alternative to vaginal breech delivery or cesarean delivery, reducing the cesarean delivery rate for breech by 50%. The ACOG, in its 2000 Practice Bulletin, recommends offering ECV to all women with a breech fetus near term. Consider adjuncts such as tocolysis, regional anesthesia, and acoustic stimulation to improve ECV success rates. Before performing a delivery or ECV on a mother whose fetus is in a breech presentation, assess for any underlying fetal abnormalities or uterine conditions that may result in a malpresentation
FACTORS ASSOCIATED WITH SUCCESSFUL VERSION
The most consistent factor associated with the success of external cephalic version is parity (Zhang and colleagues, 1993). Gestational age is also important; the earlier external version is performed, the more likely it will be successful. Conversely, the more remote from term external version is performed, the higher the rate of spontaneous reversion (Westgren and colleagues, 1985b). Other reported, albeit controversial, determinants of unsuccessful version include diminished amnionic fluid volume, excessive maternal weight, anterior placental location, cervical dilatation, descent of the breech into the pelvis, and anterior or posterior positioning of the fetal spine (Newman and colleagues, 1993, Zhang and co-authors, 1993). Remarkably, Johnson and Elliott (1995) used fetal acoustic stimulation to startle breech fetuses to shift their spines laterally for successful external version! Fernandez and co-workers (1996) randomized 103 women with term antepartum singleton breech presentations to receive terbutaline 250 mg subcutaneously or placebo. Use of terbutaline significantly enhanced the success of external cephalic version from 27 to 52 percent. Marquette and colleagues (1996) reported similar results using ritodrine infusions.
Women with a transverse lie are usually excluded from analyses of breech version because the overall success rate approaches 90 percent (Newman and colleagues, 1993).
External cephalic version is typically carried out in a labor and delivery unit (Newman and colleagues, 1993), although Kornman and colleagues (1995) have performed selected versions in an office setting. Real-time ultrasonic examination is performed to confirm nonvertex presentation, the adequacy of amnionic fluid volume (vertical pocket of 2 cm or greater), fetal measurements consistent with term gestation, and estimated fetal weight; to rule out obvious fetal anomalies; and to identify placental location. A nonstress test is performed to assess fetal heart rate reactivity. Terbutaline sulfate, 250 mg, is given subcutaneously and version attempted 20 minutes later. “Forward roll” of the fetus is usually attempted first and the “back flip” technique is then tried if unsuccessful. Version attempts are discontinued for excessive discomfort, persistently abnormal fetal heart rate, or after multiple failed attempts. D-immune globulin is given to D-negative, unsensitized women. The nonstress test is repeated after the version until a normal test result is obtained. This process takes about half a day and may cost as much as $1700 (Newman and colleagues, 1993).
According to Zhang and colleagues (1993), there have been no reported fetal deaths in the United States resulting directly from external version since 1980. Reported nonfatal complications include fetal heart rate decelerations in almost 40 percent of fetuses (Phelan and co-workers, 1984) and fetomaternal hemorrhage in 4 percent (Stine and colleagues, 1985). Petrikovsky and colleagues (1987) reported a case of fetal brachial plexus injury after a successful external version. Stine and co-workers (1985) reported a maternal death due to amnionic fluid embolus.
Fig. 8 Longitudinal lie. Cephalic presentation. Differences in attitude of fetal body in (A) vertex, (B) sinciput, (C) brow, and (D) face presentations. Note changes in fetal attitude in relation to fetal vertex as the fetal head becomes less flexed.
The deflexed vertex presentation. The deflexed vertex presentation is a I degree of head extension.
Diagnosis. The diagnosis of the deflexed vertex presentation bases on the results of the vaginal palpation: the sagittal suture, the large and the small fontanels on the same level. The fetal head presents with a fronto-occipital diameter, a leader point is the large fontanel.
The cardinal movements of labor in deflexed vertex presentation are:
· internal rotation;
· internal rotation of the fetal body and external rotation of the fetal head.
1. Deflexion. The sagittal suture is in the transverse or oblique size of the pelvic inlet. The head fixes to the inlet and some deflexed. The large fontanel becomes the leader point.
2. Internal rotation. This movement is a manner that the occiput gradually moves from its original position posteriorly towards the sacrum os. The rotation is complete when the head reaches the pelvic floor; the sagittal suture is in the anteroposterior diameter.
3. Flexion of the head. Flexion begins when the head fixes by its root of the nose (the first fixing point) to the inferior margin of symphysis pubis. The flexion finishes when the occiput comes to the tip of sacrum and the second fixing point forms.
4. Extension of the head. After internal rotation and flexion the fetal head closely touched with the area of the occiput to the tip of the sacrum. The head extends and deliveries.
5. Internal rotation of the fetal trunk and external rotation of the fetal head. This moment realizes as in anterior occiput presentation.
The brow presentation is a II degree of extension.
With the brow presentation, that portion of the fetal head between the orbital ridge and the frontal suture presents at the pelvic inlet. The fetal head thus occupies a position midway between full flexion (occiput) and full extension (mentum or face). Except when the fetal head is very small or the pelvis is unusually large, engagement of the fetal head and subsequent delivery cannot take place as long as the brow presentation persists.
Diagnosis. The diagnosis of the brow presentation bases on the results of the external obstetrics examination and vaginal palpation. The brow presentation may be recognized by abdominal palpation when both the occiput and chin can be easily palpated. The reliable information can be felt by the vaginal examination: the frontal suture, the large fontanel, orbital ridges, eyes, and root of the nose. The nose and mouth can not be palpable.
The fetal head presents with a mento-occipital diameter, a leader point is the middle of the frontal suture.
Fig.9 Brow posterior presentation.
The delivery at term in brow presentation is impossible. The preterm delivery, when the fetus is small is possible and the characteristically deforms of the head occurred. The caput succedaneum is over the fore head and may be so extensive that identification of the brow by palpation is impossible.
If the labor is possible the cardinal movements in brow presentation are:
1. Deflexion. The frontal suture is in the transverse size of the pelvic inlet. The head fixes to the inlet and deflexed. The middle of the frontal suture becomes the leading point.
2. Internal rotation.
3. Flexion of the head.
4. Extension of the head.
5. Internal rotation of the fetal trunk and external rotation of the fetal head.
In the face presentation, the head is hyperextended so that the occiput is in contact with the fetal back and the chin (mentum) is presenting part.
Diagnosis. By abdominal palpation the occiput, the chin and the angle between the fetal back and the occiput can be easily palpated. The fetal heart sound are the loudest from the side of the fetal thorax. On vaginal palpation, the distinctive features of the face presentation are the mouth, nose, the malar bones, and the orbital ridges.
Face presentation is rarely observed above the pelvic inlet. The brow generally presents and is converted to a face presentation after further extension of the head during descent through the pelvis.
The cardinal movements of labor in face posterior presentation are:
1. Deflexion. The face linea is in the transverse size of the pelvic inlet. Descent is brought about by the same factors as vertex presentation. The head presented its vertical diameter. The chin is the leading point.
2. Internal rotation. The object of internal rotation of the face is to bring the chin under the symphysis. Only in this way the neck subtend the posterior surface of the symphysis pubis. If the chin rotates directly posteriorly, the birth of the head is impossible.
3. Extension of the head. After the rotation and descent, the chin and mouth appear at the vulva, the undersurface of the chin presses against the symphysis, and the head is delivered by flexion. The nose, eyes, brow and occiput then appeared in succession over the anterior margin of the perineum.
4. Internal rotation of the fetal trunk and external rotation of the fetal head. The shoulders are born as in vertex presentations.
Fig. 10 Biomechanism of labor in face posterior presentation
Macrosomia is a term used rather imprecisely to describe a very large fetus/newborn. There is general agreement among obstetricians that newborns weighing less than 4000 g are not excessively large; but a similar consensus has not been reached that permits a precise definition of macrosomia. In the contemporary literature, newborn weights greater than 4000, 4100, or 4500 g (10 pounds) have been suggested as appropriate to define macrosomia (Boyd and colleagues 1983; Modenlau and colleagues 1980; Neiger, 1992). There is no doubt that fetuses who are born weighing 4500 to 5000 g are at less risk of a poor perinatal outcome than those who weigh more than 5000 g (Spellacy and co-workers, 1985). But even within a group of large fetuses of a rather restricted weight range, neonatal outcome with macrosomia can be affected by the presence or absence of compounding variables (e.g., maternal diabetes). Among macrosomic fetuses of diabetic women, for example, there is a greater shoulder circumference and a greater shoulder circumference-to-head circumference ratio, and consequently, a greater risk of shoulder dystocia, compared with fetuses of similar body weight of nondiabetic women (Modenlau and colleagues, 1982; Neiger, 1992; Sachs, 1993). Among macrosomic fetuses of similar body weight, the presence of a relatively greater proportion of body fat tissue is associated independently with an increased risk of labor dystocia and, in consequence, cesarean delivery (Bernstein and Catalano, 1994). For these reasons, and in the absence of a commonly agreed-upon definition of macrosomia, a generally accepted obstetrical management plan optimal for this pregnancy complication has not evolved.
Based on ultrasonic measurements of the fetus, some relatively complex computations have been proposed to identify macrosomia: the ponderal index, 100 times the body weight of the infant divided by the cube of its length; or the symmetry index, the ratio between newborn length and weight, each divided by the length and weight of the population’s 50th percentile (Keller and associates, 1990; Sachs, 1993; Walther and Ramaekers, 1982). The American College of Obstetricians and Gynecologists (1991) concluded that the term “macrosomia” was an appropriate designation for fetuses who, at birth, weigh 4500 g or more.
Maternal diabetes, obesity, or both are the most important of known risk factors for development of fetal macrosomia. There are several other factors, however, that also favor the likelihood of a large fetus: (1) large size of the parents, especially the mother; (2) multiparity; (3) prolonged gestation; (4) male fetus; (5) previous delivery of an infant weighing more than 4000 g; (6) smoking status of the mother; and (7) race and ethnicity (Benito and co-workers, 1996; Chervenak, 1992; Johnson and co-workers, 1992; Perlow and associates, 1992; Sachs, 1993). When the pregnant woman weighs more than 300 pounds, her fetus is at greater risk of macrosomia (30 percent) or, conversely, growth retardation (8 percent). Among women who are simultaneously diabetic, obese, and postterm, the incidence of fetal macrosomia can range from 5 to 15 percent (Arias, 1987; Chervenak, 1992). Known maternal risk factors, however, are identified in only 40 percent of women who deliver macrosomic fetuses (Boyd and associates, 1983).
INCIDENCE OF MACROSOMIA
There are wide variations in mean birthweights of various peoples of the world, to wit: 2400 g among the Lumi of New Guinea, but 3830 g among the native American Cheyenne Indians (Meredith, 1970; Sachs, 1993). In the Obstetrical Statistical Cooperative study of more than 104,000 deliveries, 5.3 percent of the newborns weighed more than 4000 g, but only 0.4 percent weighed more than 4500 g. Among the more than 15,000 deliveries at Parkland Hospital in 1991, 7.7 percent of the newborns weighed 4000 g or more but only approximately 1 percent weighed more than 4500 g (Ramin and Cunningham, 1995). These data are noteworthy because this obstetrical population is comprised of predominantly young women who often are socioeconomically deprived and present with a relatively low prevalence of diabetes. Moreover, the incidence of excessively large babies in each of the birthweight groups cited in this population has increased during the past two decades.
The excessively large newborn is still a curiosity. Newborn weight rarely exceeds 11 pounds (5000 g). Indeed, the birth of a 16-pound (7300 g) infant in the United States in 1979 was widely publicized; delayed maternal glucose metabolism was identified, and this woman previously had delivered several infants weighing 9 to 10 pounds. Two of the largest newborn weights ever recorded were that of a nearly 24-pound (10,800 g) infant, as described by Beach in 1879 (Barnes, 1957), and a 25-pound stillborn cited in Chapter 5. There were only 23 newborns who weighed 5000 g or more (1.5 per 1000 births) delivered in Parkland Hospital in 1991. Among approximately 74,000 infants who were delivered at this institution between 1987 and 1991, only two weighed 6000 g or more, an incidence of 2.7 per 100,000 deliveries. The larger of these two infants, 6065 g (13 lb 51¤2 oz), was delivered by cesarean section (Fig. 37–1 ); but the other, 6050 g, was delivered per vagina without complications.
Presently, an accurate estimate of excessive fetal size (weight) is not possible; consequently, the diagnosis of macrosomia most commonly is not made until after the fetus is delivered. Inaccuracy in clinical estimates of fetal weight by physical examination is often attributable, at least in part, to maternal obesity.
Numerous attempts have been made to improve the accuracy of fetal weight estimations by analyses of various measurements obtained by ultrasonography. A number of formulas have been proposed for analyses using ultrasonic measurements of fetal head, femur, and abdomen to estimate fetal weight. The estimates provided by these computations are reasonably accurate for predicting the weight of small, preterm fetuses; but using this approach, estimates of fetal weight with very large fetuses are not as reliable. The relationship between actual and predicted newborn weight, using the most commonly applied formulas proposed by Shepard and co-workers (1982) and Watson and Seeds (1991), are presented in Table 37–1. Among fetuses estimated to weigh more than 4000 g or more than 4500 g, the probability that the actual birthweight would correspond with that predicted was only 50 percent. In another study of more than 300 fetuses who, at birth weighed in excess of 4000 g, Benacerraf and co-workers (1988) found a sensitivity of predictability of only 65 percent. These investigators were able to exclude 90 percent of fetuses as not having macrosomia, but because 90 percent of term newborns weigh less than 4000 g, this prediction is not particularly useful. Pollack and colleagues (1992), in a study confined to postterm pregnancies, used a formula (with ultrasonic measurements) proposed by Hadlock and associates (1984) to estimate fetal weight. The measurements applied to this formula were the abdominal circumference and the femur length. They found that only half of fetuses with macrosomia—greater than 4000 g—were correctly identified, and that only 65 percent of the fetuses that were predicted to be macrosomic actually weighed more than 4000 g at birth. These investigators deduced that to achieve 70 percent confidence that the actual birthweight would be greater than 4000 g, the estimated fetal weight must be greater than 4750 g. Similar findings and conclusions were presented by Chervenak and associates (1989) and Combs and co-workers (1993). In a comparison of the accuracy of fetal weight estimates made from computations with three different formulas (using sonographic measurements), Miller and colleagues (1987) found that the positive predictive value of macrosomia by these several estimates was 60 percent or less. O’Reilly-Green (1996) studied 202 consecutive postterm pregnancies and found a positive predictive value of 79 percent for 4000 g but only 33 percent for 4500 g.
