UTERINE RUPTURE

Williams Obstetrics 24th Edition (HAL 617 Chapter 31)

CLASSIFICATION
Uterine rupture typically is classified as either (1) complete when all layers of the uterine
wall are separated, or (2) incomplete when the uterine muscle is separated but the viscera
peritoneum is intact. Incomplete rupture is also commonly referred to as uterine
dehiscence. As expected, morbidity and mortality rates are appreciably greater when
rupture is compleat. The greatest risk factor for either from of rupture is prior cesarean
delivery. In a review of all uterine rupture cases in Nova Scotia between 1988 and 1997,
Kieser and Baskett (2002) reported that 92 percent were in women with a prior cesarean
birth. Holmgren and associates (2012) described 42 cases of rupture in women with a
prior hysterotomy. Of these, 36 were in labor at the time of rupture.
DIAGNOSIS
Progress of labor in women attempting VBAC is similar to regular labor, and there is no
specific pattern that presages uterine rupture (Graseck, 2012 ; harper, 2012b). Before
hypovolemic shock devekops, symptoms and physical findings in women with uterine
rupture may appear bizarre unless the possibility is kept in mind. For example,
hemoperiteoneum from a ruptured uterus may result in diaphragmatic irritation with pain
referred to the chest-directing one to a diagnosis of pulmonary or amnionic fluid
embolism instead of uterine rupture. The most common sign of uterine rupture is a
nonreassuring fetal heart rate pattern with variable heart rate decelerations that may
evolve into late decelerations and bradycardia as shown in Figure 31-4 (American
Academy of Pediatrics and American Colege of Obstetricians and Gynecologists, 2012).
In 36 cases of such rupture during a trial of labor, there were fetal signs in 24, maternal in
eight, and both in three (Holmgren, 2012). Few women experience cessation of
contractions following uterine rupture, and the use of intrauterine pressure catheters has
not been shown to assist reliably in the diagnosis (Rodriguez, 1989).
In some women, the appeatance of uterine rupture is indentical to that of placental
abruption. In most, however, the is remarkably little appreciable pain or tenderness. Also,
because most women in labor are treated for discomfort with either narcotics or epidural

analgesia, pain and tenderness may not be readily apparent. The condition usually
becomes evident bacause of fetal distress sign and occasionally because of maternal
hypovolemia from concealed hemorrhage.
If the fetal presenting part has entered the pelvis with labor, loss of station may be
detected by pelvic examination. If the fetus is pattly or totally extruded from the uterine
rupture site, abdominal palpation or vaginal examination may be helpful to identify the
presenting part, which will have moved away from the pelvic inlet. A firm contracted
uterus may at times be felt alongside the fetus.
DECISION-TO-DELIVERY TIME
With rupture and expulsion of the fetus into the peritoneal cavity, the chances for
intact fetal survival are dismal, and reported mortality rates range from 50 to 75 percent.
Fetal condition depends on the degree to which the placental implantation remains
intact, although this can change within minutes.With rupture the only chance of fetal
survival is afforded by immediate delivery-most often by laparotomy-otherwisse, hypoxia
is inevitable. If rupture is followed by immediate total placental separation, then very few
intact fetuses will be salvaged. Thus, even in the best of circumstnces, fetal salvage will
be impaired. The Utah experiences are instructive here (Holmgren, 2012).
Of the 35 laboring patients with a uterine rupture, the decision-to-delivery time was
< 18 minutes in 17, and none of these infants had an adverse neurological outcome. Of
the 18 born > 18 minutes from decision time, the three infants with long-term
neurological impairments were delivered at 31,40, and 42 minutes. There were no deaths,
thus severe neonatal neurological morbidity developed in 8 percent of these 35 women
with uterine rupture.
In a study using the Swedish Birth Registry, Kaczmarczyk and colleagues (2007)
found that the risk of neonatal death following uterine rupture was 5 percent-a 60-fold
increase in risk compared with pregnancies not complicated by uterine ripture. In the
Network study seven of the 114 uterine rupture-6 percent-associated with a trial of labor
were complicated by the development of neonatal hypoxic ischemic encephalopathy
(Spong,2007)

Maternal deaths from rupture are uncommon, For example, of 2.5 milion women
who gave birt in Canada between 1991 and 2001, there were 1898 cases of uterine
rupture, and four of these-0.2 percent-resulted in maternal death (Wen, 2005). In other
regions of the world, however, maternal motality rates associated with uterine rupture are
much higher. In a report from rural India, for example, the maternal mortality rate
associated with uterine rupture was 30 percent (Chatterjee,2007).
HYSTERECTOMY VERSUS REPAIR
With complete rupture during a trial of labor, hysterectomy may be required. In the
reports by McMahon (1996) and Miller (1997) and their coworkers, 10 to 20 percent of
such women required hysterectomy for hemostasis. In selected cases, however, suture
repair with uterine preservation may be performed. Sheth (1968) described outcomes
from a series of 66 women in whom repair of a uterine rupture was elected rather than
hysterectomy. In 25 instances, the repair was accompanied by tubal sterilization. Thirteen
of the 41 mothers who did not have tubal sterilization had a total of 21 subsequent
pregnancies. Uterine rupture recurred in four of these-approximately 25 persent. Usta and
associates (2007) identified 37 women with a prior complete uterine rupture delivered
during a 25-year period in Lebanon. Hysterectomy was performed in 11, and in the
remaining 26 women, the rupture was repaired. Twelve if these women had 24
subsequent pregnancies, one third of which were complicated by recurrent uterine
rupture. Inanother study, however, women with a uterine dehiscence were not more likely
to have uterine rupture with a subsequent pregnancy (Baron,2013b).
COMPLICATIONS WITH MULTIPLE REPEAT CESAREAN DELIVERIES
Because of the concerns with attempting a terial of labor-even in the women with
excellent criteria that forecast succesfull VBAC-most women in the United States
Undergo elective repeat cesarean delivery. This choice in not without several significant
maternal complication, and rates of these increase inwomen who have multiple repeat
operations. The incidences of some common complications for women with one prior
transverse cesarean delivery who undergo an elective repeat cesarean delivery were show
in tabele 31-2. Finally, half of cesarean hysterectomies done at Parkland Hospital are in

women with one or more prior cesarean deliveries (Hernandez, 2013).

