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26
tubercle
(symphysis pubis)
Superior view Medial view
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T. Widelock et al.
outlet) [1–3]. Collectively, these physical and
physiological changes are progressive and coordinated to culminate in the delivery of the fetus.
While these processes and changes of pregnancy
and childbirth are impressive in their design and
result, they are however also fraught with potential for pathology and lasting maternal effects.
In general, information regarding the normal
physiologic processes as they pertain to maternal
alterations of anatomy are scattered throughout
the obstetric literature and difcult for the busy
clinician to glean a gestalt or clear understanding.
The authors of this chapter hopefully have separated the wheat from the chaff for readers by
scouring said literature and compiling these
important events into a succinct and coherent
chapter. We begin our chapter with a description
of the anatomical and physiological changes of
pregnancy and childbirth to provide a working
framework and perspective for the clinician caring for women during and after pregnancy. We
conclude the chapter with both a description of
the associated pathologies that often result from
the changes and processes of pregnancy and labor
and delivery and a discussion of the implications
these pathologies may have for a woman.
3.2 Clinical Anatomy
ofthePelvis-Perineum
3.2.1 The Bony Pelvis
The pelvic canal is the gateway to ex utero life for
the developed fetus. The pelvis is composed of
four bones: the sacrum, the coccyx, and the two
innominate bones (formed by the fusion of the
ilium, ischium, and pubis); see Fig.3.1.
The pelvis may be further divided into the
false and true pelvis. The false pelvis lies above
the linea terminalis, and the true pelvis lies below
the linea terminalis; see Fig.3.2. The true pelvis
is the portion important in childbearing. The
superior aspect of the true pelvis delineates the
pelvic inlet. The pelvic inlet is bounded by the
sacral promontory and the alae of the sacrum, the
linea terminalis, and the upper margins of the
pubic bones. The cavity of the true pelvis may be
described as an oblique bent cylinder with the
greatest height posteriorly [4]. The posterior wall
of the true pelvis is the anterior surface of the
sacrum. The lateral walls of the true pelvis are
formed by the ilial and ischial bones and the
sacrospinous and sacrotuberous ligaments and
Anterior
longitudinal
ligament
Anterior
sacroiliac
ligament
Greater
sciatic
foramen
Anterior
superior
iliac spine
lliofemoral
ligament
Inguinal
ligament
Pubic
Fig. 3.1 The female bony pelvis and ligaments
lleum
Anterior
superior
iliac spine
Ischium
Body of
pubis
Pubis
Articular surface
lliac crest
Articular surface
(with sacrum)
Body of ileum
Spine of ischium
Body of ischium
Ramus of ischium
Inferior ramus of pubis
Pe
Pelvic outlet
lliofemora
Supraspinous
sacrococcygeal
sacroilia
ligament
ligament
ligament
Posterior view Anterior view
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27
corresponding sciatic foremen; see Fig.3.3. The
anterior wall is formed by the pubic bones, the
ascending superior rami of the ischial bones and
the obturator foramen. Inferiorly, the true pelvis
is delineated by the pelvic outlet.
False pelvis
Tr ue pelvis
Pelvic inlet
lvic cavity
Fig. 3.2 Cross-section of the pelvic bones
The pelvic outlet is described as a diamondshaped area constructed by (1) the connes of the
tip of the coccyx and sacrotuberous ligaments
laying the oor; (2) anked laterally by the
ischial tuberosities; and, (3) roofed by the left
and right rami of the pubic arch joining to form
the pubic symphysis; see Fig.3.4.
3.2.2 The Pelvic Joints
There are two pelvic joints—the pubic symphysis and the sacroiliac joints—which are signicant to the discussion of the anatomical
adaptations of pregnancy and parturition. The
pubic symphysis joins the pelvic bones anteriorly and consists of brocartilage and the convergence of the arcuate ligaments of the pubis.