Other sonographic measurements for use in estimating the weight of the fetus who may have macrosomia have been proposed: chest circumference, femur length/abdominal circumference ratio, soft-tissue thickness of the proximal humerus or femur, thickness of fetal abdominal fat line, and cheek-to-cheek diameter (Abramowicz, 1993; Miller, 1987; Mintz, 1989; Petrikovsky, 1996; Santolaya-Forgas, 1994, and their colleagues).
Unfortunately, a formula that gives estimates of fetal macrosomia with sufficiently accurate predictive value to be useful in constructing clinical management decisions has not been derived or evaluated (American College of Obstetricians and Gynecologists, 1991). In a comprehensive review of estimates of fetal weight from ultrasonic measurements to identify macrosomia, Sandmire (1993) argued that the use of such data in clinical decision making may cause more harm than good. He suggested that a moratorium be placed on the reporting and clinical use of sonographic data in estimates of excess fetal weight. Indeed, Adashek and colleagues (1996) found that women who had ultrasonography in the last 4 weeks of pregnancy were at significantly increased risk for cesarean delivery if estimated fetal size exceeded 4000 g, regardless of actual newborn weight.
We conclude that the estimation of fetal weight from ultrasonic measurements is not proven to be reliable. Nonetheless, sonographic measurements to evaluate excess fetal weight to assist in clinical management decisions may be warranted in rare circumstances. Routine use of these estimates to identify macrosomia are not recommended; indeed, the findings of several studies are indictive that estimates of fetal weight by physician-conducted physical examination of the pregnant woman are as reliable as, or even superior to, those made from ultrasonic fetal measurements (Chauhan and colleagues, 1992, 1993; Hanretty and co-workers, 1990; Sandmire, 1993; Watson and associates, 1988). Chauhan and associates (1992) suggested that the parous woman in labor at term can herself predict fetal weight with a degree of accuracy comparable to that predicted by physician examination or by ultrasonographic measurements!
COMPLICATIONS OF MACROSOMIA
The accurate estimation of fetal weight in pregnancies in which a macrosomic fetus is suspected could prove useful for two reasons.
Fetopelvic Disproportion with Macrosomia. Knowledge of fetal weight might permit the avoidance of vaginal delivery of pregnancies in which labor most likely would be arrested because of true fetopelvic disproportion. Unfortunately, however, even with a very accurate prediction of fetal weight, variations in size and shape of the maternal pelvis, variable effects of soft tissue on the course of labor, or flexibility of the joints of the pelvic girdle would not be taken into account. The diagnosis of cephalopelvic disproportion often cannot be established by any criteria other than the outcome of an adequate trial of labor (American College of Obstetricians and Gynecologists, 1989). Labor itself, however, is unlikely to cause harm to the macrosomic fetus or the mother in a carefully managed pregnancy that ultimately must be delivered by cesarean section because of arrest of labor.
SHOULDER DYSTOCIA WITH MACROSOMIA
. Fetal shoulder dystocia, and the attendant risk of permanent brachial plexus palsy, in pregnancies with a macrosomic fetus is cause for considerable concern. Shoulder dystocia occurs when the maternal pelvis is of sufficient size to permit delivery of the fetal head, but not large enough to allow delivery of the very large-diameter fetal shoulders. In this circumstance, the anterior shoulder becomes impacted against the maternal symphysis pubis (Chap. 42 ); and even with expert obstetrical assistance at delivery, stretching and injury of the brachial plexus of the affected shoulder may be inevitable. It must be recognized, however, that the risk of brachial plexus injury is increased substantially when inappropriate force is applied during attempts to complete vaginal delivery (Allen and co-workers, 1994). Only 30 percent of all brachial plexus injuries caused by shoulder dystocia are sustained by infants who weigh more than 4000 g (Walle and Hartkainen-Sorri, 1993). Nevertheless, the relative risk of this complication is appreciably greater with macrosomic fetuses; and it is very likely that some of these injuries could be avoided if cesarean delivery were elected.
On the one hand, therefore, the prospective identification of fetuses at risk for macrosomia and shoulder dystocia is a desirable goal. But on the other hand, the success of management plans that include cesarean delivery for macrosomia (based upon estimates of fetal size) is highly dependent on the precision of the estimations of fetal weight to predict brachial plexus injury. Otherwise, the greater maternal morbidity that accrues with operative deliveries is not justified. As emphasized by Sandmire (1993), clavicular fracture and cephalohematoma do not cause long-term disabilities; consequently, strict avoidance of these complications may not be sufficiently warranted to justify the obliged increase in cesarean deliveries. Fortunately, 95 percent of brachial plexus palsies are transient (Gordon and associates, 1973); but unfortunately, a significant proportion of brachial plexus impairments occur in non-macrosomic infants, or else are not caused directly by shoulder dystocia.
Some obstetricians have suggested that cesarean delivery should be elected when the fetus is estimated to weigh in excess of 4000 or 4250 g in pregnancies of diabetic women, or 4500 g in pregnancies of nondiabetic women. Data in support of this proposal (i.e., a documented reduction in the incidence of permanent brachial plexus palsy or other birth injury resulting from the implementation of this management plan), however, has not been provided (Acker and associates, 1985; Langer and colleagues, 1991; Sandmire, 1993; Spellacy and co-workers, 1985). Even assuming that the weight of macrosomic fetuses could be estimated accurately, obligatory cesarean delivery based on specific, but arbitrarily chosen, fetal weight thresholds would result in many unnecessary operations. Consider the following: at Parkland Hospital in 1991, 1162 infants weighing 4000 g or more were delivered; of these, 847 (73 percent) were uncomplicated vaginal births (Ramin and Cunningham, 1995). Brachial plexus injuries, of varying severity, occurred in 4 of 737 infants weighing 4000 to 4500 g, and in 4 of 118 weighing more than 4500 g. Stated differently, 99.5 percent of fetuses weighing 4000 to 4500 g were delivered per vagina without injury, as were 96.6 percent of fetuses weighing more than 4500 g.
In the absence of clearly established benefits, which were documented in well-designed clinical trials, a recommendation of cesarean delivery based solely upon estimated fetal weight is not justified. Several of the recognized risk factors for macrosomia also constitute substantial increased risk factors for maternal operative morbidity and mortality. Consequently, maternal risks that accompany cesarean delivery must be considered critically in the development of management plans for the pregnancy with a suspected macrosomic fetus. For example, in the case of a 300-pound woman with poorly controlled diabetes and a fetus estimated to weigh in excess of 4000 g, cesarean delivery might reduce fetal risk. The risks for the woman described that accompany cesarean delivery may be sufficiently great, however, as to mitigate against the overall benefit to mother and child of this management approach. In several studies, there was an increased cesarean delivery rate but no improvement in neonatal outcome or reduction in birth injury among pregnancies in which labor was electively induced because of fetal macrosomia (Boyd and associates, 1983; Combs and colleagues, 1993; Delpapa and Mueller-Heubach, 1991).
Management of Shoulder Dystocia
Management of Shoulder Dystocia. The occurrence of fetal shoulder dystocia cannot be accurately predicted; therefore, the obstetrician must be expert in the management of this potentially devastating complication of childbirth. Reduction in the time interval from delivery of the head to delivery of the body is important to neonatal survival. An initial attempt to deliver the anterion shoulder with gentle traction, assisted by maternal expulsive efforts, is recommended by the American College of Obstetricians and Gynecologists (1991). Excessive traction on the fetal head or neck, or excessive rotation of the fetal body during delivery, however, may cause serious damage to the infant. A number of maneuvers have been described that can be used to relieve shoulder dystocia and effect delivery
Pregnancy interrupting. Postterm pregnancy. Uterine contractions abnormalities.
PRETERM AND POSTTERM LABOR
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.
A wide spectrum of causes and demographic factors has been implicated in the birth of preterm infants.
· chronic tonsillitis
· urinary tract infection
· TORCH – infection
· viral infection
· chronic inflammatory diseases of the female sexual organs (vaginatis, bacterial vaginosis)
· 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.
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. 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.
· adrenal impairment – hyperandrogeny
· thyroid gland impairment - hypothoroidism
· placental abruption, placental previa
· pregnancy induced hypertension
· multiple pregnancy
· 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
· short stature
· occupational factors
· psychological stress in the mother.
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.
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).
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
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.
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.
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.
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.
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
Profound muscular paralysisa
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.
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.
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.
“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.
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.
ETIOLOGY, CLINICS, DIAGNOSIS AND TREATMENT OF PREGNANCY INDUCED HYPERTENSION
The term pregnancy-induced hypertension (PIH) has not been discarded, because the development of hypertension, especially in nulliparas, cannot be differentiated from transient hypertension except retrospectively. Therefore, the development of hypertension in a previously normotensive pregnant woman should and must be considered potentially dangerous to both her and her fetus. Thus, clinical situations should be designated pregnancy-induced hypertension and considered precursors to preeclampsia and eclampsia until after safe management of pregnancy. At this time, it may then be appropriate to reclassify the hypertension as transient.
1. primigravid status, new paternity;
2. family history of preeclampsia or eclampsia;
3. previous preeclampsia or eclampsia;
4. extremes of maternal age (younger than 20 y or older than 35 years of age);
5. preexisting hypertensive vascular, autoimmune, or renal disease;
6. preexisting renal, pulmonary, thyroid dysfunction;
7. Diabetes mellitus;
8. Multiple gestation;
9. Nonimmune or alloimmune fetal hydrops;
10. Hydatidiform Mole.
1. Generalized vasospasm.
4. Disseminated intravascular coagulopathy.
5. Metabolic impairment as result of hypoxia.
6.Organ dysfunction – renal, hepatic, cardiac and pulmonary, hematological, cerebral problems.
7. Placental dysfunction because the vasospastic changes.
Theories about the Cause of Pregnancy-induced Hypertension
Any satisfactory theory must account for the observation that pregnancy-induced or -aggravated hypertension is very much more likely to develop in the woman who (1) is exposed to chorionic villi for the first time; (2) is exposed to a superabundance of chorionic villi, as with twins or hydatidiform mole; (3) has preexisting vascular disease; or (4) is genetically predisposed to hypertension developing during pregnancy. Although chorionic villi are essential, they need not support a fetus or be located within the uterus.
The risk of pregnancy-induced hypertension is appreciably enhanced in circumstances where formation of blocking antibodies to antigenic sites on the placenta might be impaired. This may arise during immunosuppressive therapy to protect a renal transplant; where effective immunization by a previous pregnancy is lacking, as in first pregnancies; or where the number of antigenic sites provided by the placenta is unusually great compared with the amount of antibody, as with multiple fetuses (Beer, 1978). Strickland and associates (1986), however, provided data that do not support “immunization” by a previous pregnancy. They analyzed the outcomes of over 29,000 pregnancies at Parkland Hospital and reported that pregnancy-induced hypertension was decreased only slightly (22 versus 25 percent) in women who previously had aborted and were now having their first baby. The immunization concept is supported, however, by the observation that preeclampsia develops more frequently in multiparous women impregnated by a new consort (Feeney and Scott, 1980; Robillard and colleagues, 1994). Also, Dekker (1996) provided evidence that oral sex before pregnancy provided protection against preeclampsia. He hypothesized that “tolerization” to paternal antigens was operative.
Cooper and associates (1988) and Jagadeesan (1988) found no association of complement fractions C3, C3F, and CH50 with preeclampsia, and Hofmeyr and colleagues (1991) reported C4 concentrations to be reduced only in hypertensive pregnant women with proteinuria. Simon and co-workers (1988) reported no association of histocompatibility antigens HLA-A and -B with preeclampsia. They did report a higher incidence of recurrent hypertension in pregnancy in women with HLA-DR4 phenotypes, an observation consistent with an increased incidence of chronic hypertension and not preeclampsia. As cited previously, Hoff and associates (1992) found a maternal–fetal HLA-DR relationship with pregnancy-induced hypertension. Haeger and associates (1992) reported that complement, neutrophils, and macrophages are activated in women with severe preeclampsia. Despite such appealing theories, convincing proof of clinical significance is lacking.
Cooper and Liston (1979) examined the possibility that susceptibility to preeclampsia is dependent upon a single recessive gene. They calculated the expected first-pregnancy frequencies of daughters of women with eclampsia; daughters-in-law served as controls. The frequencies calculated by them and those actually observed by Chesley and co-workers (1968) in daughters and daughters-in-law of women with eclampsia are remarkably close. Subsequently, Chesley and Cooper (1986) concluded that the single-gene hypothesis fits well, but multifactorial inheritance cannot be excluded. Ward and associates (1993) reported that women carrying the angiotensinogen gene variant T235 had a higher incidence of pregnancy-induced hypertension. Morgan and colleagues (1995), however, could not confirm these findings. Although Arngrimsson and co-workers (1994) found no association between the renin gene and preeclampsia, Dizon-Townsend and colleagues (1996) found a higher incidence of factor V Leiden mutations in preeclamptic women.
Various dietary deficiencies have been suspected as a cause of preeclampsia; however, these hypotheses lack supportive data. For example, because pregnancy “depletes” a woman nutritionally, preeclampsia should be more common in multiparous women compared with nulliparas; but it is not. Moreover, various types of dietary supplementation do not decrease the frequency of hypertension. Finally, the incidence of hypertension is higher in obese women, and the incidence increases with prepregnancy weight (Sibai and co-workers, 1995a). Zlatnik and Burmeister (1983) provided convincing evidence that the incidence of preeclampsia is not related to the level of dietary protein.
Calcium deficiency has been implicated by some, and calcium supplementation appears to reduce the risk of preeclampsia (Carroli and colleagues, 1994). Belizán (1991), López-Jaramillo (1989), Sanchez-Ramos (1994b), and their associates reported that after midpregnancy, daily dietary supplementation with 2 g of elemental calcium significantly reduced the incidence of hyper-tension. Conversely, Sanchez-Ramos and co-workers (1995) found that severe preeclampsia was not prevented in women with mild preeclampsia who were treated with the 2-g dose. Certainly, decreased urinary excretion of calcium has been documented in preeclamptic and future hypertensive women (August and associates, 1992; Sanchez-Ramos and colleagues, 1991). What remains to be established is whether there is decreased dietary intake, altered calcium absorption, or intrinsic renal tubular dysfunction. Tolaymat and colleagues (1994) have provided evidence that calcium absorption is not impaired in preeclampsia. The apparent effectiveness of supplemental calcium may be explained by an overriding of impaired absorption or defective renal handling of calcium. Other possibilities exist, however, including changes in vasodilation and vascular reactivity mediated by increased prostacyclin or nitric oxide production (Gant and Gilstrap, 1990; López-Jaramillo and colleagues, 1990; St-Louis and Sicotte, 1992).