The Network addressed issuer of increased morbidity in a cohort 0f 30,132 women
who had from one to six repeat cesarean deliveries (Silver, 2006). This report addressed a
list of morbidities, most of which increased as a trend sith increasing number of repeat
operations. The rates of some of the more common or serious complication are depicted
in figure 31-5. In addition to the ones shown, rates of bowel or bladder injury, admission
to an intensive care unit or ventilator therapy, and maternal mortality, as well as operative
and hospitalization length, showed significantly increasing trends. Similar results have
been reported by others (Nisenblat, 2006;Usta,2005). More difficult to quantify are risks
for bowel obstructions and pelvic pain from peritoneal adhesive disease, both of which
inctease with each successive cesarean delivery (Andolf, 2010;Mankuta, 2013).
Cook and colleagues (2013) from the United Kingdom Obstertic Surveillance system
(UKOSS) described adverse sequelae of women with multiple cesarean deliveries.
Outcomes of those undergoing a fifth or greater operation were compared with those
from women having a second through fourth procedure. Those having five or more
cesarean deliveries had significantly increased rates if morbidity compared with rates in
women having fewer than five procedures. Specifically, the major hemorrhage rate
increased 18-fold; visceral damage, 17-fold; critical care admissions, 150fold; and
delivery < 37 weeks, sixfold. Much of this morbidity was in the 18 percent who had
placenta previa or accrete syndromes (Chap.41p.799). A percreta may invade the bladder
or other adjacent structures. With this, difficult resection carries an inordinately high risk
of hysterectomy, massive hemorrhage with transfusion, and maternal maotality.
STATE OF VAGINAL BIRTH AFTER CESAREAN-2014
The best answer for a given women with a prior cesarean delivery in unknown. We
agree with scott (2011) regarding a common-sense approach. Thus, the women- and her
partner if she wishes-are encouraged to actively participate with her health-care provider
in the final decision after appropriate counseling. For women who wish TOLAC despite a
factor that increases their specific risk, additions to the consent form are recommended
(American College of Obstetricians and Gynecologiss, 2013a). Bpnanno and colleagues
(2011) have provided such an example.

Williams Obstetrics 24th Edition (hal 790-793 section 11 & chapter 41)
RUPTURE OF THE UTERUS
Uterine rupture may be primary, defined as accurring in a previously intact or
unscarred unterus, or may be secondary and associated with a preexisting myometrial
incision, injury, or anomaly. Some of the etiologies associated with uterine rupture are
presented in table 41-3. Importantly, the contribution of each of these underlying causes
has changed remarkably during the ppast 50 years. Specifically, befor 1960, when the
cesarean delivery rate was much lower than it is currently and when women of great
parity were numerous, primary uterine rupture predominated. As the incidence of
cesarean delivery increased and especially as a subsequent trial of labor in these women
became prevalent through the 1990s, uterine rupture through the cesarean hysterotomy
scar became preeminent. As discussed in detail in Chapter 31 (p.17) along with
diminished enthusiasm for trial of labor in women with prior cesarean delivery, the two
types of rupture likely now have equivalent incidences. Indeed, in a 2006 study of 41
cases of uterine rupture from the Hospital Corporation of America, half were in women
with a prior cesarean delivery (Porreco,2009)
PREDISPOSING FACTORS AND CAUSES
In addition to the pprior cesarean hysterotomy incision already discussed, risk for
uterine rupture include other previous operations or manipulations thah traumatize the
muometrium. Examples are uterine curettage or perforation, endometrial ablation,
myomectomy, or hysteroscopy (Kieser, 2002; Pelosi, 1997). In the study by porreco and
colleagues (2009) cited earlier, seven of 21 women with-out a prior cesarean delivery had
undergone prior uterine surgery.
In developed countries, the incidence of rupture was cited by getahun and associates
(2012) as 1 in 4800 deliveriies. The frequency of primary rupture approximates 1 in
10,000 to 15,000 births (Miller, 1997;Porreco, 2009). One reason is a decreased incidence
of women of great parity (Maymim, 1991;Miller, 1997). Another is that excessive or
inappropriate unterine stimulation eith oxytocin-previously a frequent cause-has mostly
disappeared. Anecdotally, however, we have encountered primary unterine rupture in a
disparate number of women in whom labor was induced with prostaglandin E1.

PATHOGENESIS
Rupture of the previously intact uterus during labor most often involver the thinnedout lower uterine segment. When the rent is in the immediate vicinity of the cervix, it
freequently extends trensversely or obliquely. Where the rent is in the portion of the
uterus adjacent to the broad ligament, the tear is usually longitudinal. Although these
rears develop primarily in the lower uterine segment, it is not unusual for them to extend
upward into the active segment or downward through the cervix and into the vagina
(fig.41-13). In some cases, the bladder may also be lacerated (Rachagan, 1991). If the
rupture is of sufficient size, the uterine contents will usually escape into the peritoneal
cavity. If the presenting fetal part is firmly engaged, however, then only a portition of the
fetus may be extruded from the uterus. Fetal prognosis is largely dependent on the degree
of placental separation and magnitude of maternal hemorrhage and hypovolemia. In some
cases, the overlying peritoneum remains intact, and this usually is accompanied by
hemorrhage that extends into the broad ligment to cause a large retroperitoneal hematoma
with extensive blood loss.
Occasionally, there is an inherent weakness in the myomatrium in which the rupture
takes place. Some examples include anatomical anomaalies, adenomyosis, and
connectivetissue defects such as Ehlers-Danlos syndrome (Arici, 2013;Nikolaou, 2013)
MANAGEMENT AND OUTCOMES
The varied clinical presentations of uterine rupture and its management are discussed
in detail in chapter 31 (p.617).
In the recent maternal mortality statistics from the centers for Disease Control and
Prevention, uterine rupture accounted for 14 of deaths caused by hemorrhage (Berg,
2010). Maternal morbidity includes hysterectomy that may be necessary to control
hemorrhage. There is also considerably increased perinatal morbidity and mortality
associated with uterine rupture. A major concern is that surviving infants develop severe
neurological impairment (Porreco, 2009).

TRAUMATIC UTERINE RUPTURE

Although the distended pregnant uterus is surprisingly resistant to blunt trauma,
pregnant women sustaining such trauma to the abdomen should be watched carefully, for
sign of a ruptured uterus (Chap.47, p.954). Even so, blunt trauma is more likely to cause
placental abruption as described subsequently. In a study by miller and paul (1996),
trauma accounted for only three cases of uterine rupture in more than 150 women. Other
causes of traumatic rupture that are uncommon today are those due to internal podalic
version and extraction, difficult forceps delivery, breech extraction, and unsual fetal
enlrgement such as with hydrocephaly.
TABLE 41-3. Some causes of Uterine Rupture
Preexisting Uterine Injury or Anomaly
Surgery involving the myometrium :
Cesarean delivery or hysterotomy
Previously repaired uterine rupture
Myomectomy incision through or the endometrium
Deep cornual resection of interstitial fallopian tube
Metroplasty
Coincidental uterine trauma :
Abortion with instrumentation-sharp or suction
curette, sounds
Sharp or blunt trauma-assaults, vehicular accidents,
bullets,knives
Silent rupture in previous pregnancy
Congenital :
Pregnancy in undeveloped uterine horn
Defective tissue-Marfan or Ehlers-Danlos Syndrome