Posteriorly, the pubic bones are joined by articulations of the sacrum and the iliac portion of
the innominate bones, forming the sacroiliac
joints.
ligament
lliolumbar
ligament
l
ligament
Dorsal
sacrococcygeal
ligament
Anterior
c
ligament
Arcuate pubic
Short posterior
sacroiliac
ligament
Long posterior
sacroiliac
ligament
Sacrotuberous
ligament
lliolumbar
ligament
Anterior
longitudinal
ligament
Sacrospinous
ligament
lliofemoral
ligament
Anterior
sacroiliac
ligament
lliofemoral
ligament
Sacrospinous
ligament
Fig. 3.3 The female pelvic cavity
Obturator
membrane
Inguinal
lliolumbar
ligament
Anterior
longitudinal
ligament
Inferior viewSuperior view
Dorsal
ligament
Sacrotuberous
ligament
Arcuate pubic
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1 symphysis pubis
2 inferior pubic lig. (arcuate lig.)
3 transverse perineal lig. (Krause lig.)
4 urethrovaginal m.
5 inferior ischio-pubic ramus
6 deep transversal perineal m. (urogenital diaphragm)
T. Widelock et al.
1
2
3
4
5
6
7
8
9
10
11
12
7 bulbospongiosus m.
8 superficial transversal perineal m.
9 tendinous center of the perineum
(perineal body)
10 levator ani m.
11 ischial tuberosity
12 external anal sphincter m.
Fig. 3.4 Cross-section of the female pelvis
3.2.3 Obstetrical Pelvic Dimensions
Obstetricians have correlated various pelvic
dimensions with obstetrical outcomes. The signicant anteroposterior dimensions include the
following:
1. True or anatomical conjugate: the distance
between the sacral promontory and the upper
edge of the pubic symphysis (mean 11cm)
2. Obstetric conjugate (the “lesser anteroposterior diameter”): the distance between the
sacral promontory and the bulge on the posterior most portion of the symphysis pubis
(mean 10.5cm)
3. Diagonal conjugate: the distance between the
sacral promontory and lower edge of the pubic
symphysis (mean 12.5cm)
The obstetrical conjugate is important clinically, in that it represents the shortest distance
between the promontory of the sacrum and the
pubic symphysis (shortest anterioposterior diameter). This is distinct from the anterioposterior
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see Fig.3.6. The transverse diameter is the greatest distance between the linea terminalis at the
pelvic inlet, and typically averages approximately 13.5cm. At the level of the midpelvis, the
interspinous diameter is the most clinically relevant transverse diameter as it typically represents
smallest transverse pelvic diameter. The interspinous diameter is typically 10 cm or slightly
greater.
3.2.4 Variants inObstetrical Pelvic
Shapes
Variations in dimensions of the maternal pelvis
have implications for both the success of and
complications with the birthing process for both
Fig. 3.5 Female pelvic outlet. (a) Conjugate diameter at
pelvic inlet; (b) true conjugate; (c) diagonal conjugate; (d)
pelvic cavity at its widest; (e) pelvic cavity at its narrowest;
(f) pelvic outlet; (g) pelvic inclination (60°)
Fig. 3.6 Obstetrical dimensions. (a) Conjugate; (b)
oblique; (c) transverse; (d) pelvic cavity between ischial
spines; (e) intercristal distance; (f) interspinous distance
diameter of the pelvic inlet, otherwise known as
the true conjugate. The obstetrical conjugate cannot be measured directly, but rather is estimated
by subtracting 1.5–2cm from the diagonal conjugate (Fig.3.5).
The transverse diameter and the interspinous
diameter are important anatomical landmarks;
mother and fetus. These variances are manifest
by hormonal and genetic inuences likely
evolved for the essential need for the female pelvis having varied reproductive purpose from that
of the male pelvis.
The Caldwell and Moley classication of pelvic shapes is based on measurements of the greatest transverse diameter of the pelvic inlet and its
division into anterior and posterior sections. The
character of the posterior segment determines the
type of pelvis, and the character of the anterior
segment determines the tendency of the pelvis—
essentially further characterizing the pelvic shape
as most pelvises are actually mixed types. The
four parent pelvic types of the Caldwell–Moley
classication are: gynecoid, platypelloid, anthropoid, and android. Any discussion regarding
maternal pelvic shape and labor discussion inherently leads to how the pelvic type impacts presentation of the fetal head through the birth canal;
see Fig.3.7.
