Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 276 - файл
.pdf
36
https://t.me/medicina_free
T. Widelock et al.
3.5 Denitions ofLabor/Preterm
Labor
Labor is dened as active and persistent contractions that cause cervical change and ultimately
result in delivery. Term labor occurs after the
achievement of 37 completed weeks’ gestational
age, whereas preterm labor occurs after the completion of 20weeks but prior to the achievement
of 37 completed weeks’ gestational age (20–36
6/7). Contractions and cervical change leading to
delivery prior to 20weeks’ gestational age constitutes a miscarriage and is not categorized as
labor [28, 31].
3.6 Stages ofLabor
3.6.1 Prelabor: Cervical Remodeling
(“Ripening”)
The uterus exhibits contractions throughout gestation. The uterine contractions in the early and
midtrimesters of pregnancy are characterized by
being infrequent, irregular, generally painless,
discoordinated, and focal within the contractile
apparatus of the uterine myometrium. This is in
stark contrast to the uterine contractions experienced during labor which are typically characterized as cyclical and repetitive, coordinated, and
globally effect myometrial activity across a functional uterine syncytium that occurs during the
rst phase of latent and active labor. Unlike the
discoordinated contractions in the early and
midtrimesters of pregnancy, these coordinated
contractions result in signicant alteration in cervical length, consistency, and ultimately in dilation [31, 32].
A number of physiologic and cellular changes
occur over the course of the late trimester, especially within the month leading up to labor. Such
pre-labor changes are key to setting the stage for
the three phases of labor during which progressive
dilation of the cervix occurs until the fetus and
placenta may be delivered in succession [32, 33].
The concept of the “cervical coefcient” was
coined a half-century ago when Hendricks
described pre-labor changes to the cervix observed
via serial cervical examinations in a cohort of 303
patients. Hendricks simplied the complex biology surrounding prelabor changes into a mathematical function generated by the product of two
factors—cervical dilation and effacement. The
resulting cervical coefcient demonstrated strong
inverse association with duration of labor; i.e., the
larger the coefcient, the shorter period of labor
to effect delivery, highlighting the importance of
prelabor cervical changes [34].
Similarly, Bishop generated a scoring system
that is commonly used to categorize a woman’s
cervix as favorable or unfavorable for induction
as based on cervical and obstetrical descriptors
that predict successful vaginal delivery [33]; see
Table3.1.
Hormonal and cellular changes drive the
aforementioned observations. Inammatory
mediators converge on the myometrial tissues to
trigger downstream signaling cascades that create a syncytial milieu across the uterine fundus
and thus coordinating the process of labor.
Progesterone withdrawal and downregulation of
progesterone receptors are key components of
this process and occur in concert with upregulation of oxytocin receptors [35, 36]. Initially, the
cervix undergoes softening, which is effectively
the rst measurable alteration evident on exami-
Table 3.1 Bishop cervical scoring system
Dilation, cm Closed 1–2 3–4
Effacement, % 0–30 40–50 60–70
a
Station
Cervical consistency Firm Medium Soft
Position of the cervix Posterior Midposition Anterior
a
Based on a −3 to +3 scale
0 1 2 3
−3 −2 −1, 0
≥5 to 6
≥80
+1, +2
ab
3 Pregnancy andParturition: ThePhysical andPhysiological Changes andTheir Pathologies
https://t.me/medicina_free
37
nation. This measurable decline in tensile
strength and increase in tissue compliance is
described in both biomechanical studies in animal model studies and from clinical examination in human pregnancies by digital
examination. The palpable or measured softening is due to a progressive and incremental
remodeling of the cervix owing to activation of
metalloproteinases in the cervical stroma that
effectively decrease the density of the connective tissue in the cervix [37, 38]. This decrease
in tissue density leads to both softening and
thinning of the cervix [39].
Many of these changes coincide with, and are
a consequence of, the metalloproteinasemediated destruction of the collagen matrix of
the cervix. Collagen is notably the most abundant
protein of the cervix and as such, destruction of
the brillar collagen matrix leads to decreased
tensile strength and rmness of the cervix.