Uterine injury or Abnormality incurred in current

Pregnancy
Before delivery :
Persistent, Intense, Spontaneous contractions
Labor stimulation-oxytocin or prostaglandins
Intraamnionic instillation-saline or prostaglandins
Perforation by internal uterine pressure catheter
External trauma-sharp or blunt
External Version
Uterine overdistention-hydramnios, multifetal pregnancy
During delivery :
Internal version second twin
Difficult forceps delivery
Rapid tumultuous labor and delivery
Breech extraction
Fetal anomaly distending lower segment
Vigorous uterine pressure during delivery
Difficult manual removal of placenta
Acquired :
Placental accrete syndromes
Gestational trophoblastic neoplasia
Adenomyosis
Sacculation of entrapped retroverted uterus

REFERENCES
Williams Obstetrics /(edited bay) F.Gary Cunningham, Kenneth J.Leveno, Steven L.
Bloom, Catherine Y. Spong, Jodi S. Dashe, Barbara L. Hoffman, Brian M.Casey,
Jeanne S. Sheffied.-24 th edition. hal 617 Chapter 31 & hal 790-793 section 11 &
chapter 41, 2014)

TABEL 31-4 Some Recommendations of Professional Sucieties Concerning a trial af labor to Attempt VBAC
American College of

Counseling
Offter to most women with one

Facilities
Safest with ability for

Other
Not precluded; twins,

obstetricians and Gynecologist

prior low-transverse incision;

immediate cesrean delivery;

macrosomia, prior lowvertical

(2013a)

consider for two prior low-

patients should be allowed to

or unknown type of incision

tranverse incisions

accept increased risk when not

available

Society of

Offer to women with one prior

Should deliver in hospital in

Obstetricians and gynaeclogists

transverse low-segment cesarean

which timely cesarean delivery induction safe, but

of canada (2005)

delivery; with>1 prior CD then

is available; approximate

prostaglandins should not be

VBAC likely successful but

timeframe o 30 minutes

used;macrosomia, diabetes,

increased risks

Oxytocin or foley catheter

postterm pregnancy, twins are

not contraindications

Royal College of Obstetricians

Discuss VBAC option with women

Suitable delivery suite with

Caution with twins and

and Gynaecologists (2007)

with prior low-segment cesarean

continuous care and

macrosomia

delivery; decision between

monitoring;immediate

obstetrician and patient

CD = cesarean delivery;VBAC= Vaginal birth after cesarean.

cesarean delivery capability

Berief synopses of professional society guidelines are shown in table 31-4. Guidelines that tend to be more conservative are show
in table 31-5.
TABLE 31-5. Conservative Guidelines to approach a trial of labor following cesarean delivery
Follow ACOG practice guidelines
Education and counseling
Preconceptionally
Provide ACOG patient pamphlet
Early during prenatal care
Develop preliminary plan
Revisit at least each trimester
Be willing to alter decision
Have facilities availability
Risk assessment
Review previous operative note (s)
Review relative and absolute contraindications
Reconside risk as pregnancy progresses
Tread carefully : > 1 prior transverse CD, unknown incision, twins, macrosomia
Labor and delivery
Cautions for induction-unfavorable cervix, high station
Consider AROM
Avoid prostaglandins
Respect oxytocin-know when to quit
Beware of abnormal labor progress
Respect EFM pattern abnormalities
Know when to abandon a trial of labor
ACOG = American College of Obstetricians and Gynecologists; AROM = artificial rupture of membranes; CD= Cesarean Delivery ;
EFM = eleectronic fetal monitoring.

Williams Obstetrics 24th Edition (hal 491-500 chapter 24)

FETAL DISTRESS
The terms fetal distress and birth asphyxia are to broad and vague to be applied
with any precision to clinical situations ( American collage of obstetricians and
gynecologists, 2005). Uncertainty regarding the diagnosis based on interpretation of
fetal hearth rate patterns has given rise to descriptions such as reassuring or non
rearssuring. The terms reassuring suggests a restoration of confidence by particular
pattern, whereas nonreassuring suggests inability to remove doubt. These patterns
during labor are dynamic they can rapidly change from reassuring to nonreassuring
and viceversa. In this situation, obstetrician lose confidence or cannot assuage doubts
about fetal condition. These assessments are subjective clinical judgments that are
inevitably subject to imperfection and must be recognized as such.
Pathophysiology
Why is the diagnosis of fetal distress based on hearth rate patterns so tenuous?
One explanation, is that these patterns are more a reflection of fetal physiology than of
pathology. Physiological control of hearth rate includes various interconnected
mechanisms that depend on blood flow ande oxygenation. Moreover, the activity of
these control mecanisms influenced by the preexisting state of fetal oxygenation, for
example, as seen with chronic plasental insufficiency. Importantly, the fetus is
tethered by an umbilical cord, whereby blood flow is constanly in jeopardy.
Moreover, normar labor is a process of increasing acidemia ( rogers 1968). Thus,
normal labor is a process of repeated fetal hypoxic events resulting inevitably in
academia.
Put another way, and assuming that asphyxia can be defined hypoxia leading to
acidemia, normal parturition is an as phyxiating event for the fetus.
Diagnosis
Because of the above uncertainties it follows that identifications of fetal
distress based on fetal heart rate patterns is imprecise and controversial. It is well
known that experts in interpretations of these patterns of ten dissagre with each order.
In fact, parer (1997), a strong advocate of electronic fetal heart rate monitoring and an
organizer of the 1997 NICHD fetal monitoring workshop, light heartedly compared

the experts in attendance to marine iguanas of the Galapagos Islands, to wit: all on
the same beach but facing different direntions and spitting at one another constantly!
Ayres-de-Campos and colleagues (1999) investigated interobserver agreement of
fetal heart rate pattern interpretation and found that agreement or conversely,
disagreementwas related to whether the pattern was normal, suspicious, or
pathological. Specifically, experts agreed on 62 percent of normal patterns, 42 percent
of suspicious patterns, and only 25 percent of pathological pattens. Keith and
coworkers (1995) asked each of 17 experts to review 50 tracings on two occasions, at
least 1 month apart. Approximately 20 percent changed their own interpratations, and
approximately 25 percent did not agree with the interpretations of their collagues. And
although Murphy and associates (2003) conclude that at least part of the interpretation
problem is due to a lack of formalized education in America training program, this is
obviously only on a small modifier. Put another way, how can the teacher enlighten
the student if the teacher is uncertain?
National Institutes of Healt Workshops Three-Tier Classification System
The NICHD (1997) held a succession of workshops in 1995 and 1996 to develop
standardized and unambiguous defitions of fetal heart rate (FHR) tarcings and
published recommendations for interpreting these patterns. In 2008, a second
workshops was convened to reevaluate the 1997 recommendations and to clarify
terminology (see table 24-1) (Macones,2008). A major result was the recommendation
of a three-tier system for classification of FHR patterns (table 24-2). The American
College of Obstetricians and Gynecologist (2013b) subsequently recommended use of
this tiered system.
A few studies have been done to assets the three-tiered systems. Jackson and
cowokers (2011) studied 48,444 women in labor and found that category I (normal
FHR) patterns were observed during labor in 99.5 percent of tracings. Category II
(indeterminate FHR) patterns were found in 84.1 percent of tracings, and category III
(abnormal FHR) patterns were seen in 0.1 percent (54 women). Most 84 percent of
women had a mix of categories during labor. Cahill and colleagues (2012)
retrospectively studied the incidence of umbilical cord academia (Ph 7.10)
correlated with fetal heart rate characteristics during the 30 minutes preceding
delivery. None of the three categories demonstrated a significant association with cord
blood academia. The American College of Obstetricians and Gynecologist and the