A wide variety of cellular and serum vasoactive factors likely play a role in the etiology or pathogenesis of pregnancy-induced hypertension. Endothelins are potent vasoconstrictors, and endothelin-1 is the only species produced by human endothelium (Mastrogiannis and co-workers, 1991). Plasma endothelin-1 is increased in normotensive laboring and nonlaboring women, and even higher levels have been reported in preeclamptic women (Clark, 1992; Mastrogiannis, 1991; Nova, 1991; Schiff, 1992; and their associates). Otani and colleagues (1991), however, did not observe increased plasma endothelin levels, and Barton and associates (1993) did not find increased urinary endothelin-1 levels in preeclamptic women.
Nitric oxide, previously termed endothelium-derived relaxing factor (EDRF), is synthesized by endothelial cells from L-arginine (Palmer and associates, 1988). It is a potent vasodilator whose absence or decreased concentration might play a role in the etiology of pregnancy-induced hypertension. Inhibition of nitric oxide has been shown to increase mean arterial pressure, decrease heart rate, and reverse the pregnancy-induced refractoriness to vasopressors in some animals. Equally important, it appears to maintain the normal low-pressure vasodilated state characteristic of fetoplacental perfusion in the sheep, guinea pig, and human (Chang and colleagues, 1992; Myatt and co-workers, 1992; Weiner and associates, 1992). Kupferminc and collaborators (1996) found no differences in circulating nitrite and nitrate levels in women with severe preeclampsia compared with normal controls. Morris and colleagues (1996) recently provided a scholarly review of these interactions.
Wang and colleagues (1991a,b) reported that normotensive pregnancies are characterized by progressive increases in the ratios of prostacyclin to thromboxane and vitamin E to lipid peroxides. They concluded that the vasodilating actions of prostacyclin and the antioxidant activity of vitamin E were favored progressively with advancing gestation. With increasing severity of preeclampsia, both ratios were progressively reversed. Thus, increased thromboxane resulted in increased vasospasm and platelet destruction, and increased lipid peroxides increased endothelial damage. Davidge and associates (1992), using a different assay, found similar findings in antioxidant activity in preeclamptic women.
Cigarette smoking has been reported to reduce the incidence of pregnancy-induced hypertension (Klonoff-Cohen and co-workers, 1993; Sibai and colleagues, 1995a). Smoking may stimulate a decrease in the specific activity of platelet-activating factor-acetylhydrolase. This enzyme is known to degrade platelet-activating factor, an extremely powerful vasodilator and platelet-aggregating factor (Miyaura and associates, 1992). The decrease in PAF-acetylhydrolase would lead to an increase in plasma platelet activating factor and vasodilation, a known effect of normal pregnancy (Maki and colleagues, 1993).
Evidence has accumulated for a pathogenic model of preeclampsia whereby an immunologically mediated deficiency in the trophoblast invasion of the placental bed spiral arteries leads to a poorly perfused fetoplacental unit. This results in the secretion of a factor (or factors) into the maternal circulation, which leads to “activation” of the vascular endothelium, with the clinical syndrome resulting from widespread changes in endothelial cell function (de Groot and colleagues, 1995; Friedman and associates, 1995; Roberts and Redman, 1993; Smárason and co-workers, 1996). Intact endothelium has anticoagulant properties and blunts the response of vascular smooth muscle to agonists. Damaged endothelium activates endothelial cells to promote coagulation, and increases sensitivity to vasopressor agents. Further evidence of endothelial activation in preeclampsia includes characteristic changes in glomerular capillary endothelial morphology, increased capillary permeability, and elevated blood levels of substances associated with endothelial cell activation (see the preceding section). Serum from preeclamptic women stimulates cultured endothelial cells to produce greater amounts of prostacyclin than sera from normotensive pregnant women.
The nature of the circulating factor(s) and the mechanism by which endothelium is activated are not known. Studies by Endresen and associates (1995) indicate that preeclamptic sera are not cytotoxic to endothelial cells. Baker and colleagues (1995) have shown that vascular endothelial growth factor (VEGF) levels are elevated in serum of preeclamptic women, and postulate that this may activate endothelial cells. Similarly, platelet-derived growth factor may be operative (Gurski and colleagues, 1996; Krueger and co-workers, 1996).
Pathophysiology of Preeclampsia–Eclampsia
Vasospasm is basic to the pathophysiology of preeclampsia–eclampsia. This concept, first advanced by Volhard (1918), is based upon direct observations of small blood vessels in the nail beds, ocular fundi, and bulbar conjunctivae, and it has been surmised from histological changes seen in various affected organs (Hinselmann, 1924; Landesman and co-workers, 1954). Vascular constriction causes resistance to blood flow and accounts for the development of arterial hypertension. It is likely that vasospasm itself also exerts a damaging effect on vessels. Moreover, angiotensin II causes endothelial cells to contract. These changes likely lead to endothelial cell damage and interendothelial cell leaks through which blood constituents, including platelets and fibrinogen, are deposited subendothelially (Brunner and Gavras, 1975). The vascular changes, together with local hypoxia of the surrounding tissues, presumably lead to hemorrhage, necrosis, and other end-organ disturbances that have been observed at times with severe preeclampsia. With this scheme, fibrin deposition is then likely to be prominent, as seen in fatal cases (McKay, 1965).
Increased Pressor Responses
Normally pregnant women develop refractoriness to infused vasopressors (Abdul-Karim and Assali, 1961). Increased vascular reactivity to pressors in women with early preeclampsia has been identified by Raab and co-workers (1956) and Talledo and associates (1968) using either norepinephrine or angiotensin II, and by Dieckmann and Michel (1937) and Browne (1946) using vasopressin. Gant and co-workers (1973) demonstrated that increased vascular sensitivity to angiotensin II clearly preceded the onset of pregnancy-induced hypertension. As shown in Figure 31–1 , nulliparas who remained normotensive were refractory to the pressor effect of infused angiotensin II, while women who subsequently became hypertensive lost this refractoriness weeks before the onset of hypertension. Of women who required more than 8 ng/kg per minute of angiotensin II to provoke a standardized pressor response between 28 and 32 weeks, 90 percent remained normotensive throughout pregnancy. Conversely, among normotensive nulliparas who required less than 8 ng/kg per minute at 28 to 32 weeks, 90 percent subsequently developed overt hypertension. Similar results from 231 women were subsequently reported by Öney and Kaulhausen (1982).
Supine Pressor Response
A hypertensive response induced by having the woman assume the supine position after lying laterally recumbent was demonstrated in some pregnant women by Gant and co-workers (1974b). The majority of nulliparous women at 28 to 32 weeks who had increased diastolic pressure of at least 20 mm Hg when the maneuver was performed later developed pregnancy-induced hypertension. Conversely, most women whose blood pressure did not become elevated when this was done remained normotensive. Although not all investigators have reported equally good predictive results (Dekker and Sibai, 1991), this so-called rollover test remains an effective screening test to identify asymptomatic women who will likely develop pregnancy-induced hypertension (O’Brien, 1990). Women who demonstrated a supine pressor response were also abnormally sensitive to infused angiotensin II, while those without a hypertensive response were normally refractory. The mechanism by which this maneuver incites a rise in blood pressure is not clear, but it is likely a manifestation of increased vascular responsitivity or sympathetic overactivity in those who will later develop pregnancy-induced hypertension (Sander and colleagues, 1995).
Women with underlying chronic hypertension have similar responses. An identically performed study of angiotensin II pressor responsiveness was conducted in women whose pregnancies were complicated by chronic hypertension (Gant and colleagues, 1977). Two groups were identified on the basis of clinical outcome and serial determinations of vascular reactivity to infused angiotensin II. All women were refractory to angiotensin II between 21 and 25 weeks; however, women who subsequently developed pregnancy-aggravated hypertension began to lose this refractoriness after 27 weeks.
It appears unlikely that the normally blunted pressor response to angiotensin II is due to down-regulation or decreased affinity of angiotensin II vascular smooth-muscle receptors (MacKanjee and associates, 1991). The metabolic clearance rate of angiotensin II is not altered in women with pregnancy-induced hypertension (Magness and co-workers, 1994). Other factors may be operative; for example, aldosterone secretion is increased strikingly in pregnant women. This is modulated by the effects of angiotensin II on the zona glomerulosa of the adrenal cortex. Based on the findings of a number of studies, it was concluded that the blunted pressor response was due principally to decreased vascular responsiveness mediated in part by vascular endothelial synthesis of prostaglandins or prostaglandin-like substances (Cunningham and associates, 1975; Gant and co-workers, 1974a). For example, refractoriness to angiotensin II in pregnant women is abolished by large doses of the prostaglandin synthase inhibitors (Everett and colleagues, 1978).
The exact mechanism by which prostaglandin(s) or related substances mediate vascular reactivity during pregnancy is unknown. Goodman and colleagues (1982) reported increased concentrations of vasodilating prostaglandins during normal pregnancy. Everett and colleagues (1978) demonstrated that large doses of indomethacin and aspirin increased vascular sensitivity to infused angiotensin II. They postulated that prostaglandin(s) synthesis was suppressed, returning the vascular system to a nonpregnant sensitive state. Sanchez-Ramos and colleagues (1987) documented a diminished vascular response within 2 hours of ingestion of 40 mg of aspirin likely due to a preferential suppression of the vasoconstrictor thromboxane.
Walsh (1985) showed that, compared with normal pregnancy, placental production of prostacyclin is decreased significantly and thromboxane A2 significantly increased in preeclampsia. Walsh (1988) reported that progesterone production is increased in vitro in placentas of preeclamptic pregnancies, and hypothesized that increased progesterone concentrations may inhibit prostacyclin production. Spitz and colleagues (1988) reported that 81 mg of aspirin given daily to future hypertensive women restored angiotensin II refractoriness by suppressing synthesis of thromboxane A2 by about 75 percent; however, prostacyclin synthesis was decreased by 20 percent and prostaglandin E2 by 30 percent. Thus, arachidonic acid, an essential fatty acid, is converted by cyclooxygenase into prostacyclin, prostaglandin E2, and thromboxane. In preeclamptic women, thromboxane is increased and prostacyclin and prostaglandin E2 are decreased, resulting in vasoconstriction and sensitivity to infused angiotensin II.
Low-dose aspirin therapy markedly decreases thromboxane production but only partially blocks prostacyclin and prostaglandin E2 production, allowing these two vasodilating prostanoids to restore refractoriness to infused angiotensin II.
Fig. Arachidonic acid (AA) may be converted into prostacyclin (PGI2), prostaglandin E2 (PGE2), and thromboxane A2 (TxA2). Low-dose aspirin therapy usually blocks thromboxane A2 production more than production of prostacyclin and prostaglandin E2.
Brown and associates (1990) reported similar findings in angiotensin II-sensitive women rendered refractory to angiotensin II by low-dose aspirin. In women remaining sensitive despite aspirin, however, all three prostaglandins were reduced significantly by low-dose aspirin. These observations indicate that vessel reactivity may be mediated through a delicate balance of production and metabolism of at least these three vasoactive prostaglandins. In this scheme, preeclampsia may follow inappropriately increased production or destruction of one prostaglandin, diminished synthesis or release of the other, or perhaps both.
The role of nitric oxide—endothelium-derived relaxing factor—or its endothelial loss is unclear. Withdrawal of nitric oxide from pregnant rats and guinea pigs results in the development of a clinical picture similar to preeclampsia (Conrad and Vernier, 1989; Weiner and associates, 1989). Nitric oxide appears to be important in the maintenance of a low fetal vascular resistance in the placental circulation (Chaudhuri and co-workers, 1991; Gude and co-workers, 1990; Myatt and associates, 1991). Decreased nitric oxide release or production has not been shown to develop prior to the onset of hypertension. Thus, the changes in nitric oxide concentrations in women with pregnancy-induced hypertension appear to be the consequence of hypertension and not the inciting event (Morris and colleagues, 1996).
At least two vasoconstrictor mechanisms may be operative in preeclamptic women in whom arachidonic acid is converted by cyclooxygenase into thromboxane A2 with an accompanying reduction of prostacyclin and prostaglandin E2 (Catella and associates, 1990; Fitzgerald and colleagues, 1990; Mitchell and Koenig, 1991; Tannirandorn and co-workers, 1991). This pathway is responsive to low-dose aspirin therapy. The second route is via the lipoxygenase pathway, which results in an increased placental production of 15-hydroxyeicosatetraenoic acid (15-HETE). This inhibits prostacyclin production, resulting in further vasoconstriction (Mitchell and Koenig, 1991). Biagi and co-workers (1990) also reported an increased lipoxygenase pathway activation in placentas from hypertensive women.
Maternal and Fetal Consequences of Preeclampsia–Eclampsia
Deterioration of function in a number of organs and systems, presumably as a consequence of vasospasm, has been identified in severe preeclampsia and eclampsia. For descriptive purposes, these effects are separated into maternal and fetal consequences; however, these aberrations often occur simultaneously. Although there are many possible maternal consequences of pregnancy-induced hypertension, for simplicity these effects are considered by analysis of cardiovascular, hematological, endocrine and metabolic, and regional blood flow changes with subsequent end-organ derangements. The major cause of fetal compromise occurs as a consequence of reduced uteroplacental perfusion.
Hemodynamic changes accompanying severe preeclampsia and eclampsia have been studied by a number of investigators. Key issues addressed include the cardiovascular status of these women before treatment, as well as volume expansion and pharmacological attempts to relieve vasospasm. Elucidation of the mechanisms that cause heart failure and pulmonary edema complicating the course of some women has also been pursued. In assessing cardiac function, four areas must be addressed:
(1) preload—end-diastolic pressure and chamber volume;
(2) afterload—intramyocardial systolic tension or resistance to ejection;
(3) contractile or inotropic state of the myocardium;
and (4) heart rate.
Variables that define cardiovascular status range from high cardiac output with low vascular resistance to low cardiac output with high vascular resistance. Similarly, left ventricular filling pressures, estimated by pulmonary capillary wedge pressure determination, range from low to pathologically high. At least three factors may explain these differences: (1) women with preeclampsia might present with a spectrum of cardiovascular findings dependent upon both severity and duration, (2) chronic underlying disease may modify the clinical presentation, or (3) therapeutic interventions may significantly alter these findings. It is likely that more than one of these is operative.
Cardiac function was hyperdynamic in all women, but filling pressures varied markedly.
Hemodynamic data obtained prior to active treatment of preeclampsia identified normal left ventricular filling pressures, high systemic vascular resistances, and hyperdynamic ventricular function. Benedetti (1980a), Hankins (1984), and their associates reported similar findings in women with severe preeclampsia or eclampsia who were being treated with magnesium sulfate, hydralazine, and intravenous crystalloid given at 75 to 100 mL/hour. Cardiac function in these women was appropriate, and the lower systemic vascular resistance was most likely due to hydralazine treatment.