Additionally, glycosaminoglycans (GAGs)
increase as gestation progresses and are expressed
abundantly in the cervical stroma. GAGs modulate collagen bril size and regulate the disorganization of the collagen extracellular matrix
(ECM). Such changes are mediated by inammatory cells and pro-inammatory cytokines that
not only lead to activation of the metalloproteinase enzymes but also cell-mediated clearance of
the cervical stroma by tissue monocytes, neutrophils, and leukocytes [37–39]. This clearance of
the cervical stroma is what leads to the clinically
evident changes Hendricks was able to rst
describe and reduce to the cervical coefcient as
well as the more commonly used Bishop score.
As opposed to the average prelabor cervical
dilation relative to parity—1.8cm for nulliparas
versus 2.2cm for multiparas—the cervical coefcient demonstrates positive correlation irrespective of parity with predicting onset of and duration
of labor. Similarly, observational studies of
women undergoing induction based on “favorable” Bishop scores, dened as at least 6–8
depending on the study performed, have demonstrated success that varies signicantly by parity.
Hence, subsequent authors have deduced that
modifying a woman’s Bishop score by adding 2
points for women with prior successful vaginal
birth adds prognostic quality to the Bishop score.
Such variation in success is rooted in the physiologic and histologic alteration that occurs during
pregnancy and delivery and persists postpartum
for parous women [35–37]. Women with prior
vaginal deliveries have long been described as
having parous cervical os, whereby the cervical
os takes on a relaxed and collapsed ovoid shape
rather than the nulliparous pinhole- like appearance; see Fig.3.10.
Nulliparous cervix Multiparous cervix
Fig. 3.10 Variation in cervical appearance by parity. Typical cervical appearance based on maternal parity
38
https://t.me/medicina_free
T. Widelock et al.
The characteristic appearance of a parous cervix is a consequence of the stretching and
increased laxity in the cervical stroma that persists after a delivery even after a completely
dilated and effaced cervix “closes” and reconstitutes itself postpartum. These changes are evident on elastography studies. Elastography
technology enables an objective evaluation of the
mechanical stamina of tissue walls as dened by
a measured displacement of moving tissues in
response to oscillatory pressure [40–42]. Cervical
stiffness is assessed by the resistance of tissues to
displacement and deformation. Nulliparous cervices demonstrate increased stiffness and resistance to displacement by elastography as
compared to parous cervices. Accordingly, the
mechanical strain imparted by a prior delivery
has measurably created a persistent injury or
deformation that is not only observable in appearance and measurable by elastography but also is
functionally more efcient at effecting a vaginal
delivery as demonstrated by the need to modify
Bishop score to account for the positive effect of
parity in childbirthing success [33, 40, 31, 42].
Following cervical remodeling are the three
classic stages of labor. These stages of labor and
timeline of the alterations to the maternal pelvic
anatomy is highlighted in Fig.3.11.
3.6.2 First Stage ofLabor:
Progressive Cervical Dilation
Following weakening and decreased tensile
strength during cervical remodeling, the onset of
repetitive uterine contractions leads to further
widening of the cervix. Mechanical pressure
from uterine contractions repeatedly and forcefully moves the presenting fetal part (e.g., fetal
head in cephalic fetuses or buttocks in the breech
fetus) toward and through the cervical os. This
leads to progressive and active cervical dilation
from the current threshold of cervical dilation of
6cm (dening active labor) to 10cm (complete
cervical dilation) [39].
3.6.3 Second Stage ofLabor:
Expulsion oftheFetus(es)
Following complete cervical dilation, the fetus
may be delivered through the cervix, vaginal
vault, and onto the introitus. Delivery of the
infant typically ensues shortly thereafter when
maternal expulsive efforts are urged by the overall pressure of the presenting part being sensed in
the birth canal. Given the greatly decreased tensile strength and increased compliance of the cervix, the ability of the cervix to pass the fetus
without tearing or lacerations is very high.
However, some women will sense the urge to
push prior to the achievement of complete dilation or are urged to push prior to the achievement
of complete dilation; these scenarios have a propensity for cervical laceration [31, 43].
Retrospective data indicate that in spite of
such injuries, cervical lacerations are not associated with increase in cervical insufciency (as
indicated by need for cerclage) in subsequent
pregnancies, cervical laceration in subsequent
deliveries, labor dystocias/protracted labor in
subsequent pregnancies, or with preterm delivery in subsequent pregnancies. Likewise, a history of cervical lacerations does not inuence
mode of delivery in subsequent pregnancies.