3.2.5 The Pelvic Floor
The pelvic oor or diaphragm is elegantly
designed, in that it functions to both support the
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ab
cd
Fig. 3.7 Pelvic diameters. Caldwell-Moley classication of pelvic diameters and shapes. (a) Anthropoid; (b) Gynecoid;
(c) Android; (d) Platypelloid
pelvic viscera and to also accommodate for the
passage of the cranially dominant human fetus
during parturition. The pelvic oor is comprised
primarily from the pudendal nerve (S2, S3, S4)
with secondary contribution of direct branches
from the sacral plexus.
of the levator ani muscle (LAM) complex (containing the bulbocavernosus muscle, transverse
perineal muscle, and ischiocavernosus muscle)
3.2.6 The Pelvic Viscera
and the perineal membrane [5, 6]; see Fig. 3.8.
The fascial attachments of the vagina to the pelvic walls and the LAM complex comprise the
mainstay support of the pelvic viscera; consequently, either direct or indirect damage to these
structures may result in pelvic organ prolapse.
The nerve innervation to the pelvic oor arises
The viscera of the pelvis includes the vagina,
uterus, adnexal structures, and the broad ligament. For the purposes of this chapter, we will
also discuss the lower urinary tract (specically
the bladder and urethra) as pregnancy and parturition notably impacts urinary function [5–7].
Superior view
Medial vie
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Urethra
Obturator canal
Obturator
internus muscle
Vagina
Rectum
31
Tendinous arch
Levator
ani muscle
Levator
ani muscle
Pubococcygeus
sacrococcygeal
w
Obturator canal
internus muscle
Tendinous arch
Pubococcygeus
urethrae muscle
lliococcygeus
Puborectalis
Anterior
ligament
Obturator
lliococcygeus
Urethra
Sphincter
Vagina
Ischial spine
Coccygeus
Piriformis
muscle
Piriformis
muscle
Ischial spine
Coccygeus
Levator ani
muscle (cut)
Rectum
External anal
sphincter muscle
Superficial and deep
transverse perineal muscles
Fig. 3.8 Caldwell–Motoy pelvic types
3.3 The Adaptations
ofPregnancy
Pregnancy is a remarkable time of adaptive biological processes and mechanical forces working
in concert to change the maternal anatomy and
physiology in order to accommodate the developing fetal life. These pregnancy changes primarily
result from two key elements: the sheer mass
effect from mechanical stretch and pressure and
hormonal changes triggering increased tissue
compliance and laxity [1, 8]. In this section, we
will describe these changes in relation to the
anatomy and later discuss how these changes are
affected by hormonal processes.
3.3.1 The Uterus
Maternal weight gain and uterine enlargement
impart mechanical force on the abdominal wall
and pelvic oor. Starting in early gestation, the
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growing uterus leads to a downward displacement of the pelvic oor that is evident on perineal
ultrasound. Over the course of pregnancy, the
uterus expands its capacity both in housing the
growing fetus(es) to term size and in the ability to
deliver adequate blood ow for utero-placental
delivery of oxygenated blood and nutrients and
capture of metabolic byproducts generated by the
fetus(es) [9, 10]. To accommodate the need to
increase in size, gene activation within the connective tissues of the uterus leads to a signicant
increase in collagen content. In fact, collagen
content for a term uterus is eightfold higher than
the non-gravid uterus value (60g vs. 7g; mean
increase 53g). Total uterine weight undergoes a
tenfold increase during pregnancy. While the collagen content and uterine mass increase in parallel, percentage of collagen per gram of uterine
mass decreases over pregnancy in primigravid
women. Notably, this change in composition persists 5weeks postpartum [9, 10]. After delivery,
the collagen content begins diminishing and is
evident by 14 hours postpartum. This process is
so rapid that by postpartum day 8, the collagen
content is 28% (16g) of that seen at term prior to
delivery. At 5 weeks postpartum, collagen content is only 3.9g reective of persistent alteration
of collagen content of the uterus following the
pregnancy event from delivery to the end of the
puerperium. Uterine weight likewise increases
from non- gravid 130g to term 1300g and then
by 2days postpartum more than halves to 500g
and decreases to 98g by 4weeks postpartum [9].