Women similarly treated with magnesium sulfate and hydralazine plus aggressive intravenous therapy or volume expansion had the lowest systemic vascular resistances and highest cardiac outputs. A comparison of volume-restricted women with those hydrated aggressively shows hyperdynamic ventricular function in both groups, and two responses with respect to left ventricular stroke work index and pulmonary capillary wedge pressure . Fluid restriction resulted in wedge pressures of less than 10 mm Hg, and most were less than 5 mm Hg. Thus, hyperdynamic ventricular function was largely a result of low wedge pressures and not a result of augmented left ventricular stroke work index, which more directly measures myocardial contractility. By comparison, women given appreciably larger volumes of fluid commonly had pulmonary capillary wedge pressures that exceeded normal; however, ventricular function remained hyperdynamic because of increased cardiac output. Subsequently, Cotton and co-workers (1988) reported findings from 45 women with severe preeclampsia or eclampsia and described high systemic vascular resistance and hyperdynamic ventricular function in most. It is reasonable to conclude that aggressive fluid administration given to women with severe preeclampsia causes normal left-sided filling pressures to become substantively elevated, while increasing an already normal cardiac output to supranormal levels.
Easterling and colleagues (1990) provided evidence that preeclampsia is caused by high cardiac output. In their prospective longitudinal study of 179 nulliparas, they found that women who subsequently developed preeclampsia had elevated cardiac outputs throughout pregnancy. They challenged the concept of hypoperfusion as the hallmark of pathophysiology in preeclampsia. These intriguing results need to be corroborated.
Hemoconcentration in women with eclampsia was emphasized earlier by Dieckmann (1952). Pritchard and co-workers (1984) reported that in eclamptic women hypervolemia is usually absent . Women of average size should have a blood volume of nearly 5000 mL during the last several weeks of a normal pregnancy, compared with about 3500 mL when nonpregnant. With eclampsia, however, much or all of the anticipated 1500 mL of blood normally present late in pregnancy is absent. The virtual absence of an expanded blood volume is likely the consequence of generalized vasoconstriction made worse by increased vascular permeability. In women with preeclampsia, these differences are not as marked (Silver and Seebeck, 1996).
Dieckmann (1952) believed that clinical improvement was characterized by hemodilution, as reflected by a fall in hematocrit. An acute fall in hematocrit is more likely the consequence of blood loss at delivery in the absence of normal pregnancy hypervolemia; or occasionally it is the result of intense erythrocyte destruction, as described below.
In the absence of hemorrhage, the intravascular compartment in eclamptic women is usually not underfilled. Vasospasm has contracted the space to be filled; the reduction persists until after delivery when the vascular system typically dilates, blood volume increases, and hematocrit falls. The woman with eclampsia, therefore, is unduly sensitive to vigorous fluid therapy administered in an attempt to expand the contracted blood volume to normal pregnancy levels. She is sensitive as well to even normal blood loss at delivery.
Hematological abnormalities develop in some, but certainly not all, women who develop pregnancy-induced or -aggravated hypertension. These include thrombocytopenia, which at times may become so severe as to be life threatening; the level of some plasma clotting factors may be decreased; and erythrocytes may be so traumatized that they display bizarre shapes and undergo rapid hemolysis.
Hematological changes consistent with intravascular coagulation, and less often erythrocyte destruction, may complicate preeclampsia and especially eclampsia. Renewed interest in these changes has led to the concept by some investigators that disseminated intravascular coagulation is not only a characteristic feature of preeclampsia but also plays a dominant role in its pathogenesis.
Since the early description by Pritchard and co-workers (1954) of an eclamptic coagulopathy, we have found little evidence that it is common. Thrombocytopenia, infrequently severe, was the most common finding. Serum fibrin degradation products were elevated only occasionally. Nolan and associates (1993) found significant elevations of D-dimer fragment of fibrin degradation with preeclampsia; however, these were clinically insignificant. Unless some degree of placental abruption develops, plasma fibrinogen does not differ remarkably from levels found late in normal pregnancy. Similar results have been reported by Leduc and associates (1992). The thrombin time was somewhat prolonged in a third of the cases of eclampsia even when elevated levels of fibrin degradation products were not identified. The reason for this elevation is not known, but it has been attributed to hepatic derangements discussed subsequently. The coagulation changes just described are also identified in women with severe preeclampsia, but are certainly no more common. These observations in eclampsia are most consistent with the concept that coagulation changes are the consequence of preeclampsia–eclampsia, rather than the cause.
Maternal thrombocytopenia can be induced acutely by preeclampsia–eclampsia. After delivery, the platelet count will increase progressively to reach a normal level within a few days (Katz and associates, 1990; Romero and colleagues, 1989). The frequency and intensity of maternal thrombocytopenia vary in different studies, apparently dependent upon the intensity of the disease process, the length of delay between the onset of preeclampsia and delivery, and the frequency with which platelet counts are performed (Leduc and associates, 1992). Overt thrombocytopenia, defined by a platelet count less than 100,000/mL, is an ominous sign. It indicates severe disease and delivery is usually indicated because the platelet count most often continues to decrease.
The cause of the thrombocytopenia is not known. Platelet aggregation is increased in preeclamptic women (Torres and associates, 1996). Immunological processes or simply platelet deposition at sites of endothelial damage may be the cause (Pritchard and colleagues, 1976). Samuels and colleagues (1987) performed direct and indirect antiglobulin tests and found that platelet-bound and circulating platelet-bindable immunoglobulin were increased in preeclamptic women and their neonates. They interpreted these findings to suggest platelet surface alterations. Burrows and colleagues (1987) reported that platelets from preeclamptic women were more likely to have platelet-associated IgG, even if thrombocytopenia did not develop. Although they believed this mechanism implied an autoimmune process, IgG could also be bound to platelets damaged by any mechanism.
Kelton and colleagues (1985) showed that thrombocytopenia with preeclampsia was frequently associated with a prolonged bleeding time. This was true even with normal platelet levels. They attributed this to impaired thromboxane synthesis. Kilby and associates (1990) and Barr and colleagues (1989) found increased intracellular free calcium concentrations in platelets from preeclamptic women. Louden and colleagues (1991) interpret this and other evidence to mean that platelets from preeclamptic women are exhausted, that is, platelet aggregation and release are decreased.
The clinical significance of thrombocytopenia, in addition to the obvious impairment in coagulation, is that it reflects the severity of the pathological process. In general, the lower the platelet count, the greater are maternal and fetal morbidity and mortality (Leduc and co-workers, 1992; Verhaeghe and colleagues, 1991). The addition of elevated liver enzymes to this clinical picture is even more ominous. Weinstein (1982) referred to this combination of events as the HELLP syndrome—that is, hemolysis (H), elevated liver enzymes (EL), and low platelets (LP) (see “HELLP Syndrome” below ).
Thiagarajah and co-workers (1984) and Weinstein (1985) reported thrombocytopenia in neonates whose mothers had preeclampsia. Conversely, Pritchard and colleagues (1987), in a large clinical study, did not observe severe thrombocytopenia in the fetus or infant at or very soon after delivery. No cases of fetal or neonatal thrombocytopenia were identified, despite severe maternal thrombocytopenia. Thrombocytopenia did develop later in some of these infants after hypoxia, acidosis, and sepsis developed. Hence, maternal thrombocytopenia in hypertensive women is not a fetal indication for cesarean delivery.
Thrombocytopenia that accompanies severe preeclampsia and eclampsia may be accompanied by evidence of erythrocyte destruction characterized by hemolysis, schizocytosis, spherocytosis, reticulocytosis, hemoglobinuria, and occasionally hemoglobinemia (Pritchard and colleagues 1954, 1976). These derangements result in part from microangiopathic hemolysis, and human and animal studies are suggestive that intense vasospasm causes endothelial disruption, with platelet adherence and fibrin deposition. Cunningham and associates (1985) described erythrocyte morphological characteristics using scanning electron microscopy. Women with eclampsia, and to a lesser degree those with severe preeclampsia, demonstrated schizocytosis and echinocytosis but not spherocytosis when compared with normally pregnant women. Sanchez-Ramos and colleagues (1994a) described increased erythrocyte membrane fluidity in women with HELLP syndrome and postulated that these changes predispose to hemolysis.
Other Clotting Factors
A severe deficiency of any of the soluble coagulation factors is very uncommon in severe preeclampsia–eclampsia unless another event coexists that predisposes to consumptive coagulopathy, such as placental abruption or hepatic infarction.
Antithrombin III has been reported to be lower in women with preeclampsia compared with normally pregnant women and those with chronic hypertension (Chang and co-workers, 1992; Saleh and associates, 1987; Weiner and associates, 1985). Unfortunately, early hope that antithrombin III levels could be used to predict the future development of pregnancy-induced hypertension and separate chronic hypertensive women from those with preeclampsia has not proven to be true (Sen and colleagues, 1994). Fibronectin, a glycoprotein associated with vascular endothelial cell basement membrane, is elevated in women with preeclampsia (Brubaker, 1992; Saleh, 1988; Taylor, 1991; and their associates). Hsu and colleagues (1995) also reported that thrombomodulin was elevated with severe disease. Ballegeer and associates (1992) and Sen and co-workers (1994) reported that fibronectin and laminin were increased 4 weeks prior to hypertension. These observations are consistent with others that preeclampsia causes vascular endothelial injury with subsequent hematological aberrations. The clinical utility of serial antithrombin III or fibronectin measurements for the prediction, diagnosis, and management of preeclampsia awaits further evaluation.
Thrombin levels are elevated in normal and preeclamptic women. This is likely due to an enhanced inactivation of protein C by a1-antitrypsin, which is increased in preeclampsia but not chronic hypertension (De Boer and co-workers, 1989; Espaa and associates, 1991). This results in an increased level of activated protein C/a1-antitrypsin complex. Protein C inhibitor also appears to be decreased by kallikrein, which is increased as a consequence of activation of the intrinsic coagulation pathway.
Endocrine and Metabolic Changes
Plasma levels of renin, angiotensin II, and aldosterone are increased during normal pregnancy. Pregnancy-induced hypertension results in a decrease of these values toward the normal nonpregnant range (Weir and colleagues, 1973). With sodium retention, hypertension, or both, renin secretion by the juxtaglomerular apparatus decreases. Because renin catalyzes the conversion of angiotensinogen to angiotensin I (which is then transformed into angiotensin II by converting enzyme), angiotensin II levels decline, resulting in a decrease in aldosterone secretion. Despite this, women with preeclampsia avidly retain infused sodium (Brown and colleagues, 1988b).
Another potent mineralocorticoid, deoxycorticosterone (DOC), is increased strikingly in third-trimester plasma. Its increase is not from increased secretion by maternal adrenal glands but from conversion from plasma progesterone. Thus, it is not reduced by sodium retention or hypertension, and it may play a role in the pathogenesis or perpetuation of preeclampsia.
Antidiuretic hormone activity is normal or even low (Elias and colleagues, 1988). Plasma chorionic gonadotropin levels are elevated inconstantly; conversely, placental lactogen levels are reduced inconstantly.
Atrial natriuretic peptide is released upon atrial wall stretching from blood volume expansion. It is vasoactive and promotes sodium and water excretion likely by inhibiting aldosterone, renin activity, angiotensin II, and vasopressin. This peptide is increased in normal pregnancy. Atrial natriuretic peptide is increased substantively in women with preeclampsia. With volume expansion, there is an augmented release of the compound in preeclamptic compared with normotensive pregnant women. Increases in atrial natriuretic peptide following volume expansion result in comparable increases in cardiac output and decreases in peripheral vascular resistance in both normotensive and preeclamptic women (Nisell and associates, 1992). This observation may in part explain observations of a fall in peripheral vascular resistance following volume expansion in preeclamptic women.
Ouabain-like natriuretic factor is being studied in pregnancy because it is elevated in essential hypertension. It cross-reacts with some antidigoxin antibodies, and because of this, it also is called digoxin-like immunoreactive substance. The factor inhibits the sodium-potassium-ATPase pump, which causes increased peripheral vascular resistance. Ouabain-like natriuretic factor is increased in normal pregnancy. It is progressively more increased in women with pregnancy-induced hypertension alone, and even more increased in those with preeclampsia (Gregoire and colleagues, 1988; Kaminski and associates, 1991).
Fluid and Electrolyte Changes
Commonly, the volume of extracellular fluid in women with severe preeclampsia–eclampsia has expanded beyond the normally increased volume that characterizes pregnancy. The mechanism responsible for the pathological expansion is not clear. Edema is evident at a time when, paradoxically, aldosterone levels are reduced compared with the remarkably elevated levels of normal pregnancy. As discussed earlier, however, plasma deoxycorticosterone levels remain elevated, but they are not consistently greater than those in normotensive women. Electrolyte concentrations do not differ appreciably from those of normal pregnancy unless there has been vigorous diuretic therapy, sodium restriction, or administration of water with sufficient oxytocin to produce antidiuresis. Edema does not ensure a poor prognosis, and absence of edema does not ensure a favorable outcome.
Following an eclamptic convulsion, the bicarbonate concentration is lowered due to lactic acid acidosis and compensatory respiratory loss of carbon dioxide. The intensity of acidosis relates to the amount of lactic acid produced and its metabolic rate, as well as the rate at which carbon dioxide is exhaled.
During normal pregnancy, renal blood flow and glomerular filtration rate are increased appreciably. With development of preeclampsia, renal perfusion and glomerular filtration are reduced. Levels that are much below normal nonpregnant values are the consequence of severe disease. Plasma uric acid concentration is typically elevated, especially in women with more severe disease. The elevation exceeds the reduction in glomerular filtration rate and creatinine clearance that accompanies preeclampsia (Chesley and Williams, 1945). Despite this, plasma uric acid measurements are generally of little practical value for diagnosis, management, or prognosis.
In the majority of preeclamptic women, mild to moderately diminished glomerular filtration appears to result from a reduced plasma volume; thus, plasma creatinine seldom is below normal nonpregnant levels. In some cases of severe preeclampsia, however, renal involvement is profound, and plasma creatinine may be elevated two to three times over nonpregnant normal values. This is likely due to intrinsic renal changes caused by severe vasospasm (Pritchard and colleagues, 1984). Total renal perfusion does not appear to be reduced in preeclamptic women (Levine and associates, 1992). Lee and associates (1987) reported normal ventricular filling pressures in seven severely preeclamptic women with oliguria, and concluded that this was consistent with intrarenal vasospasm. In most, urine sodium concentration was elevated abnormally, suggesting an intrinsic renal etiology. Urine osmolality, urine–plasma creatinine ratio, and fractional excretion of sodium were also indicative that a prerenal mechanism was involved. Importantly, intensive intravenous fluid therapy was not indicated for these women with oliguria. When dopamine was infused into oliguric preeclamptic women, this renal vasodilator caused increased urine output, fractional sodium excretion, and free water clearance (Kirshon and co-workers, 1988).