American Academy of Pediatrics (2014) concluded that a category I or II tracing with

a 5-minutes Apgar score > 7 or normal arterial blodd acid-base values was not
consistent with an acute hypoxic-ischemic event.
Sholapurkar (2012) also challenged the validity of the three tier system because
most abnormal fetal rate patterns fall into the inderterminate category II, that is, one
for which no definite management recommendations can be made. It was further
suggested that this resulted from most fetal heart rate decelerations being
inappropriately classified as variable decelerations due to cord compression.
Paree and King (2010) compared the current situation in the United States with
that of other countries in which a consensus on classification and management has
been reached by a number of professional societies. Some of these include the Royal
College of Obstetricians and Gynecologist, the Society of Obstetricians and
Gynecologists of Canada, the Royal Australian and New Zealand College of
Obstetricians and Gynecologists and the Japan Society of Obstetricians and
Gynecology. Parer and King (2010) further comment that the NICHD three-tier
system is inadfequate because category IIinderteminate FHRconsist of a vast
heterogenous mixture of patterns that prevent development of a management
strategy. Peter and Ikeda (2007) had previously proposed a color-coded five-tier
system for both FHR interpretation and management. There have been two reports
comparing the five-tier and three-tier systems. Bannerman and associates (2011)
found that the two system were similar in fetal heart rate interpretations for tracing
that were either very normal or very abnormal. Coletta and cowokers (2012) found
that the five-tier system had better sensitivity than the three-tier system. It is apparent
that, after 50 years of continuous electronic fetal heart rate monitoring use, there is not
a consensus on interpretation and management recommendations for FHR patterns
(Parer,2011).
Table 24.2 Three-tier fetal heart rate interpretation system
Category I-NORMAL
Include all of the following:
Baseline rate : 110 160 bpm
Baseline FHR variability : moderate
Late or variable decelerations : absent
Early decelerations : present or absent
Accelerations : present or absent

Category II INDETERMINATE
Include all FHR tracings not categorized as category I or III.
Category II tracings may represent an appreciable fraction of those encountered in
clinical care. Examples include any of the following:
Baseline rate
Bradycardia not accompanied by absent baseline variability
Tachycardia
Baseline FHR VARIABILITY
Minimal baseline variability
Absent baseline variability not accompanied by recurrent decelerations
Marked baseline variability
ACCELETATIONS
Absence of induced accelerations after fetal stimulation periodic or episodic
decelerations
Recurrent variable decelerations accompanied by minimal moderate baseline
variability
Prolonged deceleration min 2 but < 10 min
Recurrent late decelerations with moderate baseline variability
Variable decelerations with other characterististic, such as slow return to
baseline, overshoot, or shoulders
Category III
Include either :
Absent baseline FHR variability and any of the following recurrent late
decelerations, recurrent variable decelerations, bradycardia
Sinuisoidal pattern
Bpm = beats per minute ; FHR = fetal heart rate
From Macones, 2008, with permission
Meconium in the amniotic fluid
Obstetrical teaching throughout the past century has included the concept that
meconium passage is a potential warning of fetal asphyxia. In 1903, J. Whitridge
Williams observed and attributed meconium passage to relaxation of the sphincter
ani muscle induced by faulty aeration of the (fetal) blood. Even so, obstetricians have
also long realized that the detection of meconium during labor is problematic in the
prediction of fetal distress or asphyxia. In their review, Katz and Bowes (1992)
emphasized the prognostic uncertainty of meconium by referring to the topic as a
murky subject. Indeed, although 12 tp 22 percent of labors are complicated by
meconium, only a few are linked to infant mortality. In an investigation from Parkland

Hospital, meconium was found to be a low-risk obstetrical hazard because the

perinatal mortality rate attribubutable to meconium was I death per 1000 live births
(Nathan,1994)
The theories have been suggested to explain fetal passage of meconium and in
part may explain the tenuous conection between its detection and infant mortality.
First, the phatological explanation proposes that fetuses pass meconium in response to
hypoxia and that meconium therefore signals fetal crompomise (walker, 1953)
Second, the physiological explanation is that in utero passage of meconium represents
normal gastrointestinal tract maturation under neural control (Mathews, 1979). A final
theory posits that meconium passage follows vagal stimulation from common but
transient umbilical cord entrapment with resultant increased bowel peristalsis
(Hon,1961). Thus, meconium release may represent physiological processes.
Ramin and associates (1996) studied almost 8000 pregnancies with meconium
stained amniotic fluid delivered at Parkland Hospital. Meconium aspiration ayndrome
was significantly associated with fetal academia at birth. Other significant correlates
of aspiration included cesarean delivery, forceps to expedite delivery, intrapartum
heart rate abnormalities, depressed apgar scores, and need for assisted ventilation at
delivery. Analysis of the type of fetal academia based on umbilical blood gases
suggested that the fetal compromise associated with meconium aspiration syndrome
was an acute event. This is because most academic fetuses had abnormally increased
PCO2 values rather than a pure metabolic academia.
Dawes and coworkers (1972) observed that such hypercarbia in fetal lambs
induces gasping and resultant increased amnionis fluid inhalation. Jovanovic and
Nguyen (1989) observed that meconium gasped into the fetal lungs caused aspiration
syndrome only in asphyxiated animals. Ramin and colleagues (1996) hypothesized
that the pathophysiology of meconium aspiration syndrome includes, but is not
limited to, fetal hypercarbia, which stimulates fetal respiration leading to aspiration of
meconium into alveoli. Lung parenchymal injury is secondary to academia induced
alveolar cell damage. In this phatophysiological scenario, meconium in amniotic fluid
is a fetal environmental hazard rather than a marker of preexistent compromise. This
proposed pathophysiological sequence is not all inclusive, because is does not account
for approximately half of the cases of meconium aspiration syndrome in which the
fetus was not academic at birth.
Thus, it was concluded that the high incidence of meconium observed in the