Uterine proteases and prolidases have been
shown to effect the destruction in the reticular
framework for pregnancy that is no longer needed
following delivery; essentially, these proteases
and prolidases decrease collagen content postpartum. Inammation and endothelial disruption
within the uterus occurs during this consumptive/
resorptive process and leads to transient histologic edema of the uterus in the rst 2 weeks
postpartum [9].
During the rst 2weeks after a spontaneous
vaginal delivery, the uterus involutes or exhibits a
series of dynamic changes that lead to reconstitu-
tion of the nongravid state. Coordinated contractions and extrusion of blood volume lead to the
restoration of the uterine body and cavity size.
Breast-feeding augments this process by triggering oxytocin release leading to uterine contractions and in effect hastening the dramatic decrease
in uterine size due to the nongravid state. While
ultrasound data collected in the puerperium (up
to day 40) have not shown signicant difference
in length of the uterine corpus in breast-feeding
vs. bottle-feeding mothers, an inverse correlation
in uterine size and breast-feeding has been demonstrated at 3-months postpartum (r = −0.395;
p<0.001) [9].
3.3.2 The Lower Uterine Segment
As the uterine cavity expands and the uterine corpus stretches to accommodate the growing conceptus, the lower uterine segment undergoes
signicant alterations to withstand the strain
without rupture [9, 10]. Morphologic studies
using both ultrasound and MRI imaging along
with tissue biopsy demonstrate that the uterine
myometrium hypertrophies as gestation advances
[10]. While some proliferation of myocytes
occurs over the course of gestation, the bulk of
the changes result from hypertrophy of the existing myocytes (increased cell size) along with a
complimentary accumulation of brous tissue of
the uterine wall, especially true in the lower uterine segment.
Ultrasound data demonstrate thinning of the
lower uterine segment as the uterine cavity is
stretched [11]; such changes are seen earlier and
more evidently in multiple gestations [12].
Interestingly, the thinner the lower uterine segment in twin gestation at increasingly early gestational age, the more likely it is for preterm labor
to occur at correspondingly earlier gestational
ages and earlier preterm delivery; such relationship points toward mechanical stretch and activation of labor [11]. Hormonal changes induce
hypertrophy early in pregnancy as evidenced by
wall thickening. Later in gestation, the lower
3 Pregnancy andParturition: ThePhysical andPhysiological Changes andTheir Pathologies
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uterine segment thins considerably. Elastography
studies demonstrate increasing compliance and
decreasing density of the lower uterine segment
with advancing gestational age—a biologic adaptation key to avoiding uterine rupture.
3.3.3 The Pelvic Floor andLower
Urogenital Tract
There is a decrease in the contraction of pelvic
oor muscles and consequential increase in bladder and urethral mobility that is progressive and
most evident in the late trimester [13, 14]. Thus,
merely carrying a conceptus to the late trimester
exposes the uterine, cervical, lower urogenital
tract, pelvic oor, and entirety of the pelvis to
macroscopic connective tissue alterations that are
evident with a variety of imaging studies
[13–17].