Taufield and associates (1987) reported that preeclampsia is associated with diminished urinary excretion of calcium because of increased tubular reabsorption. This mechanism would explain the decreased calcium excretion in hypertensive and future hypertensive pregnant women.
After delivery, in the absence of underlying chronic renovascular disease, complete recovery of renal function usually can be anticipated. This would not be the case, of course, if renal cortical necrosis, an irreversible but rare lesion, develops (Sibai and associates, 1990c).
There should be some degree of proteinuria to establish the diagnosis of preeclampsia–eclampsia (Chesley, 1985). Because proteinuria develops late, however, some women may be delivered before it appears, and thus still have preeclampsia without proteinuria. Meyer and colleagues (1994) emphasized that 24-hour urine excretion should be measured. They found that a urinary dipstick of 1+ proteinuria or greater was predictive of at least 300 mg per 24 hours in 92 percent of cases. Conversely, trace or negative proteinuria had a negative predictive value of only 34 percent in hypertensive women. Urine dipstick values of 3+ to 4+ were positively predictive of severe preeclampsia in only 36 percent of cases.
Albuminuria is an incorrect term to describe proteinuria of preeclampsia. As with any other glomerulopathy, there is increased permeability to most large-molecular-weight proteins; thus, abnormal albumin excretion is accompanied by other proteins, such as hemoglobin, globulins, and transferrin. Normally, these large protein molecules are not filtered by the glomerulus, and their appearance in urine signifies a glomerulopathic process. Some of the smaller proteins that usually are filtered but reabsorbed are also detected in urine.
Changes identifiable by light and electron microscopy are commonly found in the kidney. Sheehan (1950) observed that the glomeruli were enlarged by about 20 percent. The capillary loops variably are dilated and contracted. The endothelial cells are swollen, and deposited within and beneath them are fibrils that have been mistaken for thickening of the basement membrane.
Most electron microscopical studies of renal biopsies are consistent with glomerular capillary endothelial swelling. These changes, accompanied by subendothelial deposits of protein material, were called glomerular capillary endotheliosis by Spargo and associates (1959). The endothelial cells are often so swollen that they block or partially block the capillary lumens. Homogeneous deposits of an electron-dense substance are found between basal lamina and endothelial cells and within the cells themselves. On the basis of immuno-fluorescent staining, Lichtig and co-workers (1975) identified deposited fibrinogen or its derivatives in 13 of 30 renal biopsy specimens from women with preeclampsia. The amount of fibrin was graded as more than a trace in only two. Kincaid-Smith (1991) found that these deposits disappear progressively in the first week postpartum. Petrucco and colleagues (1974) detected IgM, IgG, and sometimes complement in the glomeruli of preeclamptic women in proportion to disease severity.
The renal changes identified by electron microscopy have been advanced as being pathognomonic of preeclampsia. The uncertainties of clinical diagnosis are so great, however, as to preclude acceptance of such a one-to-one relation. The history of other alleged pathognomonic lesions in eclampsia engenders such skepticism. The subject was recently reviewed in detail by Gaber and colleagues (1994).
Renal tubular lesions are common in women with eclampsia, but what has been interpreted as degenerative changes may represent only an accumulation within cells of protein reabsorbed from the glomerular filtrate. The collecting tubules may appear obstructed by casts from derivatives of protein, including, at times, hemoglobin.
Acute renal failure from tubular necrosis may develop. Although this is more common in neglected cases, it is invariably induced by hypovolemic shock, usually associated with hemorrhage at delivery, for which adequate blood replacement is not given. Sibai and colleagues (1993b) reported that 7 percent of women with hemolysis, elevated liver enzymes, and thrombocytopenia—HELLP syndrome—developed acute renal failure. Moreover, half of these also had a placental abruption, and most had postpartum hemorrhages. Rarely, renal cortical necrosis develops when the major portion of the cortex of both kidneys undergoes necrosis. Both cause acute renal failure characterized clinically by oliguria or anuria and rapidly developing azotemia. Renal cortical necrosis is irreversible, and although it develops in nonpregnant women and in men, the lesion has most often been associated with pregnancy.
With severe preeclampsia, at times there are alterations in tests of hepatic function and integrity, including delayed excretion of bromosulfophthalein and elevation of serum aspartate aminotransferase levels (Combes and Adams, 1972). Severe hyperbilirubinemia is uncommon with preeclampsia (Pritchard and colleagues, 1976). Much of the increase in serum alkaline phosphatase is due to heat-stable alkaline phosphatase of placental origin. Oosterhof and co-workers (1994) described increased hepatic artery resistance using Doppler sonography in 37 women with preeclampsia.
Periportal hemorrhagic necrosis in the periphery of the liver lobule is the most likely reason for increased serum liver enzymes. In the past, this lesion was often identified at autopsy and was long considered to be the characteristic lesion of eclampsia. Such extensive lesions are seldom identified in nonfatal cases with liver biopsy (Barton and colleagues, 1992). Bleeding from these lesions may cause hepatic rupture or they may extend beneath the hepatic capsule and form a subcapsular hematoma. Such hemorrhages without rupture may be more common than previously suspected. Using computed tomography, Manas and colleagues (1985) showed that 5 of 7 women with preeclampsia and upper abdominal pain had hepatic hemorrhage. Prompt surgical intervention may be life saving. Smith and co-workers (1991) reviewed 28 cases of spontaneous hepatic rupture associated with preeclampsia and added seven cases of their own. The mortality rate was 30 percent, and they concluded that packing and drainage was superior to lobectomy. One such woman at Parkland Hospital survived after receiving blood and blood products from more than 200 donors. Hunter and co-workers (1995) described a similar woman in whom liver transplant was considered life saving.
It is not known precisely what effects preeclampsia has on cerebral blood flow. Evidence is consistent with vasospasm or with impairment of autoregulation with passive overdistension of cerebral arterioles. Morriss and colleagues (1997) used magnetic resonance angiography to measure cerebral artery flow in severely preeclamptic and eclamptic women. Although cerebral blood flow was not altered, these women had been given magnesium sulfate after their eclamptic seizures and before angiography was performed. Naidu and associates (1996) provided evidence that magnesium sulfate therapy relieves cerebral vasospasm.
Nonspecific electroencephalographic abnormalities can usually be demonstrated for some time after eclamptic convulsions. Sibai and colleagues (1985a) observed that 75 percent of 65 eclamptic women had abnormal electroencephalograms within 48 hours of seizures. Half of these abnormalities persisted past 1 week, but most were normal by 3 months. An increased incidence of electroencephalographic abnormalities has been described in family members of eclamptic women, a finding suggestive that some eclamptic women who convulse have an inherited predisposition to do so (Rosenbaum and Maltby, 1943).
The principal postmortem cerebral lesions are edema, hyperemia, focal anemia, thrombosis, and hemorrhage. Sheehan (1950) examined the brains of 48 eclamptic women very soon after death, and hemorrhages, ranging from petechiae to gross bleeding, were found in 56 percent. According to Sheehan, if the brain is examined within an hour after death, most often it is as firm as normal, and there is no obvious edema. Govan (1961) investigated the cause of death in 110 fatal cases of eclampsia and concluded that cerebral hemorrhage was responsible in 39. Small cerebral hemorrhagic lesions were also found in 85 percent of the 47 women who died of cardiorespiratory failure. A regular finding was fibrinoid changes in the walls of cerebral vessels. The lesions sometimes appeared to have been present for some time, as judged from the surrounding leukocytic response and hemosiderin-pigmented macrophages. These findings are consistent with the view that prodromal neurological symptoms and convulsions may be related to these lesions.
Using cranial computed tomography scanning, Brown and colleagues (1988a) found that nearly half of eclamptic women studied had abnormal findings. The most common findings were hypodense cortical areas, which corresponded to petechial hemorrhage and infarction sites reported at autopsy by Sheehan and Lynch (1973). Using magnetic resonance imaging, Morriss and colleagues (1997) confirmed remarkable changes, especially in the area of the posterior cerebral artery. These findings may provide an explanation of why some women with preeclampsia convulse but others do not. The brain, like the liver and kidney, may be more involved in some women than in others. Thus, the extent of ischemic and petechial subcortical lesions, further altered by an inherent seizure threshold, influences the incidence of eclampsia.
Although visual disturbances are common with severe preeclampsia, blindness, either alone or accompanying convulsions, is not. Some women with varying degrees of amaurosis are found to have radiographic evidence of extensive occipital lobe hypodensities; this is likely an exaggeration of the lesions described earlier and shown in Figure 31–9. Herzog and colleagues (1990) reported that magnetic resonance imaging was superior to computed tomography in identifying specific brain lesions responsible for this type of blindness. Over a 14-year period, we described 15 women with severe preeclampsia or eclampsia who also had blindness (Cunningham and associates, 1995). This persisted for 4 hours to 8 days, but in all it resolved completely.
Retinal artery vasospasm may be associated with visual disturbances. Fortuitously, Belfort and associates (1992) showed that a 6-g bolus of magnesium sulfate caused retinal artery vasodilation. Retinal detachment may also cause altered vision, although it is usually one sided and seldom causes total visual loss as in some women with cortical blindness. Surgical treatment is seldom indicated; prognosis is good, and vision usually returns to normal within a week.
It is rare for a woman with eclampsia not to awaken after a seizure. It is also rare for a woman with severe preeclampsia to become comatose without an antecedent seizure. Prognosis for these women is guarded. In two eclamptic women with coma that we have managed, extensive cerebral edema was documented by computed tomography. It does not appear that coma results from an extension of the ischemic and hemorrhagic lesions described above, because eclamptic women without coma have minimal cerebral edema (Brown and colleagues, 1988a; Morriss and associates, 1997). Because coma usually follows sudden and severe blood pressure elevations, it is more likely that this phenomenon represents an inability to autoregulate cerebral blood flow with severe acute hypertension; the result is generalized cerebral edema.
Coma may result from intracranial hemorrhage from a ruptured intracerebral vessel, an arteriovenous malformation, or a berry aneurysm. Sheehan and Lynch (1973) reported that 6 of 76 women with fatal eclampsia had massive white matter hemorrhage that caused coma and death. They also reported a high mortality rate with bleeding into the basal ganglia or pons. Treatment is the same as for any nonpregnant woman.
Compromised placental perfusion from vasospasm is almost certainly a major culprit in the genesis of increased perinatal morbidity and mortality associated with preeclampsia.
Attempts to measure human maternal placental blood flow have been hampered by several obstacles, including inaccessibility of the placenta, the complexity of its venous effluent, and the unsuitability of certain investigative techniques for humans. Despite formidable problems, Assali and associates (1953) and Metcalfe and co-workers (1955) measured uterine blood flow in pregnant women and obtained reasonably consistent results. Both groups used a nitrous oxide Fick principle method that required cannulation of a uterine vein. Total uterine perfusion was measured, rather than maternal placental blood flow. Uterine blood flow in normal-term pregnant women was approximately 500 to 700 mL/min.
Browne and Veall (1953) estimated changes in maternal placental flow through the use of a 24Na clearance technique. This method required needle insertion into the intervillous space. They, as well as Weis and associates (1958), observed that 24Na was cleared two to three times more rapidly in normotensive pregnant women than in preeclamptic women. This implied a two- to threefold decrease in uteroplacental perfusion in hypertensive women compared with normotensive controls.
The consistent results and conclusions obtained from these early studies continue to be supported by other methods of investigation. For instance, Brosens and associates (1972) reported that the mean diameter of myometrial spiral arterioles of 50 normal pregnant women was 500 mm. The same measurement in 36 women with preeclampsia was 200 mm.
Everett and colleagues (1980) presented evidence that the clearance rate of dehydroisoandrosterone sulfate through placental conversion to estradiol-17b was an accurate reflection of maternal placental perfusion. Fritz and colleagues (1985) reported that the technique paralleled uteroplacental perfusion in primates. Normally, as pregnancy advances, this measurement increases greatly. The placental clearance rate decreases before the onset of overt hypertension (Worley and associates, 1975). Finally, placental clearance is decreased in women given diuretics or hydralazine (Gant and co-workers, 1976).
Doppler measurement of blood velocity through uterine arteries has been used to estimate uteroplacental blood flow Vascular resistance is estimated by comparing arterial systolic and diastolic velocity waveforms. Fleischer and colleagues (1986) and Trudinger and associates (1990) reported increased systolic–diastolic ratio in uterine arteries of women with preeclampsia. Others have not confirmed this (Hanretty and colleagues, 1988). Absent end-diastolic flow or reversal of flow is associated with increased fetal morbidity and mortality in hypertensive women (Fairlie and co-workers, 1991; Kofinas and associates, 1990). Thaler and colleagues (1992) reported that the presence of a systolic or diastolic notch, or a combination of both, is associated with elevated resistance indexes in the uterine and umbilical vessels. Nifedipine therapy and epidural analgesia have been reported to decrease abnormally elevated systolic-diastolic ratios (Pirhonen, 1990; Puzey, 1991; Ramos-Santos, 1991; and their colleagues).
Ducey and associates (1987) described systolic– diastolic velocity ratios from both uterine and umbilical arteries in 136 pregnancies complicated by hypertension. Among 51 women considered to have preeclampsia, 20 percent had normal umbilical artery velocity ratios; 15 percent had normal umbilical but abnormal uterine artery ratios; and in 40 percent both ratios were abnormal. Atkinson and associates (1994b) showed that elevated umbilical artery S/D ratio is not a clinically useful predictor for preeclampsia in a low-risk population.
In our experiences, diminished uterine artery flow velocities are seldom encountered with uncomplicated preeclampsia. This is true even with severely elevated blood pressures. With associated fetal growth restriction, however, aberrant flow velocities are often seen in both umbilical and aortic vessels (Cameron and colleagues, 1988). In some reports, women were studied because of growth retardation. Thus, it appears that preeclampsia alone may not be associated with significant changes in the uterine artery systolic–diastolic ratio. Aberrations in fetal blood flow velocities detected in hypertensive pregnancies are much more likely if there is retarded fetal growth (Lowery and associates, 1990; Villar and colleagues, 1989a).
Histological Changes in the Placental Bed
Hertig (1945) identified in preeclamptic pregnancies a lesion of uteroplacental arteries characterized by prominent lipid-rich foam cells. Zeek and Assali (1950) termed this acute atherosis. Most investigators are now in accord that there is a lesion, but they do not agree on its precise nature. Classically, in normal pregnancy, spiral arteries are invaded by endovascular trophoblast. It seems that, in preeclampsia, decidual vessels, but not myometrial vessels, are invaded by endovascular trophoblasts. Using electron microscopical studies of arteries taken from the uteroplacental implantation site, De Wolf and co-workers (1980) reported that early preeclamptic changes included endothelial damage, insudation of plasma constituents into vessel walls, proliferation of myointimal cells, and medial necrosis. They also found that lipid accumulates first in myointimal cells and then in macrophages. Importantly, Meekins and associates (1994) showed that these changes are a continuum from normal pregnancies to those with severe preeclampsia.