While rare and unavoidable, the presence of
broblasts deposition (scar) and potential for
decreased compliance or integrity of the cervix
for maintenance of pregnancy to term and being
able to dilate and accommodate passage of the
fetus, the presence of the scar tissue from prior
laceration does not appear to have an adverse
effect on subsequent pregnancy outcome [31, 32,
43].
The descent of the fetus through the birth
canal and vaginal delivery leads to mechanical
stretch that may tear and damage nerves, muscles, fascia, and ligamentous structures of the
pelvic oor. Excessive stretch, tearing, and
mechanical strain may lead to permanent anatomical and effectively irreversible functional
alterations. The effect of the passage of the fetus
cloud that is process type eect view window le object select view window
untitled cm
document unf
window setup type to searc to here int worik moring fresh medium the great all the medincine home selec
coulud vnhefhigh quality bnjec
cloud that is process type e
untitled cm
document unf
window setup type to searc to here int worik moring fresh medium the great all the medincine home selec
coulud vnhefhigh quality bnjec
cloud that is process type e
untitled cm
document unf
window setup type to searc to here int worik moring fresh medium the great all the medincine home selec
coulud vnhefhigh quality bnject share medi
3 Pregnancy andParturition: ThePhysical andPhysiological Changes andTheir Pathologies
https://t.me/medicina_free
39
t
t
t
t share medi
t share medi
ect view window le object select view window
o transform untiled cmyk preview type here to search documents share type here type share
yk character could area type le view contact dashed line
o transform untiled cmyk preview type here to search documents share type here type share
yk character could area type le view contact dashed line
ect view window le object select view window
o transform untiled cmyk preview type here to search documents share type here type share
yk character could area type le view contact dashed line
Fig. 3.11 Is absent (Timeline of changes and alterations of maternal pelvic anatomy)
40
https://t.me/medicina_free
T. Widelock et al.
on these injuries is supported by the nding that
subsequent childbirths continually expose the
pelvic oor to injury and denervation and alteration of muscle tone (overstretched) that leads to
decreased sensation, resting pelvic tone, and
strength of the pelvic oor long term [31, 32, 43].
3.6.4 Third Phase ofLabor:
Placental Separation
During pregnancy, the placental site is characterized by an attachment in which the cotyledons
actually extend into the decidua basalis; this
interface of the placental cotyledons with the
decidua is not only the exchange site during the
gestation but also the functional cleavage plane
during the third stage of labor [44, 45]. Placental
separation occurs by a progressive shearing force
of the placenta from the uterine wall. The shearing forces are created by the uterine contractions
leading to a decrease in uterine size after expulsion of the fetus along with an inherent decrease
in the surface area of the uterine cavity; this
effectively shears or tears the placenta away from
the uterine wall along the natural cleavage plane
[44, 45].
During this process, the placenta is naturally
thickened and decreased in overall diameter due
to the constrictive forces of the uterine muscle.
The ability of the placenta to decrease its surface
area (given mass and density) is overcome by the
force of the uterine contractions and is sheared
away from the uterine wall. Upon separation, the
uterine contractions result in expulsion of the placenta. Notably, the decidual vessels must be
kinked/compressed by the muscle contraction
since the decidualization process in pregnancy
involves loss of the muscular intima of the spiral
arteries. Without adequate uterine contraction
and involution, obstetric hemorrhage can and will
occur. As the postpartum period progresses, the
associated estrogen and progesterone withdrawal
lead to shedding of the thickened decidua from
gestation [44–46].
3.7 Pathologies ofParturition
Previously, we have described many of the histological, physiological, and anatomical changes of
parturition. For the remainder of the chapter, we
begin to discuss the pathologies of labor and their
implications for a woman’s future health.
The mechanism of obstetrical trauma is
believed to be several fold: trauma to the pelvic
support system, denervation injury, ischemia,
combined neurovascular injury, and defective
soft-tissue remodeling have all been implicated
and associated with the pathologies seen following childbirth [47].