3.3.4 Hormonal Changes
ofPregnancy andParturition
Concurrent with the mechanical changes of pregnancy, hormonal alterations consisting of
increased circulating levels of relaxin, estrogen,
and progesterone, induce cellular and histologic
modications of the maternal tissues. Perhaps
one of the most signicant histological alterations of the maternal skeletal system, the ligament relaxation of the pelvis, is caused by the
aforementioned increased levels of circulating
estrogen, progesterone, and relaxin. The pelvic
laxity of pregnancy is progressive, increasing
over the course of pregnancy in concert with the
hormonal changes of pregnancy [1, 18]. For
example, the ovarian release of the hormone
aptly named relaxin begins in the rst trimester
and effects joint laxity as early as the 10th week
of pregnancy. These changes persist 4–12weeks
postpartum [19–23]. These hormonal alterations,
such as the relaxation of the pubic symphysis and
sacroiliac joints, are biologically necessary and
advantageous to facilitate delivery of the fetus by
widening the pelvic inlet.
It is important to note that in addition to
increased skeletal and joint laxity, there is also
increased soft tissue laxity during pregnancy. For
example, the vagina is noted to become increasingly distensible during pregnancy. This process
is believed to be mediated by hormonal changes
causing increased collagen and elastic synthesis
in the broblasts of the pelvic oor. In fact, animal models have been used to demonstrate that
the vaginal wall and its supportive tissue complex
are far more distensible and less stiff during pregnancy [24]. In conclusion, the gestational hormonal milieu contributes to the development of a
progressive and generalized compliance and
laxity.
3.3.5 Antepartum Alterations
ofGross Maternal Anatomy
As a consequence of both the aforementioned
mechanical and hormonal processes of pregnancy, there occurs a series of anatomical adaptive alterations of the maternal musculoskeletal
system. Some of these changes are highlighted
in Fig.3.9 and include the following: (1) a shift
in the axis of gravity; (2) increased force across
joints; (3) postural adjustments (increased lordosis of the lower back, forward exion of the
neck, and downward movement of the shoulders); (4) joint laxity of the anterior and posterior longitudinal ligaments; (5) widening and
increased mobility of the sacroiliac joints and
pubic symphysis; (6) anterior tilt of the pelvis
with increased use of the hip extensor, abductor,
and ankle plantar exor muscles; (7) ligamentous laxity; (8) vaginal lengthening, genital hiatal widening, and posterior vaginal relaxation
[13, 25, 26].
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~12
1st trimester
• Goodell’s sign: softening of the
cervix and vagina
• Increased mucous secretion
by endocervical glands (leukorrhea)
• Chadwick’s sign: bluish-purple
discoloration on the vaginal mucosa
• Desidualization occurs as the
trophoblasts clears the muscular
intima of the spiral arterioles and in
effect increase capacitance and
decrease resistance across the
utero placental interface.
• Hypertrophy of the myometrium and
initiation of atraumatic stretching of
the uterine corpus.
• Pear shaped uterine lengthens
vertically as it approaches the height
of the symphysis pubis at 12 weeks.
~26
weeks
2nd trimester
• Continued hypertrophy of the
myometrium and atraumatic
stretching of the uterine corpus in to
more of an ovoid shape.
• Progesterone,estrogen and relaxin
secretion by the maternal ovaries
signal alteration in the connective
tissues of the pelvis musculature,
ligaments in the pelvis and uterine
ligaments (ex: round, uterosacral) to
relax and increase laxity
• Onset of irregular and focal
contractures of the myometrium
triggered by stretching and activation
of myocytes
• Vascular endothelial growth factor
(VEGF) and other angiogenic factors
lead to increased vascularity of the
uterus, vagina and perineal body
~38
weeks
3rd trimester
• Further atraumatic stretching of the uterine
corpus leads to Thinning of the lower
uterine segment to 5-10 mm in thickness
• Broad, round and uterosacral ligaments
continue to stretch and trigger sharp pains
as the nerve fiber along the pelvic floor are
triggered
• Waddle sign: complete progression of the
laxity of the pelvic ligaments leads to the
15 to 50 mm separation of the symphysis
pubic and sacroiliac joint leading to gait
Stability
• Uterine contractions become more
organized by the signalling coordinating
the gap junctions between the myometrial
cells this effects the uterine fundus function
as a syncytium and creates coordinated
albeits irregularly timed contraction prior
to labor (Braxton-Hicks)
• Musculature of the pelvic floor continues to
increase in laxity due to molecular signaling
and alterations of collagen
• As the lower uterine segment thins as the
fetus descends/engages in to the maternal
pelvis, the presenting fetal part compresses
the maternal bladder anteriorly reducing the
volume capacity near term. Such change
effectively increase urinary frequency.