Classification on pregnancy induced hypertension.
1. Hypertensive disorders during pregnancy.
2. Edema during pregnancy.
3. Proteinuria during pregnancy.
4. Mild preeclampsia.
5. Moderate preeclampsia.
6. Severe preeclampsia.
“Superimposed” hypertensive disorders develop on the underlying preexisting diseases, such as Diabetes Mellitus, Hypertensive disease, kidneys inflammatory diseases, thyroid and pulmonary dysfunction. They have such peculiarities as:
1. early beginning;
2. severe duration;
3. isolated symptoms only presenting (isolated proteinuria, edema, or hypertension);
4. presence of atypical clinical findings such as paresthesia, insomnia, hypersalivation.
Is defined as hypertension present before the twentieth week of gestation or beyond 6 weeks' postpartum.
Diagnosis of Coincidental (Chronic) Hypertension
All chronic hypertensive disorders, regardless of their cause, predispose to development of superimposed preeclampsia or eclampsia. These disorders can create difficult problems with diagnosis and management in women who are not seen until after midpregnancy. The diagnosis of coincidental or chronic underlying hypertension is suggested by (1) hypertension (140/90 mm Hg or greater) antecedent to pregnancy, (2) hypertension (140/90 mm Hg or greater) detected before 20 weeks (unless there is gestational trophoblastic disease), or (3) persistent hypertension long after delivery. Additional historical factors that help support the diagnosis are multiparity and hypertension complicating a previous pregnancy other than the first. There is also usually a strong family history.
The diagnosis of chronic hypertension may be difficult to make if the woman is not seen until the latter half of pregnancy. This is because blood pressure decreases during the second and early third trimesters in both normotensive and chronically hypertensive women. Thus, a woman with chronic vascular disease, who is seen for the first time at 20 weeks, will frequently have a normal blood pressure. During the third trimester, however, blood pressure returns to its former hypertensive level, presenting a diagnostic problem as to whether the hypertension is chronic or pregnancy induced.
There are many causes of underlying hypertension that are encountered during pregnancy are present in the Table .
UNDERLYING CHRONIC HYPERTENSIVE DISORDERS
Essential familial hypertension (hypertensive vascular disease)
Coarctation of the aorta
Glomerulonephritis (acute and chronic)
Chronic renal insufficiency
Essential hypertension is the cause of underlying vascular disease in more than 90 percent of pregnant women. McCartney (1964) studied renal biopsies from women with “clinical preeclampsia,” and found chronic glomerulonephritis in 20 percent of nulliparas and in nearly 70 percent of multiparas. Fisher and co-workers (1969), however, did not confirm this high prevalence of chronic glomerulonephritis.
Chronic hypertension causes morbidity whether or not a woman is pregnant. Specifically, chronic hypertension may lead to premature cardiovascular deterioration, resulting in cardiac decompensation and/or cerebrovascular accidents. Intrinsic renal damage may also result from chronic hypertensive disease. More commonly in young women, hypertension develops as a consequence of underlying renal parenchymal disease. Dangers specific to pregnancy complicated by chronic hypertension include the risk of pregnancy-aggravated hypertension, which may develop in as many as 20 percent of these women. Additionally, the risk of abruptio placentae is increased substantively. Moreover, the fetus of the woman with chronic hypertension is at increased risk for growth restriction and death.
Diagnosis of Pregnancy-aggravated Hypertension
Preexisting chronic hypertension worsens in some women, typically after 24 weeks. Such pregnancy-aggravated hypertension may be accompanied by proteinuria or pathological edema; the condition is then termed superimposed preeclampsia. Often, the onset of superimposed preeclampsia develops earlier in pregnancy than pure preeclampsia, and it tends to be quite severe and accompanied in many cases by fetal growth restriction.
The most common hazard faced by pregnant women with chronic hypertensive vascular disease is the superimposition of preeclampsia. The frequency of pregnancy-aggravated hypertension is difficult to specify precisely because the incidence varies with the diagnostic criteria employed. If the diagnosis is made only on the basis of (1) significant aggravation of the hypertension, (2) sustained proteinuria, and (3) generalized edema, the incidence will be relatively low because delivery is often accomplished before intense superimposed preeclampsia or eclampsia has developed. If, however, the diagnosis is made on the basis of a modest rise in blood pressure and minimal to modest proteinuria, the incidence will be much higher. For example, with mild chronic hypertension, the incidence of superimposed preeclampsia cited in the studies in Table 31–13 varied from 6 to 46 percent!
Pregnancy-aggravated hypertension typically becomes manifest by a sudden rise in blood pressure that almost always is complicated eventually by substantive proteinuria. Extreme hypertension—systolic pressure greater than 200 mm Hg and diastolic pressure of 130 mm Hg or more, oliguria, and impaired renal clearance may rapidly ensue; the retina may have extensive hemorrhages and cotton-wool exudates; and convulsions and coma are likely. Therefore, in its most severe form, the resultant syndrome is similar to hypertensive encephalopathy. With the development of superimposed preeclampsia or eclampsia, the outlook for both infant and mother is grave unless the pregnancy is terminated. The frequency of fetal growth restriction and preterm delivery is increased appreciably because of its relatively early onset in pregnancy, as well as the marked severity of the process itself. If the infant is born alive and survives the perinatal period, however, long-term prognosis is good.
The diagnosis requires documentation of chronic underlying hypertension. Pregnancy-aggravated hypertension is characterized by worsening hypertension, keeping in mind that both systolic and diastolic pressures normally rise as gestation increases.
Gestational hypertension - occurs after 20 weeks of pregnancy and doesn’t accompanies with proteinuria.
Hypertension - In pregnancy is generally defined as a diastolic blood pressure of 90 mm Hg or greater, as a systolic blood pressure at or above 140 mm Hg at two estimations with the interval 4 hours or 160/110 mm Hg at once.
Preeclampsia - Is defined as the development of hypertension with proteinuria or edema (or both).
Differential diagnosis of chronic hypertension and preeclampsia
Onset of hypertension
Before pregnancy and in the first 20 weeks of gestation
After 20 weeks of gestation
Duration of hypertension
Constant, lasts during 3 months after delivery
It disappears after 6 weeks or 3 months after delivery
Presence of hypertensive disease in the parents, family
35-40 years old
20-25 years old
Spasm of vessels, hemorrhages
Vasospasm, edema of retina
1. Symptoms and signs
The pregnant woman is usually unaware of the two most important signs of preeclampsia—hypertension and proteinuria. By the time symptoms develop such as headache, visual disturbances, or epigastric pain, the disorder is almost always severe. Hence, the importance of prenatal care in the early detection and management of preeclampsia is obvious.
1. Hypertension in pregnancy is generally defined as a diastolic blood pressure of 90 mm Hg or greater, as a systolic blood pressure at or above 140 mm Hg, or as an increase in the diastolic blood pressure of at least 15 mm Hg or in the systolic blood pressure of 30 mm Hg or more when compared to previous blood pressures.
2. Weight gain – a sudden increase in weight may precede the development of preeclampsia. Weight increase of about much more than 400 g per week is abnormal.
A sudden increase in weight may precede the development of preeclampsia, and indeed, excessive weight gain in some women is the first sign. A weight increase of about 1 pound per week is normal, but when weight gain exceeds more than 2 pounds in any given week, or 6 pounds in a month, developing preeclampsia should be suspected. The suddenness of excessive weight gain is characteristic of preeclampsia rather than an increase distributed throughout gestation. Such weight gain is due almost entirely to abnormal fluid retention and is usually demonstrable before visible signs of nondependent edema such as swollen eyelids and puffy fingers. In cases of fulminating preeclampsia or eclampsia, fluid retention may be extreme; and in these women, a weight gain of 10 or more pounds per week is not unusual
3. Edema - peripheral edema is common in pregnancy, especially in the lower extremities; however, persistent edema unresponsive to resting in the supine position is not normal, especially, when it also involves the upper extremities and face (Fig. 3)
4. Headache - is unusual in milder cases but frequent in more severe disease. It is often frontal but may be occipital, and it is resistant to relief from ordinary analgesics.
5. Abdominal pain – epigactric or right upper quadrant pain often is a symptom of severe preeclampsia and may be indicated of imminent convulsions. It may be the result of stretching of the hepatic capsule, possibly by edema and hemorrhage. Tenderness over the liver should be presented.
6. Visual disturbances – a spectrum of visual disturbances, ranging from slight blurring of vision to scotomas to partial or complete blindness, may accompany preeclampsia. These develop as a result of vasospasm, ischemia, andpetechial hemorrhages within the occipital cortex.
7. Hyperreflexia should be presented. The patellar and achilles deep tendom reflexes should be carefully elicited and noted this symptom. The demonstration of clonus at the ankle is especially worrisome.
8. Any history of loss of consciousness or seizures, even in the patient with a known seizure disorder, may be significant (Fig. 4)..
Assessment for proteinuria, edema, weight, hyperreflexia, headache, visual disturbances, epigastric pain is obligatory daily.
Fig. 3. A. Severe edema in a young primigravida with antepartum eclampsia and a markedly reduced blood volume compared with normal pregnancy. B. The same woman 3 days after delivery. The remarkable clearance of pedal edema, accompanied by diuresis and a 28-pound weight loss, was spontaneous and unprovoked by any diuretic therapy. (From Cunningham and Pritchard, 1984.)
Fig. 4 Hematoma of tongue from laceration during eclamptic convulsion. Thrombocytopenia may have contributed to the bleeding.
2. Laboratory findings.
Test or Procedure
Proteinuria is defined as 300 mg or more urinary protein during a 24-hour period or 30-100 mg per dL or more in at least two random urine specimens collected 6 hours or more apart
Hematocrit in complete blood count / every 2 days
It increasing may signify worsening vasocanstriction and decreased intravascular volume.
Platelet count / every 2 days
Thrombocytopenia and coagulopathy are associated with worsening PIH.
Coagulation profile (PT, PTT)
Fibrin split products
Liver function studies / weekly
Hepatocellular dysfunction is associated with worsening PIH
Serum creatinine / twice weekly
Decreased renal function is associated with worsening PIH.
24-hour urine for creatinine clearance / twice weekly
24- hour for total protein / twice weekly
Serum uric acid / twice weekly
Ultrasound for fetal growth / every 2 weeks
To assess for pregnancy-associated hypertension effects on the fetus, intrauterine growth restriction.
Amniotic fluid volume
Fetal movement record / daily
Chronic fetal distress.
Biophysical profile / twice weekly
Nonstress test / twice weekly
Assessment of different stages of PIH severity
Diastolic blood pressure
90-99 mm Hg
100-109 mm Hg
> 110 mm Hg
Proteinuria in 24-hour collection
< 0.3 g
< 0.3 - 5 g
> 5 g
Diuresis per hour
> 50 ml
> 40 ml
< 40 ml
Presence of edema
In lower extremities
In lower extremities, and abdominal wall
Number of thrombocytes
80 - 150. 000
36 – 38
39 – 42
< 75 mkmol/L
75 – 120 mkmol/L
> 120 mkmol/L
< 4,5 mmol/L
4,5 – 8 mmol/L
> 8 mkmol/L
Preeclampsia is classified as severe if there is a blood pressure greater than or equal to 170 mm Hg systolic or 110 mm Hg diastolic, marked proteinuria (generally > 5 g/24-hr urine collection, or 5 g/L or more on dipstick of a random urine), oliguria, weight gain exceeds more than 900 g in a week, cerebral or visual disturbances such as headache and scotomata, pulmonary edema or cyanosis, epigastric or right upper quadrant pain, evidence of hepatic dysfunction, or thrombocytopenia. These myriad changes illustrate the multisystem alterations associated with preeclampsia.
Complications of preeclapsia:
Maternal – placenta abruption, cerebral hemorrhage (Fig. 5), renal and liver insufficiency (Fig. 6), disseminated intravascular coagulopathy (Fig. 7), adrenal insufficiency, eclampsia.
Fetal – intrauterine growth retardation, fetal distress (Fig. 8), intranatal fetal death, infant morbodity and mortality.
ECLAMPSIA is characterized typically by those same abnormalities as severe preeclampsia with the addition of convulsions that are precipitated by pregnancy-induced hypertension. The seizures are grand mal and may appear during pregnancy, during labor, or postpartum.
Fig. 5 Computed tomographic scan of liver showing a subcapsular hematoma (arrow) along the right margin of the liver. (Reproduced, with permission, from Manas KJ, Welsh JD, Rankin RA, Miller DD. Hepatic hemorrhage without rupture in preeclampsia. N Engl J Med. 312:424-426, 1985. Copyright ©1985 Massachusetts Medical Society. All rights reserved.)
Fig. 6. Gross liver specimen from a woman with preeclampsia who died from severe acidosis and liver failure. Periportal hemorrhagic necrosis was seen microscopically. (From Cunningham, 1993.)
Fig. 7. Hypertensive hemorrhage with eclampsia.
Fig. 8 Fetal bradycardia developing in a woman with an intrapartum eclamptic convulsion. Bradycardia resolved and beat-to-beat variability returned after about 5 minutes following the seizure. (From Cantrell and Cunningham, 1994.)
MODERN METHODS OF PREVENTION AND TREATMENT OF PREGNANCY INDUCED HYPERTENSION
Prophylaxis and Early Treatment
Because women are usually asymptomatic and seldom notice the signs of incipient preeclampsia, its early detection demands careful observation at appropriate intervals, especially in women known to be predisposed to preeclampsia. Major predisposing factors are (1) nulliparity, (2) familial history of preeclampsia–eclampsia, (3) multiple fetuses, (4) diabetes, (5) chronic vascular disease, (6) renal disease, (7) hydatidiform mole, and (8) fetal hydrops.
Rapid weight gain any time during the latter half of pregnancy, or an upward trend in diastolic blood pressure, even while still in the normal range, is worrisome. Every woman should be examined at least weekly during the last month of pregnancy and every 2 weeks during the previous 2 months. At these visits, weight and blood pressure measurements are made. All women should be advised to report immediately any symptoms or signs of preeclampsia, such as headache, visual disturbances, epigastric distress, and puffiness of hands or face. The reporting of any such symptoms calls for an immediate examination to confirm or exclude preeclampsia.