3.7.1 Pathological Disruption
oftheMaternal Bony Pelvis
During Childbirth
As the fetus passes through the pelvis, there is
stretching and compression of the surrounding
tissues and nerves. These mechanical forces of
stretch and compression may result in tearing or
avulsion of pelvic oor musculature, supporting
ligaments, and nervous tissue. Several normal
changes to the pelvic following uncomplicated
term vaginal delivery have been described and
include widening of the symphysis and sacroiliac
joints, and also gas in the sacroiliac joints [22].
These aforementioned adaptations of gestation,
while normal and necessary, also contribute to
the propensity for traumatic disruption of the
maternal bony pelvis during labor and delivery.
Ultimately, the disruption of these tissues may in
fact result in weakening the musculature and supporting ligaments and damaging the nervous tissue. For example, the sacroiliac joint exhibits
marked mobility at term and this displacement
functions to help increase the diameter of the pelvic outlet by 1.5–2.0cm at delivery. When this
displacement is greater than 2.5cm, progressive
injury to the posterior pelvic ring, including disruption of the sacroiliac joint or sacral fracture,
may occur. This disruption of the pubic symphysis with accompanying posterior pelvic-arch
3 Pregnancy andParturition: ThePhysical andPhysiological Changes andTheir Pathologies
https://t.me/medicina_free
41
instability after natural childbirth has been previously described [22, 23, 27, 28]. Traumatic disruptions of the pubic symphysis with vaginal
delivery may result in functional limitations and
severe pain. Fortunately, intrapartum pubic symphysis disruption rarely occurs with an incidence
ranging from 0.005 to 0.8% of live births, with an
increasing incidence with advancing maternal
age. When disruption does occur, women report
suprapubic pain, difculty sitting, standing,
change in decubitus, and a “waddling” gait is
often employed and observed [28, 34].
Abrupt intrapartum pubic symphysis separation is managed by pelvic ring stabilization with
a pelvic binder if available or a sheet applied at
the greater trochanter level. Injuries to this degree
are ultimately surgically managed with open
reduction and internal xation with strategic
placement of plates and screws to regain stability
of the maternal pelvis [48–50]. Alternatively,
conservative management with a pelvic binder
and 4weeks of bedrest has been described but all
patients reported having severe pelvic pain, ultimately leading to open reduction internal xation
to reduce and stabilize the pelvic ring diameter to
pre-pregnant state. After these procedures have
been performed, hardware is typically left in situ
even with intentions for future childbearing. On
the contrary, some orthopedic surgeons advocate
for hardware removal 1 year after the surgery
when future childbearing is desired. Regardless,
patients with persistent pain or hardware loosening are managed by hardware removal [48–50].
Obstetricians may perform pelvic examination, gently, to palpate diastasis of the pubic symphysis and may add pressure to the iliac crests to
assess for instability of the pelvic ring.
Alternatively, to avoid potential for eliciting signicant patient discomfort, the clinician may
order imaging studies (e.g., pelvic MRI) when
cued by patient’s verbal description [27, 28, 34].
Most gravidas exhibit what orthopedic surgical
subspecialists refer to as an “open-book” injury
in which there is partial instability—disruption of
anterior ligaments with residual integrity of posterior ligaments. Such “open-book” injuries are
vertically stable but rotationally unstable (Tile
type B) [49]; see Table3.2.
3.7.2 Pathological Trauma
tothePelvic Vasculature
During Childbirth
During childbirth, passage of the fetus through
the birth canal may also cause trauma by creating
macroscopic tearing in both the symphysis pubis
and venous plexus of the pelvis. Tearing and laceration of the latter (venous plexus and arterioles
in the supercial fascia of the pelvic triangle) is
evidenced by hematoma in the labia majora
(known as the Destot sign); see Fig.3.12.
Bleeding that is limited to the vulvar tissues
supercial to the anterior urogenital diaphragm
are categorized as vulvar hematomas.