amniotic fluid during labor often represents fetal passage of gastrointestinal contents
in conjunction with normal physiological processes. Althougth normal, such
meconium becomes an environmental hazard when fetal academia supervenes.
Importantly, such academia occurs acutely, and therefore meconium aspiration is
unpredictable and likely unpreventable. Moreover, Greenwood and colleagues (2003)
showed that clear amniotic fluid was also a poor predictor. In a prospective study of
8394 women with clear amniotic fluid, they found that clear fluid was an unreliable
sign of fetal well-being.
Growing evidence indicates that many infants with meconium aspiration
syndrome have suffered chronic hypoxia before birth (Ghidini,2001). Blackwell and
associates (2001) found that 60% of infants diagnosed with meconium aspiration
syndrome had umbilical artery blood PH 7,20, implying that the syndrome was
unrelated to the neonatal condition at delivery. Similary, markers of cronic hypoxia,
such as fetal arythropoietin levels and nucleated red blood cell counts in newborn
infants, suggest that chronic hypoxia is involved in many meconium aspiration
syondrome case (Dollberg, 2001: Jazayeri,2000)
In the recent past, routine obstetrical management of a newborn with meconiumstained amniotic fluid included intrapartum suctioning of the oropharynx and
nasopharynx. Guidelines from the American Academia of Pediatric and the American
College of Obstetricians and Gynecologists, however, recommend that such infants no
longer routinely receive intrapartum suctioning because it does not prevent meconium
aspiration syndrome (Peelman,2010). As discusses in chapter 32 (626), if the infant is
depressed, the trachea is intubated, and meconium suctioned from beneath the glottis.
If the newborn is vigorous, defined as having strong respiratory efforts, good muscle
tone, and a heart rate > 100 bpm, then tracheal suction is not necessary and may injure
the vocal cords.
MANAGEMENT OPTIONS
The principal management options for significantly variable fetal heart rate
patterns consist of correcting any fetal insult, if possible. Measure suggested by the
American Collage of Obstetritians and Gynecologists (2013b,c) are listed in table 243. Moving the mother to the lateral position, correcting maternal hypotension caused
by regional analgesia, and discontinuing oxytocin serve to improve uteroplasental
paerfusion. Examination is done to exclude prolapsed cord or impending delivery.

Simpson and james (2005) assessed benefits of three maneuvers in 52 women with
fetal oxygen saturation sensors already in place. The used intravenous hydration 500
to 1000 ml of lactated Ringer solution given over 20 minutes : lateral versus supine
position : and using a nonrebreathing mask that administered supplemental oxygen at
10 L/min. Each of these maneuvers significantly increased fetal oxygen saturation
levels, although the increments were small.
TOCOLYSIS
A single intravenous or subcutaneous injection of 0,25 mg of terbutaline sulfate
given to relax the uterus has been described as a temporizing maneuver in the
management of nonreassuring fetal heart rate patterns during labor. The rationale is
that inhibition of uterine contractions might improve fetal oxygenation, thus achieving
in utero resuscitation. Cook and spinnato (1994) described their experience during 10
years with tertabuline tocolysis for fetal resuscitation in 368 pregnancies. Such
resuscitation improved fetal scalp blood pH values, although all fetuses underwent
cesarean delivery. These investigators concluded that although the studies were small
and rarely randomized, most reported favorable results with terbutaline tocolysis for
nonreasuring patterns. Small intravenous doses of nitroglycerin 60 to 180 g also
have been reported to be beneficial ( mercier, 1997). The American Collage of
Obstetricians and Gyneclologist (2013b) has concluded that there is insufficient
evidence to recommend tocolysis for noreassuring fetal heart rate patterns.
AMNIOINFUSION
Gabbe and coworkers (1976) showed in monkeys that removal of amniotic fluid
produced variable decelerations and that decelerations and that replenishment of fluid
with saline reliaeved the decelerations. Miyazaki and taylor (1983) infused saline
through an intrauterine pressure catcheter in laboring women who had either variable
decelerations or prolonged decelarations attributed to cord entrapment. Such therapy
improved the harth rate pattern in half of the women who had either variable
decelerations or prolonged decelerations attributed to cord entrapment. Such theraphy
improved the heart rate pattern in half of the women studied. Later, Miyazaki and
Nevarez (1985) randomly assigned 96 nulliparous women in labor with cord
compression patterns and found that those who werw treated with amnioinfusion
required cesarean delivery for fetal distress less often.

Based on many of these early reports, transvaginal amnioinfusion has been

extended into three clinical areas. These include : (1) treatment of variable or
prolonged decelerations, (2) prophylaxis for women with oligohydramnions, as with
prolonged ruptured membranes, and (3) attempts to dilute or wash out thick
meconium (Chap.33,p.638)
Many different amnioinfusion protocols have been reported, but most include a
500 to 800 Ml bolus of warmed normal saline followed by a continuous infusion of
a approximately 3 Ml per minute (Owen, 1990 :Pressman, 1996). In another study,
Rinehart and colleagues (2000) randomly gave a 500 Ml bolus of normal saline at
room temperature alone or 500 Ml bolus plus continuous infusion of 3 Ml per minute.
Their study included 65 women with variable decelerations, and the investigators
found neither method to be superior. Wenstrom and associates (1995) surveyed use of
amnioinfusion in teaching hospitals in the 186 centers surveyed, and it was estimated
that 3 to 4 percent of all women delivered at these centers received such infusion.
Potential complications of amnioinfusion are summarized in table 24-4.
Table 24-4 Complications Associated With Amnioinfusion Form a Survey of 186
Obstetrical Units.
COMPLICATION
Uterine hypertonus
Abnormal fetal heart rate tracing
Chorioamnionitis
Cord prolapse
Uterine rupture
Maternal cardiac or respiratory compromise
Placental abruption
Maternal death
Adapted from Wenstrom, 1995

CENTERS No.(%)
27 (14)
17 (9)
7 (4)
5(2)
4(2)
3(2)
2(1)
2(1)

PROPHYLACTIC AMNIOINFUSION FOR VARIABLE DECELERATIONS

Hofmeyr and Lawrie (2012) used the Cochrane Database to specifically analyze
the effects of amnioinfusion in the management of fetal heart rate patterns associated
with umbilical cord compression. Nineteen suitable studies were identified, most with
fewer than 200 participans. It was concluded that amnioinfusion appeared to be
usefull in reducing the occurrence of variable decelerations, improving neonatal
outcome, and reducing cesarean delivery rates. The American College of Obstetricians

and Gynecologists (2013a) recommends considerations of amnioinfusion with

persistent variable decelerations.
PROPHYLACTIC AMNIOINFUSION FOR OLIOGOHYDRAMNIOS
Amnioinfusion in women with oligohydramnios has been used prophylactically
to avoid intrapartum fetal heart rate pattern from cord occlusion. Nageotte and
cowokers (1991) found that this resulted in significantly decreased frequency and
severity of variable decelarations in labor. Howefer, the cesarean delivery rate or
condition of term infants was not improved. In a randomized investigation, Macri and
colleagues (1992) studied prophylactic amnioinfusion in 170 term and postterm
pregnancies

complicated

by

both

thick

meconium

and

oligohydramnios.