Natriuretic drugs, such as chlorothiazide and its congeners, have been overused severely in the past. Although diuretics have been alleged to prevent preeclampsia, Collins and colleagues (1985) reviewed results of nine studies of more than 7000 women and concluded that perinatal mortality was not improved when diuretics were given. Furthermore, thiazides can induce serious sodium and potassium depletion, hemorrhagic pancreatitis, and severe neonatal thrombocytopenia. The failure of natriuretic drugs to prevent preeclampsia raises serious doubt about the efficacy of rigid dietary sodium restriction.
Wallenburg and co-workers (1986) reported their experiences with either 60 mg of aspirin or placebo to angiotensin-sensitive primigravid women at 28 weeks. The reduced incidence of preeclampsia in the treated group was attributed to selective suppression of thromboxane synthesis by platelets and sparing of endothelial prostacyclin production. In a group of high-risk women with prior bad pregnancy outcomes due to hypertension and placental insufficiency, Beaufils and colleagues (1985) reported that early prophylactic treatment with dipyridamole and aspirin reduced recurrences. Benigni and colleagues (1989) and Schiff and associates (1989) also reported salutary effects in high-risk women.
Spitz and colleagues (1988) reported that most angiotensin-sensitive women at high risk for developing preeclampsia could be rendered refractory to angiotensin by a 1-week course of daily 81-mg aspirin.
They confirmed that low-dose aspirin significantly decreased thromboxane synthesis. Prostacyclin and prostaglandin E2 synthesis were also decreased 20 to 30 percent by therapy. These same investigators reported that approximately 20 percent of angiotensin-sensitive pregnant women given low-dose aspirin did not become refractory to angiotensin, and all such women developed preeclampsia (Brown and associates, 1990). The nonresponders to low-dose aspirin had a significant fall in thromboxane levels, but they also had significant declines in prostacyclin and prostaglandin E2 levels.
Low-dose aspirin was not effective for women who already had mild pregnancy-induced hypertension (Schiff and associates, 1990); however, women with moderate hypertension improved. Magness and colleagues (1991) observed that less than 20 percent of women with early-onset pregnancy-induced hypertension failed to become normotensive with hospitalization. In the 20 percent who remained hypertensive after hospitalization, low-dose aspirin allowed prolongation of pregnancy compared with controls.
Low-dose aspirin may be effective in some women in preventing the development of pregnancy-induced hypertension and fetal growth restriction (Imperiale and Petrulis, 1991). Hauth and co-workers (1993) randomized 604 nulliparas to 60 mg aspirin or placebo beginning at 24 weeks. Only 1.7 percent of aspirin-treated women developed preeclampsia versus 5.6 percent of controls (P < 0.01). Studies from the National Institutes of Health sponsored Maternal–Fetal Medicine Network showed that aspirin prophylaxis significantly decreased preeclampsia to 4.6 percent compared with 6.3 percent in nontreated controls (Sibai and colleagues, 1993a). Overall, perinatal outcome was not improved, and women who took aspirin had significantly more placental abruptions, although Hauth and colleagues (1995) concluded that these abruptions were of no clinical importance.
In a study by the Royal College of Obstetricians and Gynecologists (CLASP, 1994), it was concluded that low-dose aspirin was ineffective to prevent preeclampsia. Similarly, the ECPPA Collaborative Group (1996), in a study from 12 Brazilian teaching hospitals, concluded that low-dose aspirin did not decrease the incidence of proteinuric preeclampsia in 1009 women randomized to aspirin or placebo. Both of these groups of investigators used Korotkoff IV sound for diastolic pressure, and this may overestimate diastolic pressure by 7 to 15 mm Hg (Brown and colleagues, 1994; Lindheimer and Katz, 1992; Shennan and co-workers, 1996). In their meta-analysis, the CLASP group concluded that low-dose aspirin reduced the incidence of preeclampsia by about 25 percent.
Currently, the salutary effects of low-dose aspirin therapy remain to be proven for most groups of women. The prevailing opinion is that normal women should not be treated, but selective treatment for certain high-risk groups is acceptable (Cunningham and Gant, 1989; Hauth and Cunningham, 1995; Royal College of Obstetricians and Gynecologists, 1996; Zuspan and Samuels, 1993).
Low-dose aspirin therapy appears to be safe for the fetus. Although most clinical trials have resulted in no apparent maternal risks, Brown and colleagues (1990) noted a rapid clinical deterioration if therapy was stopped suddenly.
The basic management objectives for any pregnancy complicated by pregnancy-induced hypertension are:
1. Termination of the pregnancy with the least possible trauma to the mother and the fetus.
2. Birth of the infant who subsequently thrives
3. Complete restoration of the health of the mother.
Hospitalization is considered for women with pregnancy-induced hypertension if there is a persistent or worsened elevation in blood pressure or development of proteinuria. With hospitalization, a systematic study should be instituted that includes the following:
1. A detailed medical examination followed by daily searches for development clinical findings such as headache, visual disturbances, epigastric pain, and rapid weight gain.
2. Admittance weight and every day thereafter.
3. Admittance analysis for proteinuria and at least every 2 days thereafter.
4. Blood pressure readings with an appropriate-size cuff every 4 hours, except between midnight and morning, unless the midnight pressure has increased.
5. Measurements of plasma creatinine, hematocrit, platelets, and serum liver enzymes, the frequency to be determined by the severity of hypertension.
6. Frequent evaluation of fetal size and amnionic fluid volume by the same experienced examiner and by serial sonography if remote from term.
If these observations lead to a diagnosis of severe preeclampsia, further management is the same as described for eclampsia.
Reduced physical activity throughout much of the day is beneficial. Ample, but not excessive, protein and calories should be included in the diet. Sodium and fluid intakes should not be limited or forced. Sedatives or tranquilizers have been used routinely by some; we do not recommend them. Further management depends upon (1) severity of preeclampsia, (2) duration of gestation; and (3) condition of the cervix. Fortunately, many cases prove to be sufficiently mild and near enough to term that they can be managed conservatively until labor commences spontaneously or until the cervix becomes favorable for labor induction. Complete abatement of all signs and symptoms, however, is uncommon until after delivery. Almost certainly, the underlying disease persists until after delivery!
1. Bed rest. Preferably with as much of the time as possible spent in a lateral decubitus position. In this position, cardiac function and uterine blood flow are maximized and maternal blood pressures in most cases are normalized. This improves uteroplacental function, allowing normal fetal growth and metabolism. ambulatory treatment has no place in the management of PIH; bed-rest throughout the greater part of the day is essential.
2. Sedative drugs for normalization of status of central nervous system:
1. Droperidol – 2 ml IM, Seduxen – 2 ml IM. These drugs should be combined with Droperidol – 0,25 % - 2ml IM or IV
3. Antihypertensive therapy eliminates vasospasm of macro- and microcirculation.
Antihypertensive drugs used in pregnancy:
1. spasmolytic agents – No-spani 2 % - 2-4 ml intramuscularly, Papaverine hydrochloride – 2 % - 2-4 ml IM, Plathyphillinum – 0,2 % - 2, 0 – twice a day, Dibasol – 1 % 2-4 ml IM or IV, Euphyllinum – 2,4 % 10, 0 IV;
2. Nifedipine – calcium-channel blocker – in the dose 10 mg po q 4-8 hours;
3. Labetalol – a- and b- adrenergic blockers – in the dose 20-50 mg IV q 3-6 hours;
4. Methyldopa – false neurotransmission, central nervous system effect;
5. Thiazide – decreased plasma volume and cardiac output.
If diastolic pressure is repeatedly above 110 mm Hg – Hydralazine is preferred agent because of its effectiveness and safety. An initial dose of 5 mg given as an intravenous bolus is increased by 5 to 10 mg every 20 minutes until suitable blood pressure is achieved. The goal of such therapy is to reduce the diastolic blood pressure to the 90-11 mm Hg range. Labetolol is a useful second-line drug for women whose hypertension is refractory to hydralazine.
Hydralazine is given intravenously whenever the diastolic blood pressure is 110 mm Hg or higher. It is administered in 5- to 10-mg doses at 15- to 20-minute intervals until a satisfactory response is achieved. A satisfactory response antepartum or intrapartum is defined as a decrease in diastolic blood pressure to 90 to 100 mm Hg, but not lower so that placental perfusion will not be compromised. Some recommend treatment of diastolic pressures over 100 mm Hg and some use 105 mm Hg as a cutoff (Cunningham and Lindheimer, 1992; Sibai, 1996).
Hydralazine so administered has proven remarkably effective, and importantly, cerebral hemorrhage has been avoided. At Parkland Hospital, approximately 8 percent of all women with pregnancy-induced hypertension are given hydralazine as described; this drug has been administered to more than 3500 women to control acute peripartum hypertension. Seldom was another antihypertensive agent needed because of poor response to hydralazine. In most European centers, hydralazine is also favored (Hutton and colleagues, 1992; Redman and Roberts, 1993).
The tendency to give a larger initial dose of hydralazine when the blood pressure is higher must be avoided. Figure 31–19 shows the mean arterial blood pressure responses to 5-mg hydralazine bolus doses. The response to even 5- to 10-mg doses cannot be predicted by the level of hypertension; thus we always give 5 mg as the initial dose. Hydralazine was injected more frequently than recommended in the protocol, and blood pressure decreased in less than 1 hour from 240–270/130–150 mm Hg to 110/80 mm Hg. Ominous fetal heart rate decelerations were evident when the pressure fell to 110/80 mm Hg, and the decelerations persisted until maternal blood pressure increased.
4. Magnesium Sulfate is used to arrest and prevent the convulsions of eclampsia without producing generalized central nervous system depression in either mother or the fetus. Magnesium sulfate may be given intramuscularly in the dose 25 % -5, 0 2-3 times a day or by continuos intravenous infusion in the dose 8 % - 200, 0 ml. It has spasmolytic, sedative, hypotensive and anticonvulsant effects.
Frequent evaluations of the patient's patellar reflex and respiration (> 14 respiratory act in a minute) are necessary to monitor for manifestations of toxic serum magnesium concentrations. In addition, because magnesium sulfate is excreted solely from the kidney, maintenance of urine output at > 30 ml/hr will avoid accumulation of the drug. Reversal of the effects of excessive magnesium concentrations is accomplished by the slow intravenous administration of 10% calcium gluconate along with oxygen supplementation and cardiorespiratory support if needed.
The maximal dose of magnesium during a day in the case of severe preeclampsia is 50-80 ml (12,5 – 80 gram).
Sheme of magnesium administration in the case of severe preeclampsia and eclampsia:
1) Intravenous administration of Magnesium Sulfate - 12 ml 25 % during 5 minutes. At the same time – intramuscularly administration of 4,5 – 6 g of Magnesium Sulfate in average dose 0,1 g per kg of patient’s weight. Than this dose is repeated each 6 hours intramuscularly. The general dose in 24 hour should be not exceed 24 gram. The course of treatment should be repeated after 12 hours.
2) Initial administration of 3 g IV and 4 g IM, followed by a 4,5-6 g every 4 hours maintenance dose.
3) administer 4-6 g of magnesium sulfate IV over 10-15 min, followed by a 2g/hour maintenance dose (American).
Magnesium sulfate is used to arrest and prevent convulsions due to eclampsia without producing generalized central nervous system depression in either the mother or the fetus-infant. Magnesium sulfate is not given to treat hypertension. Based on a number of studies that will be cited, as well as extensive clinical observations, magnesium most likely exerts a specific anticonvulsant action on the cerebral cortex. Typically, the mother stops convulsing after the initial administration of magnesium sulfate, and within an hour or two regains consciousness sufficiently to be oriented as to place and time.
Using these regimen, there has been no evidence of neonatal depression due to magnesium intoxication. In the unusual case in which the initial dose of 4 g intravenously plus 10 g intramuscularly has not arrested eclamptic convulsions, 2 g more, as a 20 percent solution, has been administered slowly intravenously. In a small woman, an additional 2 g dose may be used once, and twice if needed in a larger woman. In only 5 of 245 women with eclampsia was it necessary to use supplementary medication to control convulsions. The agent used was sodium amobarbital given slowly intravenously in doses up to 250 mg. Thiopental is also suitable. Maintenance magnesium sulfate therapy for eclampsia is continued intramuscularly every 4 hours for 24 hours after delivery. For eclampsia that develops postpartum, magnesium sulfate is administered for 24 hours after the onset of convulsions.
Parenterally administered magnesium is cleared almost totally by renal excretion, and magnesium intoxication is avoided by ensuring that before each dose (1) urine flow was at least 100 mL during the previous 4 hours, (2) the patellar reflex is present, and (3) there is no respiratory depression. Eclamptic convulsions are almost always prevented by plasma magnesium levels maintained at 4 to 7 mEq/L. As discussed below, loss of the patellar reflex begins with plasma levels of 8 to 10 mEq/L and, importantly, respiratory arrest occurs at levels of 12 mEq/L or more. Calcium gluconate, 1 g administered slowly intravenously, and oxygen usually suffice for treatment of respiratory depression. If respiratory arrest occurs, prompt tracheal intubation and ventilation are life saving.
Because magnesium is cleared almost exclusively by renal excretion, plasma magnesium concentration, using the doses described, will be excessive if glomerular filtration is decreased substantively. Renal function is estimated by measuring plasma creatinine, and whenever it is 1.3 mg/dL or higher, we give only half of the maintenance magnesium sulfate dose outlined in Table 31–11. Thus, the woman with eclampsia who has impaired renal function is given a loading dose of 4 g intravenously in addition to the 10 g intramuscular dose, to be followed by 2.5 g intramuscularly every 4 hours. Plasma magnesium levels are usually within the desired range of 4 to 7 mEq/L. Some prefer in these circumstances to give magnesium sulfate intravenously by continuous infusion. With either method, when there is renal insufficiency, plasma magnesium levels must be checked periodically.
Pharmacology and Toxicology of Magnesium Sulfate
Magnesium sulfate USP is MgSO4 · 7H2O and not MgSO4. When administered as described, the drug will practically always arrest eclamptic convulsions and prevent their recurrence. The initial intravenous infusion of 4 g is used to establish a prompt therapeutic level that is maintained by the nearly simultaneous intramuscular injection of 10 g of the compound, followed by 5 g intramuscularly every 4 hours, as long as there is no evidence of potentially dangerous hypermagnesemia. With this dosage schedule, therapeutically effective plasma levels of 4 to 7 mEq/L are achieved compared with pretreatment plasma levels of less than 2.0 mEq/L (Chesley and Tepper, 1957; Stone and Pritchard, 1970). Magnesium sulfate injected deeply into the upper outer quadrant of the buttocks, as described earlier, has not resulted in erratic absorption and consequent erratic plasma levels.