Vulvovaginal hematomas are likewise evident on
Table 3.2 Tile classication for fractures of the pelvis
Classication Stability Descriptors
A Stable A1: Fractures of the pelvis not involving
B Rotational unstable, vertically
C Rotationally and vertically unstable C1: Rotationally and vertically unstable
stable
the pelvic ring
A2: Minimally displaced fractures of the
pelvic ring
B1: Anteroposterior compression fracture
(open book)
B2: Lateral compression injury
(ipsilateral)
B3: Lateral compression injury
(contralateral)
C2: Bilateral
C3: Associated with acetabular fracture
42
https://t.me/medicina_free
Expanding
vulvar
hematoma
(Destot’s
sign)
Fig. 3.12 Destot sign
the vulva but bleeding extends into the paravaginal tissues. In such childbirth trauma, the bleeding and apparent contusion arises from branches
of the pudendal artery, namely, the posterior rectal, transverse perineal, and/or the posterior labial
arteries [23, 27, 28].
3.7.3 Pathologies ofthePelvic Floor
andSubsequent Development
ofPelvic Floor Disorders
(PFDs) Following Childbirth
As described previously, the levator ani muscle
complex (LAM) is a hammock-like muscle
which supports and comprises the pelvic oor
[29, 51]. Levator ani muscle (LAM) injuries
occur in 13–36% of women who have a vaginal
delivery [52]. Vaginal delivery may compromise
the integrity of the LAM complex via pathological overstretching of the muscular complex; traumatic disruption of the LAM complex via
anteromedial avulsion and/or partial or complete
detachment of the pubovisceral sling from the
pubic bone; or denervation of the LAM complex.
MRI and ultrasound data demonstrate disruptions
of the LAM complex in about one-fourth to onethird of women following a normal vaginal delivery [29, 30, 51, 53]. This traumatic disruption or
denervation may lead to loss of levator function
and ultimately result in pelvic oor disorders [30,
53] (Fig.3.13).
T. Widelock et al.
Fig. 3.13 Relationship of the urethra, vagina, perineum
and anus to the maternal boney pelvis
Pelvic oor disorders (PFDs) are common
complications dealt with by women in the postpartum period and later in life. It is estimated that
these disorders affect one-third of women in the
United States and have a signicant impact on a
woman’s overall health and quality of life [1–3].
PFD pathologies include urinary incontinence,
anal incontinence, pelvic organ prolapse, nerve
injury, and sexual dysfunction. While there is
much controversy regarding the etiology of these
pathologies as either resulting from the pregnancy itself, the delivery, or a consequence of
both, a causal role of pregnancy and childbirth in
causing PFDs is supported by the nding that
PFDs are more prevalent among women who
have delivered at least one child [2, 3, 8].
As described in the earlier section of the chapter, pregnancy itself is a risk factor for development of PFDs. However, vaginal delivery is also
an independent and signicant risk factor for several PFDs, including pelvic organ prolapse. It is
theorized that as the fetus passes through the pelvis, there is stretching, compression, and tearing
of the pelvic oor. These mechanical forces may
result in damage to the integrity and function of
the associated muscles, connective, and/or nervous tissue. Ultimately this may weaken the
integrity of the pelvic musculature resulting in
pelvic organ prolapse [54]. Similarly, with prolonged second stage of labor, there is an increased
duration of possible soft tissue injury (via direct
stretch, compression, tearing, or indirectly via
neuromuscular damage) to the pelvic oor.
3 Pregnancy andParturition: ThePhysical andPhysiological Changes andTheir Pathologies
https://t.me/medicina_free
43
Prolonged second stage has been associated with
consequential injury to the levator ani complex
and pelvic oor disorders [30, 47].
The development of pelvic oor pathologies,
specically of pelvic organ prolapse, may also
result from the mechanical disruption of the supporting connective tissue of the pelvic oor. Both
the detachment of endopelvic fascia from its lateral attachment to the pelvic side wall, and the
detachment of the arcus tendinous fascia pelvis
from the ischial spine, have been implicated in
the development of vaginal (paravaginal, anterior
vaginal) wall defects and consequentially PFDs
[51, 55]. Paravaginal defects are specically
associated with urinary incontinence and poor
anterior vaginal support [55, 56].
Incontinence of stool and atus are further
complications of vaginal delivery and are more
commonly experienced than was previously
believed. The reported frequency of incontinence
of stool in primiparous women ranges from 2 to
6% versus 17 to 62% after a severe perineal laceration [9, 10, 57]. Anal incontinence has been
classically associated with both forceps delivery
and anal sphincter laceration. In turn, anal sphincter laceration is strongly predicted by rst vaginal
birth, median episiotomy, and operative vaginal
delivery. Finally, incontinence of stool is also
more frequent among women who deliver vaginally and have had third- or fourth- degree perineal tears than among those who delivered
vaginally and had no anal sphincter tears (7.8% v.