Amnioinfusion significantly reduced cesarean delivery rates for fetal distress and
meconium aspiration syndrome. In contrast, Ogundipe and associates (1994)
randomly assigned 116 term pregnancies with an amnionic fluid index < 5 cm to
receive prophylactic amnioinfusion or standard obstetrical care. There were no
significant differences in overall cesarean delivery rates, delivery rates for fetal
distress, or umbilical cord acid base studies.
AMNIOINFUSION FOR MECONICUM STAINED AMNIONIC FLUID
Pierce and associates (2000) summarized the result of 13 prospective trials of
intrapartum amnioinfusion in 1924 women with moderate to thick meconium-stained
fluid. Infants born to women treated by amnioinfusion were significantly less likely to
have meconium below the vocal cords and were lesslikely to develop meconium
aspiration syndrome than infants born to women not undergoing amnioinfusion. The
cesarean delivery rate was also lower in the amnioinfusion goup. Similar result were
reported by Rathore and cowokers (2002). In contrast, several investigators were not
supportive of amnioinfusion for meconium staining. For example, Usta and associates
(1995) reported that amnioinfusion was not feasible in half of women with moderate
or thick meconium who were randomized to this treatment. These investigators were
unable to demonstrate any improvement in neonatal outcomes. Spong and cowokers
(1994) also concluded that although prophylactic amnioinfusion did dilute meconium,
it did not improve perinatal outcome. Last, Fraser and colleagues (2005) randomized
amnioinfusion in 1998 women with thick meconium staining of the amnionic fluid in
labor and found no benefits. Because of these findings, the Americans College of

Obstetricians and Gynecolists (2012a,2013c) does not recommended amnioinfusion to

dilute meconium-stained amnionic fluid. According to Xu and cowokers (2007), in
areas lacking continuous monitoring, amnioinfusion may be used to lower the
incidence of meconium aspiration syndrome.
FETAL HEART RATE PATTERNS AND BRAIN DAMAGE
Attemps to correlate fetal heart rate patterns with brain damge have been based
primarily on studies of infants identified as a result of medicolegal actions. Phelan and
Ahn (1994) reported that among 48 fetuses later found to be neurologically impaired,
a persistent nonreactive fetal heart rate tracing was already present at the time of
admission in 70 percent. They concluded that fetal neurological injury occurred
predominately before arrival to the hospital. When they looked retrospectively at heart
rate patterns in 209 brain-damaged infants, they concluded that there was not a single
unique pattern associated with fetal neurological injury (Ahn, 1996). Graham and
associated (2006) reviewed the world literature published between 1966 and 2006 on
the effect of fetal heart rate monitoring to prevent perinatal brain injury and found no
benefit.
EXPERIMENTAL EVIDENCE
Fetal heart rate patterns necessary for perinatal brain damage have been studied in
experimental animals. Myers (1972) describe the effects of complete and partial
asphyxia. Complete asphyxia was produced by total occlusion of umbilical blood flow
that led to prolonged deceleration (fig. 24-31). Fetal arterial Ph did not drop to 7.0
until approximately 8minutes after complete cessation of oxygenation and umbilical
flow. At least 10 minutes of such prolonged deceleration was required before these
was evidence of brain damage in surviving fetuses.
Myers (1972) also produced partial asphyxia in rhesus monkeys by impeding
maternal aortic blood flow. This resulted in late decelerations due to uterine and
placental hypoperfusion. He observed that several hours of these late decelerations did
not damage the fetal brain unless the Ph fell bellow 7.0. Inded, Adamsons and Myers
(1977) reported subsequently that late decelerations were a marker of partial asphyxia
long before brain damage occurred.
The most common fetal heart rate pattern during labordue to umbilical cord

occlusionrequires considerable time to significantly affect the fetus in experimental

animals. Clapp and colleagues (1988) partially occluded the umbilical cord for 1
minutes every 3 minutes in fetal sheep. Rocha and associates (2004) totally occluded
the umbilical cord for 90 seconds every 30 minutes for 3 to 5 hours a day for 4 days
without producing necrotic brain cell injury. Result form such studies suggest that the
effects of umbilical cord entrapment depend on the degree occlusion partial versus
total, the duration of individual occlusion, and the frequency of such occlusion.
HUMAN EVINDENCE
The contribution of intrapartum events to subsequent neurological handicaps has
been greatly overestimated, as discussed in further detail in Chapter 33 (p.368). It is
clear that for brain damage to occur, the exposed to much than a brief periode of
hypoxia. Moreover, the hypoxia must cause profound, just barely sublethal metabolic
academia. Because of this, the American College of Obstetricians and Gynecologists
(2012b) recommends umbilical cord blood gases be obtained whenever there is
cesarean delivery for fetal compromise, a law 5 minutes Apgar score, severe fetalgrowth restriction, an abnormal fetal heart rate tracing, maternal thyroid disease, or
multifetal gestation (chap. 32,p628). Fetal heart rate patterns consistent with these
sublethal conditions are fortunately rare.
BENEFITS F ELECTRONIC FETAL HEART RATE MONITORING
In perinatal outcome with electronic monitoring. One assumption is that fetal distress
is a slowly developing phenomenon and that electronic monitoring permits early
detection of the compromised fetus. This assumption is illogiocalthat is, how can
all fetuses die slowly? Another presumption is that all fetal damage develops in the
hospital. Within the past 20 years, attention has been focused on the reality that most
damaged fetuses suffered insults before arrival at labor units. The very term fetal
monitor implies that this inanimate technology in some fashion monitors. The
assumption is made that if a dead or damaged infant is delivered, the tracing strip
must provide some clue, because this device was monitoring fetal condition. All of
these assumptions led to great expetations and fostered the belief that all neonatal
deaths or injuries were preventable.
By the end of the 1970s, question regarding the efficacy, safety, and costs of