Fig. 3.9 Antepartum alterations of maternal anatomy
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3.4 Complications
oftheAnatomical
andPhysiological Changes
ofPregnancy
As described previously, the physical and physiological adaptions and changes of pregnancy to
the maternal musculoskeletal system result in a
proclivity to pelvic laxity and joint mobility. The
progressive lordosis, weight increase, change in
the center of gravity, and increases in the laxity
and mobility of the sacroiliac, sacrococcygeal,
and pubic joints, all stress and alter the maternal
musculoskeletal system. In addition to these
mechanical changes, the hormones of pregnancy
(including relaxin, progesterone, and estrogen)
cause a further predisposition to pelvic laxity and
joint mobility [1, 18]. For the most part, these
adaptations and changes to the maternal musculoskeletal system are considered normal and necessary for childbirth. In fact, without the timely
increase in laxity and skeletal exibility, the
descent of the fetal head through the birth canal
would be far more disruptive to the ligaments of
the pelvic ring and the surrounding soft tissue
structures. However, when these changes are
severe and profound, for example causing traumatic separation of the pelvic bones or ligaments,
these changes may become pathologic and result
in a variety of problems including arthralgia,
back pain, transient osteoporosis, and tendonitis
[18–22].
One such example of how a normal change
during pregnancy may cause pathology for the
woman is in how the mere increase in pelvic laxity and joint mobility may itself lead to pain with
ambulation and pelvic instability. This unsettling
sense is called symptomatic pelvic girdle relaxation. Typically, up to 4–7cm of increased circumference of the pelvis is well tolerated and
categorized as asymptomatic, but increases in
excess of this distance are met with pathologic
and symptomatic intolerance [22, 23, 27, 28].
Given that there are anatomical and physiological changes during pregnancy far in advance of
delivery, it is ostensible to note at this time that
these physiological and physical changes of gestation, from a practical standpoint, negate the
potential benet of “prophylactic cesarean.”
Essentially, the biomechanical stretch and hormonally induced changes of the connective tissue
scaffolding of the pelvis occurs well before the
fetus is delivered, and these changes may persist
past the puerperal period and contribute to pelvic
oor dysfunction [13–17]. Several studies have
demonstrated the association between pregnancy
and changes to maternal anatomy. In the Childbirth
and Pelvic Symptoms study (CAPS), a contemporary human cohort study of primiparous women,
the authors found that 23% of women having
cesarean section without labor still reported urinary incontinence symptoms at 6months postpartum [29]. Similarly, in a study by Rogers et al.,
low risk primiparous women undergoing vaginal
delivery had similar rates of bothersome pelvic
oor dysfunction at 6 months postpartum compared to primiparious women who underwent
cesarean delivery prior to entry into the second
stage of labor [30]. These studies suggest that gestation itself affects the urinary system. This effect
is further elucidated in the Weidner etal. study via
comparison of urethral sphincter neuromuscular
function among nulligravid versus primigravid
women which notes a signicant and lasting
decrease in the urethral sphincter neuromuscular
function between the two study cohort groups.
Furthermore, Weidner at al found that the decrease
in neuromuscular function of the urethral striated
sphincter persisted at 6 months postpartum—a
nding which does not coincide with the classic
temporal pattern seen with direct injuries, i.e.,
neurogenic or myopathic injuries of the pelvic
oor occurring during childbirth [5]. These studies underscore the signicant role and impact of
both the normal physiological changes of pregnancy in the pathogenesis of urinary dysfunction
following pregnancy.
In the next section of this chapter, we will
describe the relevant anatomy and processes of
labor and delivery and review the respective
changes and possible pathologies that arise from
parturition.
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