2.9%) [58, 59]. In conclusion, even a normal vaginal delivery (without the use of forceps or vacuum) predisposes a woman to issues related to
recto-anal incontinence.
3.7.4 Pathological Disruption
ofthePelvic Nervous System
During Childbirth
Descent of the fetal head may cause stretching
and compression of not only the pelvic oor
musculature and connective tissue but also of
associated pelvic nerves. For example, injuries
to the lumbosacral plexus during labor and
delivery may result in neuromuscular pathologies including denervation of the LAM complex and weakening of the musculature support
pelvic organ prolapse. The process of demyelination and subsequent denervation as an indirect mechanism of injury to the pelvic
musculature is supported by neurophysiologic
tests, including concentric needle electromyography (EMG) and pudendal nerve motor latency
tests [53, 60]. Stretching and compression
injury to the pudendal nerve has been reported
with 38–42% of vaginal deliveries [61].
Therefore, while vaginal delivery is a less
described and recognized risk factor for pelvic
oor neuropathy, even in the context of a normal vaginal delivery devoid of use of forceps or
vacuum, there does exist risk to some degree of
denervation of the pelvic oor and subsequent
pelvic oor neuropathy. Other risk factors for
denervation and pudendal nerve damage
include operative delivery, midforceps rotation,
prolonged second stage, fetal malpresentation,
high birth weight, small maternal size [6, 62].
3.7.5 Pathological Disruption
oftheLower Urinary Tract
During Childbirth
Childbirth is associated with a high rate of stress
urinary incontinence in the postpartum period.
Even women who may have been continent during the pregnancy may experience signicant urinary incontinence after vaginal delivery (de novo
urinary incontinence). The reported incidence of
de novo urinary incontinence after a rst vaginal
birth is 21% with spontaneous birth and 36%
with forceps delivery [6, 7]. This increase in
stress urinary incontinence following childbirth
is believed to be the result of damage to the pelvic oor muscles, fascia, ligaments, and nerves
supporting and controlling the bladder neck and
urethra. Multiple studies have demonstrated that
vaginal delivery may result in urinary system
neuromuscular damage and bladder neck hypermobility, and pelvic oor dysfunction [47, 56, 63,
64]. It is noteworthy to mention here again that
44
https://t.me/medicina_free
T. Widelock et al.
pregnancy itself is associated with anatomical
adaptations that may cause urinary incontinence
and that multiple studies underscore the signicant role and impact of both the normal physiological changes of pregnancy and the mechanical
alterations following a normal vaginal delivery in
the pathogenesis of urinary dysfunction following pregnancy [5, 29, 30].
3.7.6 Psychological Changes
andSexual Dysfunction (The
Fourth Trimester)
Vaginal delivery is a risk factor for sexual morbidity. During vaginal delivery and in the postpartum period, the woman may experience
lacerations, suture repair, hemorrhoids, constipation, incontinence, bleeding, and perineal or pelvic pain. These occurrences may have negative
impacts on the woman and may predispose a
woman to poor sexual functioning. In their study,
Signorello etal. explore the relationship between
obstetrical perineal lacerations and postpartum
sexual functioning (including time to resuming
sexual intercourse, dyspareunia, sexual satisfaction, sexual sensation, and likelihood of achieving orgasm). This study notes that the effect of
spontaneous birth on postpartum sexual function
is most signicantly related to occurrence of perineal trauma, thus underscoring the importance
of minimizing the extent of perineal damage during childbirth [65].
It is imperative to comment that in addition
to the aforementioned physical factors, there are
many psycho-social factors that may contribute
to the risk of postpartum sexual dysfunction.
Sexual health may also be impacted by mood
dysphoria, sleep deprivation and fatigue, degree
of partner involvement, and help with care of
the infant. An awareness of both the physical
and psychological changes and the consequential potential sexual difculties following pregnancy and childbirth are paramount to providing
women with vital and comprehensive postnatal
care [66].