electronic monitoring were being voiced from the Office OF Technology Assesment,
the United States Congress, and the Centers for Disease Control and Prevention.
Banta and Thacker (2002) reviewed 25 years of the controversy on the benefits, or
lack thereof, of electronic fetal monitoring. Using the Cochrane Database, Alfirevic
and colleagues (2013) reviewed 13 randomized trials involving more than 37,000
women. They concluded that electronic fetal monitoring in increased the rate of
cesarean and operative vaginal deliveries but produced no declines in rates of
perinatal mortality, neonatal, seizures, or cerebral palsy. Grimes and Peipert (2010)
wrote a Current Commentary on electronic fetal monitoring in Obstetrics and
Gynecology. They summarized that such monitoring, althought it has been used in 85
percent of the almost 4 million annual births in the United States, has failed as a
public health screening program. They noted that the positive predictive value of
electronic fetal monitoring for fetal death in labor or cerebral palsy is near zero
meaning that almost every positive test result is wrong.
There have been two recent attempts to study the epidemiological effect of fetal
monitoring in the United States, each using national vital statistics of births linked to
infant deaths. Chen and cowokers (2011) used 2004 data on 1,732,211 singleton live
births, 89 percent of which underwent electronic fetal monitoring. They reported that
monitoring increased operative delivery rates but decrease early neonatal mortality
rates. This benefits was gestational age dependent, however, and the highest impact
was seen in peterm fetuses. Most recently, Ananth and colleagues (2013) reported a
similar but larger epidemiological study using United States birth certificate data
linked with infant death certificate. They studied 57,983,256 nonanomalous singleton
livebirths born between 1990 and 2004. The temporal increase in fetal monitoring use
between 1990 and 2004 was associated with a decline in neonatal mortality rates,
especially in peterm gestations. In an accompanying editorial, Resnik (2013)
cautioned that an eoidemiological association between fetal monitoring and reduced
neonatal death does not establish causation. He suggested that the limitations of the
study by Ananth should make the reader skeptical of the findings. He opined that
the electronical fetal monitoring debate oes on . . . and on . . . and on. And it does
indeed.

PARKLAND HOSPITAL EXPERIENCE: SELECTIVE VERSUS UNIVERSAL

MONITORING
In july 1982, an investigation began at Parkland Hospital to ascertain whether all
women in labor should undergo electronic monitoring (Levono, 1986). In alternating
months, universal electronic monitoring was rotated with selective heart rate mo
nitoring, which was the prevailing practice. During the 3 years investigation, 17, 410
labor were managed using universal electronic monitoring, and these outcomes were
compared with a similar-sized cohort of women selectively monitored electronically.
No significant differences were found in any perinatal outcomes. There was a small
but significant increase in the cesarean delivery rate for fetal distress associated with
universal monitoring. Thus increase application of electronic monitoring at parklamd
hospital did not improve perinatal results, but it slightly increased the frequency of
cesarean delivery for fetal distress.
CURRENT RECOMMENDATIONS
The methods most commonly used for intrapartum fetal heart monitoring include
auscultation with a fetal stethoscope or a Doppler ultrasound device, or continuous
electronic monitoring of the heart and uterine contractions. No scientific evidence has
identified the most effective method, including the frequency or duration of fetal
surveillance that ensures optimum result. Summarized in Table 24-5 are the
recommendations of the America Academy of Pediatrics and the American College of
obstetricians and Gynecologists (2012). Intermittent auscultation or continuous
electronic monitoring is considered an acceptable method of intrapartum surveillance
in both low- and high- risk pregnancies. The recommended interval between checking
the heart rate, however, is longer in the uncomplicated pregnancy. When auscultation
and for 60 seconds. It also recommended that a 1-to1 nurse-patient ratio be used if
auscultation is employed. The position taken by the American College of
Obstetricians and Gynecologists (2013b) in their Practice Bulletin, however, is
somewhat different. While acknowledging that the available data do not show a clear
benefit for the use of electronic monitoring over intermittent auscultation, the
commite recommends limiting use of auscultation to low risk pregnancies and further
recommends recording the fetal heart rate every 15 minutes in active first stage labor
and every 5 minutes in the second stage.
Surveillance

Low risk pregnancies

High risk pregnancies

Acceptable methods
Intermitten auscultation

Yes

Yes a

Continuous electronic

Yes

Yes b

First-stage labor (active)

30 min

15 min a,b

Second-stage labor

15 min

5 min a,c

monitoring (internal or
external)
Evaluation intervals

a- preduring, ferably before, and after a uterine contraction.

b- includes tracing evaluation and charting at least every 15 min
c- tracing should be evaluated at least every 5 min
form the American Academy of Pediatrics and the American Collage of Obtetricians
and gynecologist, 2012.
INTRAPARTUM SURVEILLANCE OF UTERINE ACTIVITY
Analysis of electronically measured uterine activity permits some generalities
concerning the relationship of certain contraction patterns to labor outcome. There is
considerable normal variation, however, and caution must be exercised before judging
true labor or its absence solely from a monitor tracing. Uterine muscle effiociency to
effect delivery varies greatly. To use an analogy, 100-meter sprinters all have the same
muscle groups yet cross the finish line at different times.
INTERNAL UTERINE PRESSURE MONITORING
Amniotic fluid pressure is measured between and during contraction by a fluid
filled plastic catheter with its distal tiplocated above the presenting part (Fig.24-32).
The chateter is connected to a strain gauge pressure sensor adjusted to the same
level as the chateter tip in uterus. The amplified electrical signal produced in the strain
gauge by variation in pressure within the fluid system is recored on a calibrated
moving paper strip simultaneously with the fetal heart rate recording ( see fig.24-6).
Intrauterine pressure chateters are now avaible that have the pressure sensor in the
chatete tip, which obviates the need for the fluid column.
EXTERNAL MONITORING
Uterine contraction can be measured by a displacement transducer in which the

transducer button, or : plunger, is held against the abdominal wall. As the uterus
contracts, the button moves in proportion to the strength of the contraction. This
movement is convered into a measurable electrical signal that indicated the relative
intensity of the contraction. It has generally been accepted to not give an accurate
measure of intensity. Bakker and associates (2010) performed a randomized trial
comparing internal versus external monitoring of uterine contractions in 1456 women.
The two methods were equivalent in terms of operative deliveries and neonatal
outcomes.
PATTERNS OF UTERINE ACTIVITY
Caldeyro-barcia and Poseiro (1960), from Montevideo, Uruguay, were pioneers
who have done much to elucidate the pattern of spontaneous uterine activity
throughout pregnancy. Contractile waves of uterine activity werw usually measured
using intraamniotic pressure catheters. But early in their studies, as many four
simultaneous intramiometrial microballons were also used to record uterine pressure.
These investigators also introduced the concept of Montevideo units to define uterine
activity (Chap 23,p: 458). By this definition, uterine performance is the product of the
intensity increased uterine pressure above baseline tone of a contraction in mmHg
multiplied by contraction frequency per 10 minutes. For example, three contractions
in 10 minutes, each of 50 nn Hg intensity, would equal 150 Montevideo units.
During the first 30 weeks of pregnancy,uterine activity is comparatively
quiescent. Contraction are seldom greater than 20 mm Hg. And these have been
equated with those first described in 1872 by John Braxton Hicks. Uterine activity
increase gradually after 30 weeks, and it is noteworthy that these Braxton Hicks
Contractions also increase in intensity and frequency. Further increases in uterine
activity are typical of the last weeks of pregnancy, termed prelabor. During this phase.
The cervix ripens (Chap.21.P:410)
According To Caldeyro Barcia and Poseiro (1960), clinical labor usually
commences when uterine activity reaches values between 80 ande 120 Montevideo
units. This translates into approximately three contractions of 40 mm Hg every 10
minutes. Importantly, there is not clear cut division between prelabor and labor, but
rather a gradual and progressive transition.
During first-stage labor, uterine contarctions increase progressively in intensity
from approximately 25 mm Hg at commencement of labor to 50 mm Hg at the end. Et