Sibai and co-workers (1984) performed a prospective study in which they compared continuous intravenous magnesium sulfate and intramuscular magnesium sulfate. There was no significant difference between mean magnesium levels observed after intramuscular magnesium sulfate and those observed following a maintenance intravenous infusion of 2 g/hr. However, the intramuscular regimen resulted in serum magnesium levels that were significantly higher than those obtained with a continuous intravenous maintenance dose of 1 g/hr. They concluded that there was no therapeutic advantage to the intravenous route of administration except for the avoidance of pain at the intramuscular injection site. When given intravenously, magnesium sulfate should be delivered by an infusion pump, and careful attention must be given to the solution concentration and the rate of delivery. Most recommend that 2 g/hr be given, to be followed by serial magnesium determinations to avoid toxicity.
Patellar reflexes disappear when the plasma magnesium level reaches 10 mEq/L, presumably because of a curariform action. This sign serves to warn of impending magnesium toxicity, because a further increase will lead to respiratory depression. Plasma cholinesterase activity is decreased substantively in preeclamptic women, but this is not altered further by magnesium therapy (Kambam and associates, 1988).
When plasma levels rise above 10 mEq/L, respiratory depression develops, and at 12 mEq/L or more, respiratory paralysis and arrest follow. Somjen and co-workers (1966) induced in themselves, by intravenous infusion, marked hypermagnesemia, achieving plasma levels up to 15 mEq/L. Predictably, at such high plasma levels, respiratory depression developed that necessitated mechanical ventilation, but depression of the sensorium was not dramatic as long as hypoxia was prevented. Treatment with calcium gluconate, 1 g intravenously, along with the withholding of magnesium sulfate usually reverses mild to moderate respiratory depression. Unfortunately, the effects of intravenously administered calcium may be short lived. For severe respiratory depression and arrest, prompt tracheal intubation and mechanical ventilation are life saving. Direct toxic effects on the myocardium from high levels of magnesium are uncommon. In humans, it appears that a major cause of cardiac dysfunction is due to hypoxia, the consequence of respiratory arrest, rather than a direct effect of magnesium. With appropriate ventilation, cardiac action is satisfactory even when plasma levels are exceedingly high (McCubbin and associates, 1981).
Parenterally injected magnesium is filtered through the glomerulus and variably reabsorbed by the tubule. As plasma magnesium concentration increases, more magnesium is filtered and less is reabsorbed. Nonetheless, when glomerular filtration is impaired, so is magnesium clearance. Therefore, an appreciably elevated plasma creatinine level indicates diminished renal capacity to excrete magnesium .
Acute cardiovascular effects of parenteral magnesium ion in women with severe preeclampsia have been studied by Cotton and associates (1984), who obtained data using pulmonary and radial artery catheterization. Following a 4-g intravenous dose given over 15 minutes, mean arterial blood pressure fell slightly, and this was accompanied by a 13 percent increase in cardiac index. Thus, magnesium decreased systemic vascular resistance and mean arterial pressure, and at the same time increased cardiac output, without evidence of myocardial depression. While they found that these effects dissipated within 15 minutes despite continuous magnesium infusion, Scardo and colleagues (1995) demonstrated an effect of at least 4 hours.
In monkeys with angiotensin-induced hypertension late in pregnancy, Harbert and co-workers (1969) demonstrated slightly increased uterine blood flow in response to the infusion of magnesium sulfate. At the same time, arterial blood pressure decreased minimally.
Watson and colleagues (1986) reported the effects of magnesium on cultured human umbilical vein endothelial cells. In concentrations similar to those achieved in plasma with therapeutic doses described above, magnesium stimulated prostacyclin release in a dose-dependent fashion. Plasma from women given magnesium sulfate therapy stimulated a two- to fivefold increase in prostacyclin production, compared with pretherapy plasma. Presumably also mediated by prostacyclin, magnesium enhanced platelet aggregation inhibition characteristic of endothelial cells. In contrast, O’Brien and colleagues (1990) questioned magnesium stimulation of prostacyclin because they could not identify an increased renal excretion of prostaglandin metabolites following magnesium therapy. Similarly, Hsu and associates (1996) observed that magnesium sulfate therapy had no effect on nitric oxide levels in preeclamptic women.
Cerebrospinal fluid magnesium levels are unchanged in untreated severely preeclamptic women when compared with normotensive controls (Fong and associates, 1995). Thurnau and colleagues (1987) showed that there was a small but highly significant increase in cerebrospinal fluid magnesium concentration after magnesium therapy for preeclampsia. The magnitude of the increase was directly proportional to the corresponding serum concentration. Borges and Gücer (1978) provided convincing evidence that the magnesium ion exerts an effect on the central nervous system much more specific than generalized depression. The degree of suppression increased as the plasma magnesium concentration increased, and decreased as it fell. Therefore, even though elevated concentrations of plasma magnesium inhibit acetylcholine release in response to motor nerve impulses, reduce motor end-plate sensitivity to acetylcholine, and decrease motor end-plate potential, these actions do not account for, nor should they necessarily be implicated in, the explanation of the beneficial effects of magnesium sulfate in controlling the convulsions of eclampsia.
Lipton and Rosenberg (1994) attribute anticonvulsant effects to neuronal calcium influx blocking through the glutamate channel. Cotton and associates (1992) induced seizure activity in the hippocampus region of rats because it is a region with a low seizure threshold and a high density of N-methyl-D-aspartate receptors. These receptors are linked to various models of epilepsy and can be blocked by magnesium. Because the hippocampal seizures could be blocked by magnesium, the investigators believed that this implicated the N-methyl-D-aspartate receptor in eclamptic seizures. Magnesium, therefore, has a central nervous system effect in blocking seizures.
Magnesium ions in relatively high concentration will depress myometrial contractility both in vivo and in vitro. With the regimen described and the plasma levels that have resulted, no evidence of myometrial depression has been observed beyond a transient decrease in activity during and immediately after the initial intravenous loading dose. Typically, as the cutaneous flushing from the intravenous dose disappeared, uterine activity returned to preinjection intensity.
Magnesium administered parenterally to the mother promptly crosses the placenta to achieve equilibrium in fetal serum and less so in amnionic fluid (Hallak and colleagues, 1993). With a single large intravenous dose, but not with smaller doses, magnesium sulfate may transiently cause a loss of fetal heart rate beat-to-beat variability (Pritchard, 1979). Atkinson and colleagues (1994a) reported a statistically significant but clinically insignificant decrease in short-term variability. They observed no changes in long-term variability or fetal heart rate acceleration. Others, however, have reported more profound reductions both in short- and long-term variability (Guzman and co-workers, 1993). Gray and colleagues (1994) reported that therapeutic magnesium sulfate for tocolysis did not alter the biophysical profile in 25 fetuses studied. The neonate may be depressed only if severe hypermagnesemia exists at delivery. We have not observed neonatal compromise after intramuscular therapy with magnesium sulfate (Cunningham and Pritchard, 1984), nor have Green and associates (1983).
More recently, Nelson and Grether (1995) described a possible protective effect of magnesium against cerebral palsy in very-low-birthweight infants. To the contrary, Kimberlin and colleagues (1996) found no improved neonatal outcome advantage of maternal magnesium sulfate tocolysis in infants born weighing less than 1000 g.
5. Normalization of blood reology because of hemoconcentration – Trental, Curantil, Komplamin.
6. Limited intravenous fluid therapy under control of blood volume, hematocrit, 24-hours diuresis. Primarily lactated Ringer’s containing 5 % dextrose – should be given at a rate of 60-125 ml per hour (not faster) unless there is unusual fluid loss from vomiting, diarrhea, or, more likely, excessive blood loss at delivery. Oliguria is common in severe preeclampsia and eclampsia, making it tempting to administer intravenous fluids more vigorously. However, the infusion of large volumes of fluid enhances the maldistribution of extracellular fluid and in that way increases the risk of pulmonary and cerebral edema.
Lactated Ringer solution is administered routinely at the rate of 60 mL/hr to no more than 125 mL/hr unless there was unusual fluid loss from vomiting, diarrhea, or diaphoresis, or more likely, excessive blood loss at delivery. Oliguria, common in cases of severe preeclampsia and eclampsia, coupled with the knowledge that maternal blood volume is very likely constricted compared with normal pregnancy, make it tempting to administer intravenous fluids more vigorously. The rationale for controlled, conservative fluid administration is that the typical eclamptic woman already has excessive extracellular fluid that is inappropriately distributed between the intravascular and extravascular spaces of the extracellular fluid compartment. Infusion of large fluid volumes could and does enhance the maldistribution of extracellular fluid and thereby appreciably increases the risk of pulmonary and cerebral edema (Benedetti and Quilligan, 1980b; Gedekoh and associates, 1981; Sibai and co-workers, 1987b).
For the patient with worsening preeclampsia or the patient who has severe preeclampsia or eclampsia, stabilization with magnesium sulfate, antihypertensive therapy as indicated, monitoring for maternal and fetal well-being, and delivery by induction or cesarean section are required. A 24-hour delay in delivery allow steroid administration to enhance fetal pulmonary maturity may be indicated in some cases.
7. Avoidance of Diuretics and Hyperosmotic Agents. Potent diuretics further compromise placental perfusion, because their immediate effects include further intravascular volume depletion, which most often is already reduced compared with normal pregnancy. Therefore, diuretics are not used to lower blood pressure, so as not to enhance the intensity of the maternal hemoconcentration and its adverse effects on the mother and fetus (Zondervan and associates, 1988).
Once delivery is accomplished, in almost all cases of severe preeclampsia and eclampsia there is a spontaneous diuresis that usually begins within 24 hours and results in the disappearance of excessive extravascular extracellular fluid over the next 3 to 4 days..
With infusion of hyperosmotic agents, the potential exists for an appreciable intravascular influx of fluid and, in turn, subsequent escape of intravascular fluid in the form of edema into vital organs, especially the lungs and brain. Moreover, an oncotically active agent that leaks through capillaries into lungs and brain promotes accumulation of edema at these sites. Most importantly, a sustained beneficial effect from their use has not been demonstrated. For all of these reasons, hyperosmotic agents have not been administered, and use of furosemide or similar drugs has been limited to the rare instances in which pulmonary edema was identified or strongly suspected.
PROTOCOL FOR TREATING ECLAMPSIA: Turn patient on her side, establish airways and administer oxygen, magnesial therapy. If convulsions are controlled and maternal condition is stable – delivery within 3 to 6 hours. Continue to administer magnesium for at least 24 hours after delivery or last convulsion.
Attention! In the case if severe preeclampsia and eclampsia a patient should be hospitalized in the single patient ward, three cathethers should be inserted obligatory:
1 – into central vein - v. subclavia for a fluid therapy and controling of central venous pressure;
2 – into urinary bladder for controling of diuresis per hour;
3 – transnasal catheterisation of stomach for prevention of Mendelson’s syndrome.
Parkland Hospital Eclampsia Regimen
In 1955 Pritchard initiated a standardized treatment regimen at Parkland Hospital, and this has been used since then to manage women with eclampsia. The carefully analyzed results of treatment of 245 cases of eclampsia, typically the severest form of pregnancy-induced or -aggravated hypertension, were reported by Pritchard and associates in 1984. The specific plan of management is summarized here.
1. Control of convulsions with magnesium sulfate, using an intravenously administered loading dose and periodic intramuscular injections standardized in dose and frequency of administration.
2. Intermittent intravenous injections of hydralazine to lower blood pressure whenever the dia-stolic pressure is 110 mm Hg or higher.
3. Avoidance of diuretics and hyperosmotic agents.
4. Limitation of intravenous fluid administration unless fluid loss is excessive.
DURATION OF TREATMENT AND DELIVERY
The timing and route of delivery for preeclamptic women are determined by gestational age, fetal condition, and maternal condition.
If the effect of treatment of mild and moderate preeclampsia is absent during 7-10 days, and in the case of severe preeclamsia – during 24-48 hours – a question about delivery should be discussed immediately.
Immediate delivery by cesarean section during or after an eclamptic seizure in eclampsia can be dangerous. The maternal condition usually can be stabilized within 5-6 hours. It is safe to proceed with definitive treatment, which is cesarean section.
Indications to preterm delivery in preeclampsia:
Laboratory findings: proteinuria more than 1g 24-hour collection, decreased level of serum creatinine, liver insufficiency, thrombocytopenia, abnormal nonstress test and biophysical profile, fatal growth retardation, diastolic blood pressure more than 100 mm Hg during 24 hours, diastolic blood pressure more than 110 mm Hg.
Maternal indications: HELLP-syndrome, eclampsia, pulmonary edema, heart insufficiency, coagulopathy, kidney dysfunction, cerebral symptoms, epigastrial pain.
Once anticonvulsant and antihypertensive therapy is established, attention is directed toward delivery. Induction of labor with amniotomy is often attempted, although cesarean delivery may be needed either if induction is unsuccessful or not possible or if maternal or fetal status is worsening. Epidural anesthesia is very effective in labor because of antihypertensive effect.
At delivery, blood loss must be closely monitored, because patients with preeclampsia or eclampsia have significantly reduced blood volumes. After delivery, patients are kept in the labor and delivery area for 24 hours for close observation of their clinical progress and further administration of magnesium sulfate to prevent postpartum eclamptic seizures. Approximately 25% of all preeclamptic patients who have eclamptic seizures have them before labor, approximately 50% during labor, and approximately 25% after delivery. Usually, the vasospastic process begins to reverse itself in the first 24 to 48 hours, as manifest by a brisk diuresis.
Indications to cesarean section in PIH are frequent convulsions that don’t eliminated by therapy, amaurosis, retinal detachment, unuria, severe eclampsia which is not eliminated by conservative treatment during 24-48 hours if the cervix is unfavorable, eclampsia combining with obstetric (breech presentation, contracted pelvis, macrosomic fetus, disseminated intravascular coagulopathy) or extragenital pathology.
MANAGEMENT OF THE ECLAMPTIC SEIZURE
The eclamptic seizure is a time of life-threatening risk for mother and fetus. Maternal risks include musculoskeletal injury (including biting the tongue), hypoxia, and aspiration. Maternal therapy consists of turning patient on her side, inserting a padded tongue blade, restraining gently as needed, providing oxygen, and gaining an intravenous (IV) access. Eclamptic seizures are usually self-limited so that medical therapy should be directed to the initiation of magnesium therapy to prevent further seizures rather than to anticonvulsant therapy with diazepam or similar drugs. Transient uterine hyperactivity for 2 to 15 minutes is associated with fetal heart rate (FHR) changes, including bradycardia or compensatory tachycardia, decreased beat-to-beat activity, and late decelerations. These are self-limited and not dangerous to the fetus unless they continue for 20 minutes or more. Delivery during this time imposes unnecessary risk for mother and fetus and should be avoided. If convulsions are controlled and maternal condition is stable, initiate induction or delivery within 3 to 6 hours is recommended.