3.8 Concluding Remarks:
TheFourth Trimester
andBeyond
The biological processes of carrying a fetus to
ideally term gestation, and then of delivery and
the birth of the neonate, both entail and mandate
a number of anatomic and physiologic alterations
in the maternal pelvis. The endocrine and immune
systems initiate and mediate these modications
to accommodate and sustain pregnancy for the
growth, development, and birthing process of the
fetus. The early-, mid-, and late trimesters are
earmarked by a number of histologic changes of
the uterus, cervix, and pelvis as summarized in
this chapter. Upon achievement of term, endocrine signaling triggers the onset of labor and its
inherent rapid physiologic and anatomical
changes necessary to effect an atraumatic delivery for both the mother and fetus.
While childbirth occurs largely without undue
trauma, pregnancy and the delivery process nonetheless may result in a myriad of physical and
physiological changes with signicant implications for a woman’s future health. Knowledge of,
and understanding of, these changes and pathologies are paramount for clinician guiding the transition from pregnancy to parenthood. In 2018, the
American College of Obstetricians and
Gynecologists (ACOG) recognized the many
issues following pregnancy and delivery and
underscored the importance of ongoing comprehensive care that should extend into the “fourth
trimester” of pregnancy (the rst 3months following birth) [64, 67]. As part of a comprehensive care plan, the obstetric care provider should
address with the woman the following factors:
physical recovery from birth, mood and emotional well-being, infant care and feeding, sleep
and fatigue, sexuality, contraction, birth spacing,
chronic disease management, health maintenance
[67]. Finally, the obstetric care provider should
facilitate the woman’s transition to on-going
well-woman care to ensure that the implications
of pregnancy complications is considered in the
woman’s future healthcare plans. In doing so, the
3 Pregnancy andParturition: ThePhysical andPhysiological Changes andTheir Pathologies
https://t.me/medicina_free
45
obstetrical provider is able to best care for the
woman’s physical and mental health after giving
birth and enable every woman to optimize her
long-term health and well-being [67].
References
1. Menon R, Bonney E, Condon J, Mesiano S, Taylor
R.Novel concepts on pregnancy clocks and alarms:
redundancy and synergy in human parturition. Hum
Reprod Update. 2016;22(5):535–60.
2. Hall H, Cramer Holger C, Sundberg T, Ward L, Adams
J, Moore C, Sibbritt D, Lauche R.The effectiveness
of complementary manual therapies for pregnancyrelated back and pelvic pain. A systematic review
with meta-analysis. Medicine. 2016;95(38):e4723.
3. Lukacz ES, Lawrence JM, Contreras R, Nager CW,
Luber KM.Parity, mode of delivery, and pelvic oor
disorders. Obstet Gynecol. 2006;107(6):1253–60.
4. Cunningham FG, Williams JW. Williams obstetrics.
25th ed. Norwalk: Appleton & Lange; 2018.
5. Weidner AC, South MT, Sanders MD, Stinnett
SS.Change in urethral sphincter neuromuscular function during pregnancy persists after delivery. Am J
Obstet Gynecol. 2009;201(5):529.e1–6.
6. Meyer S, Schreyer A, DeGrandi P, Hohlfeld P. The
effects of birth on urinary incontinence mechanisms
and other pelvic oor characteristics. Obstet Gynecol.
1998;92:613–8.
7. Snooks SJ, Setchell M, Swash M, Henry MM.Injury
to innervation of pelvic oor sphincter musculature in
childbirth. Lancet. 1984;2(8402):546–50.
8. Fultz NH, Burgio K, Diokno AC, Kinchen KS,
Obenchain R, Bump RC. Burden of stress urinary
incontinence for community-dwelling women. Am J
Obstet Gynecol. 2003;189(5):1275–82.
9. Morrione T, Seifter S.Alteration in the collagen content of the human uterus during pregnancy and postpartum involution. J Exp Med. 1962;115:357–65.
10. Degani S, Leibovitz Z, Shapiro I, Gonen R, Ohel
G. Myometrial thickness in pregnancy: longitudinal
sonographic study. J Ultrasound Med. 1998;17:661.
11. Ginsberg Y, Goldstein I, Lowenstein L, Weiner
Z. Measurements of the lower uterine segment
during gestation. J Clin Ultrasound. 2013;41:
214–717.