the same time, frequency increases from there to five contractions per 10 minutes, and
uterine baseline tone from 8 to 20 mm Hg. Uterine activity further increases during
second stage labor, aided by maternal pushing. Indeed, contractions 0f 80 to 100
mmHg are typical and occur as frequently as five to six per 10 minutes. Interestingly,
the duration of uterine contractions 60 to 80 second does not increase appreciably
from early active labor through the second stage (Bakker,2007: Pontonnier,1975).
Presumably, this duration constanly serves fetal repiratory gas exchange. During a
uterine contarctions, as the intrauterine pressure exceeds that of the intervillous space,
respiratory gas exchange is halted. This leads to functional fetal :breath holding.
Which has a 60 to 80 second limit that remains relatively constant.
Caldeyro Barcia and Poseiro (1960) also observed empirically that uterine
contarctions are clinically palpable only after their intensity exceeds 10 mm Hg.
Moreover, until the intensity of contarctions reaches 40 mm Hg, the uterine wall can
readily be depressed by the finger. At greater intensity, the uterine wall then becomes
so hard that is resist easy depression. Uterine contarctions usually are not associated
with pain until their intensity exceeds 15 mm Hg, presumably because this is the
minimum pressure required for distending the lower uterine segment and serviks. It
follows that Braxton Hicks contractions exceeding 15 mm Hg may be perceived as
uncomfortable because distension of the uterus, cervix, and birth canal is generally
thought to produce discomfort.
Hendricks (1968) observed that the clinican makes great demands upon the
uterus. The uterus is expected to remain well relaxed during pregnancy, to contract
effectively but intermittently during labor, and then to remain in a state of almost
constant contaction for severa hours postpartum. Figure 24 33 demonstates an
example of normal uterine activity during labor. Uterine activity progressively and
gradually increases from prelabor through late labor. Interestingly, as shown in Figure
24 33, uterine contraction after birth are identical to those resulting in delivery of
the infant. It is there identical to those resulting in delivery of the infant. It is therefore
not suprising that the uterus that performs poorly before delivery is also prone to
atony and puerperal hemorrhage.

ORIGIN AND PROPAGATION OF CONTACTIONS

The uterus has not been studied extensively in term of its nonhormonal

physiological mechanisms of function. The normal contractile wave of labor

originates near the uterine and of one of the fallopian tubes. Thus, these areas act as
pacemakers (Fig.23-34). The right pacemaker usually predominates over the left
and starts most contractile waves. Contractions spreds from the pacemaker area
throughtout the uterus at 2 cm/sec, depolarizing the whole organ within 15 seconds.
This depolarizing wave propagates downward toward the cervik. Intensity is greatest
in the fundus, and it diminishes in the lower uterus. This phenomenon is thought to
reflect reductions in myometrial thickness from to the cervix. Presumably, this
descending gradient of pressure serves to direct fetal descent toward the cervix and to
efface the cervix. Importantly, all parts of the uterus are synchronized and reach their
peak pressure almost simultaneously, giving rise to the curvilinear waveform shown
in Figure 24-34. Young and Zhang (2004) have shown that the initiation of each
contarctions is triggered by a tissue-level bioelectric event.
The pacemaker theory also serves to explain the varying intensity of adjacent
coupled contarctions shown in panels A and B of Figure 24-33. Such coupling was
termed incoordination by Caldeyro Barcia and Poseiro (1960). A contractile wave
begins in one corneal region pacemaker, but does not synchronously depolarize the
entire uterus. As a result, another contraction begins in the contralateral pacemaker
and produces the second contractile wave of the couplet. These small contactions
alternating with larger ones appear to be typical of early labor. Indeed, labor may
progress with such uterine activity, albeit at a slower pace. These authors also
observed that labor would progress slowly if regular contractions were hypotonic
that is, contarctions with intensity less than 25 mm Hg or frequenly less than 2 per 10
minutes.
Hauth and coworkers (1986) quantified uterine contraction pressures in 109
women at term who received oxytocin for labor induction or augmentation. Most of
these women achieved 200 to effect delivery. The authors suggested that these levels
of uterine activity should be sought before consideration of cesarean delivelry for
presumed dystocia.

NEW TERMINOLOGY FOR UTERINE CONTRACTIONS

This has been recommended by the American College of Obstetricians and

Gynecologists (2013b), for the description and quantification of uterine contarctions.

Normal uterine activity is defined as five or fewer contactions in 10 minutes, average
over a 30 minutes window. Tachysystole was defined as more than five contarctions
in 10 minutes, averaged over 30 minutes. Tachysystole can be applied to spontaneous
or induced labor (Chap.26,p.527). the term hyperstimulation was a abandoned.
Stewart and associates (2012) prospectively studied uterine tachysystole in 584
women undergoing labor induction with misoprostol at Parkland Hospital. There was
no association of adverse infant outcomes with increasing number of contarctions per
10 minutes or per 30 minutes. Six or more contractions in 10 minutes, however, werw
significantly associated with fetal heart rate decelerations.
COMPLICALTIONS OF ELECTRONIC FETAL MONITORING
Electrodes for fetal heart rate evaluation and catheters for uterine contraction
measurement are both associated with infrequent but potentially serious
complications. Rarely, an intrauterine pressure catheter during placement may lacerate
a fetal vessel in the placenta. Also with insertion, placental and possibly uterine
perforation can cause hemorrhage, serious morbidity, and spurious recordings that
have resulted in inappropriate management. Severe cord compression has been
described from entanglement with the pressure catheter. Injury to the fetal scalp or
breech by a heart rate electrode is rarely severe. However, application at some other
site such as the eye in face presentations can be serious.
Both the fetus and the mother may be at increased risk of infection from internal
monitoring (Faro, 1990). Scalp wounds from the electrode may become infected, and
subsequent cranial osteomyelitis has been reported (Brook, 2005; Egginks, 2004;
McGregor, 1989). the American College of Obstetricians and Gynecologists (2012)
have

recommended

that

certain

maternal

infections,

including

human

immunodeficiency virus (HIV), herpes simplex virus, and hepatitis B and C virus, are
relative contraindications to internal fetal monitoring.