12. Sfakianaki AK, Buhimschi AI, Pettker CM, Magloire
L, Turan O, Hamar B, Buhimschi C.Ultrasonographic
evaluation of myometrial thickness in twin pregnancies. Am J Obstet Gynecol. 2008;198:530.e1.
13. Handa VL, Garrett E, Hendrix S, Gold E, Robbins
J.Progression and remission of pelvic organ prolapse:
a longitudinal study of menopausal women. Am J
Obstet Gynecol. 2004;190(1):27–32.
14. Karzel RP, Freedman MJ. Orthopedic injuries in
pregnancy. In: Artal R, Wiswell RA, Drinkwater BL,
editors. Exercise in pregnancy. 2nd ed. Baltimore:
Lippencott, Williams & Wilkins; 1991.
15. Oliphant SS, Nygaard IE, Zong W, Canavan TP,
Moalli PA. Maternal adaptations in preparation for
parturition predict uncomplicated spontaneous delivery outcome. Am J Obstet Gynecol. 2014;211(6):630.
e1–7. Epub 2014 Jun 12.
16. Foti T, Davids JR, Bagley A. A biomechanical analysis of gait during pregnancy. J Bone Joint Surg Am.
2000;82(5):625.
17. Stark DD, McCarthy SM, Filly RA, Parer JT, Hricak
H, Callen PW. Pelvimetry by magnetic resonance
imaging. Am J Radiol. 1985;144:947–50.
18. Wijma J, Weis Potters AE, de Wolf BT, Tinga DJ,
Aarnoudse JG. Anatomical and functional changes
in the lower urinary tract during pregnancy. BJOG.
2001;108:726–32.
19. Forczek W, Ivanenko Y, Salamaga M, Sylos-Labini
F, Fraczek B, Maslon A, Curylo M, Suder A.Pelvic
movements during walking throughout gestation—
the relationship between morphology and kinematic
parameters. Clin Biomech. 2019;71:146–51.
20. Dehghan F, Haerian BS, Muniandy S, Yusof A,
Dragoo JL, Salleh N. The effect of relaxin on the
musculoskeletal system. Scand J Med Sci Sports.
2014;24(4):e220–9.
21. Ahmad N, Wang W, Nair R, Kapila S. Relaxin
induces matrix-metalloproteinases-9 and -13 via
RXFP1: induction of MMP-9 involves the Pl3K,
ERK, Akt and PKC pathways. Mol Cell Endocrinol.
2012;363(1–2):46–61.
22. Martelli F, Youssef A, Capogna MV, Bruno A,
Bruno V, Dodaro MG, Ticconi C, Ghi T, Piccione E,
Pietropolli A.Longitudinal changes of subpubic arch
angle throughout pregnancy. Gynecol Obstet Invest.
2019;85(1):100–6.
23. Garagiola DM, Tarver RD, Gibson L, Rogers RE,
Wass JL.Anatomic changes in the pelvis after uncomplicated vaginal delivery: a CT study on 14 women.
Am J Roentgenol. 1989;153(6):1239–41.
24. Rahn DD, Ruff MD, Brown SA.Biomechanical properties of the vaginal wall: effect of pregnancy, elastic ber deciency, and pelvic organ prolapse. Am J
Obstet Gynecol. 2008;198:590.
25. O’Boyle AL, Woodman PJ, O’Boyle JD, Davis GD,
Swift SE. Pelvic organ support in nulliparous pregnant and nonpregnant women: a case control study.
Am J Obstet Gynecol 2002;187(1):99–102.
26. Henrix SL, Clark A, Nygaard I, Aragaki A, Barnabei
V, McTiernon A. Pelvic organ prolapse in the
Women’s Health Initiative: gravity and gravidity. Am
J Obstet Gynecol 2002;186(6):1160–6.
27. Hierholzer C, Ali A, Toro-Arbelaez JB, Suk M, Helfet
DL. Traumatic disruption of pubis symphysis with
accompanying posterior pelvic injury after natural
childbirth. Am J Orthop. 2007;36(11):E167–E17.
28. Kharrazi FD, Rodgers WB, Kennedy JG, Lhowe
DW.Parturition-induced pelvic dislocation: a report
of four cases. J Orthop Trauma. 1997;11(4):277–82.
Соседние файлы в папке @xirurgi_2025