CHAPTER 123 Low Back Pain and Pregnancy – Examination and Diagnostic Work-up in the Pregnant Patient

Colleen M. Fitzgerald, Christina Kerger Hynes

INTRODUCTION

Nearly any medical condition that can occur in the nonpregnant state can occur during pregnancy. In fact, because of the pregnant state, women can potentially be at higher risk of misdiagnosis due to the overall general concept that all back pain in pregnancy is somewhat ‘normal’.¹ Back pain in pregnancy is common, but when it becomes disabling it demands further diagnostic evaluation. Estimates of incidence are 50–70%.² One prospective study of back pain in pregnancy showed a prevalence rate of 60%, with 30% of those patients reporting severe limitations in their daily activities.³

Special consideration of postpartum back pain should also be made in the context of the continuum of pregnancy-related pain.

The physiologic changes of pregnancy may predispose women to back pain. The increased lumbar lordosis combined with the effects of the hormone relaxin on the joints of the lumbar spine and pelvis with the added weight of the gravid uterus result in a shift of the center of gravity anteriorly and an increased mechanical burden on the low back.^2,⁴ The abdominal wall musculature of the abdominal cavity stretches as the gravid uterus grows. The force–tension curve of the lengthened abdominal muscles restrict their contractile strength while the muscles of the low back work harder to maintain upright posture. The muscles of the pelvic floor will bear the weight of the growing uterus and will eventually allow passage of the fetus. Relaxin is a polypeptide hormone secreted by the corpus lutea and has been identified as the major contributor to joint laxity during pregnancy.⁴ It is dramatically elevated during the first trimester, declines early in the second trimester to a level that remains stable throughout the pregnancy,⁴ and then declines sharply after delivery. Widening of the symphysis pubis and increased mobility of the sacroiliac synchondroses begins in the tenth to twelfth week of pregnancy as a result of relaxin.⁵ The strong sacroiliac ligament which normally resists forward flexion of the ala will become lax with the effects of relaxin.⁵ Weight gain, maternal obesity, and fetal weight at term have not been found to be related to pregnancy-related back pain.⁶ Other studies have shown that low back pain prior to or during a previous pregnancy, nulliparity with increased body mass index (BMI), lower socioeconomic status, and placenta with a posterior fundal location were found to be risk factors for back pain in pregnancy.³⁵ A spectrum of clinical symptoms may be produced by the physiologic changes of pregnancy. However, the differential diagnosis of back pain in pregnancy should not be limited to pregnancy-related changes in the musculoskeletal system.

Clinical entities implicated as causes of back pain in pregnancy in one review article include: pelvic insufficiency (pain), sacroiliac joint (SIJ) subluxation, sciatica, lumbosacral disc pathology, spondylolisthesis, postural back pain and lumbar lordosis, thoracic back pain and coccydynia.⁶ Other studies have also included hip pathology, such as osteonecrosis of the femoral head and transient osteoporosis of pregnancy, as a potential cause of referred back pain.⁵ Other known causes of back pain include neurologic etiologies such as radiculopathy or plexopathy, vertebral segmental dysfunction, tumor, or fracture of the sacrum or pelvis. There is also growing evidence that the pelvic floor musculature is a pain generator, especially in relation to coccydynia and dyspareunia (Table 123.1).

Table 123.1 Visceral Causes of Low Back Pain in Pregnancy ⁶

GENITOURINARY
	Urinary tract infection
	Kidney stones
	Pyelonephritis
	Cystitis
	Urethritis
GYNECOLOGIC
	Ovarian cyst or torsion
	Uterine dysfunction or placental abnormality
	Pelvic inflammatory disease
GASTROINTESTINAL
	Constipation
	Hemorrhoids
	Irritable bowel syndrome
	Hernia

PELVIC OBLIQUITY

The pelvis is a ring comprised of two innominate bones that are connected anteriorly by the pubic symphysis and posteriorly to either side of the sacrum by the SIJ. The pelvis is dynamic or more mobile in the pregnant state as a result of the influence of relaxin on the ligamentous structures. Laxity itself is widespread and does not necessarily result in pain. Asymmetry of any part of the ring will cause dysfunction on the opposite side, i.e. dysfunction of the posterior pelvis will result in asymmetry and dysfunction of the anterior pelvis. They do not occur in isolation. However, there is a clear relation between asymmetric laxity of the SI joints and pregnancy-related pelvic pain (PRPP).⁸

There is an array of nomenclature to describe a given obliquity. By convention, dysfunction of pelvic ring is named on the hypomobile side. However, anecdotally, in the pregnant state the hypermobile side on physical examination can correlate with the side of pain. Damen et al. studied the prognostic value of laxity in assessing pain postpartum. Asymmetric laxity of the SI joints in pregnancy was believed to increase the presence of pelvic pain postpartum by as much as threefold.^9,¹⁰ This speaks to treatment of asymmetry of the SI joint and its associated pain during pregnancy to prevent future back pain.

In pregnancy, the innominate obliquity is commonly named for the side which gives the patient pain in order to best direct the physical therapy prescription. A number of anatomic landmarks are used to determine pelvic obliquity: the iliac crest, the posterior superior iliac spine (PSIS), the anterior superior iliac spine (ASIS), and the pubic tubercles. The inferior lateral angle of the sacrum (ILA) can also be assessed to further delineate asymmetric sacral positioning in relation to ilial positioning. By measuring the side-to-side difference between these landmarks, the type of obliquity can be determined. A problematic hemipelvis can be rotated anteriorly or posteriorly, sheared superiorly (upslip) or inferiorly (downslip), inflared or outflared. Sacral positioning can be described similarly.¹¹

SACROILIAC JOINT DYSFUNCTION

The sacroiliac joint is a true joint consisting of a synovial component inferiorly. It is auricular-shaped with the thinner sacral side lined with hyaline cartilage and the thicker ilial side with fibrocartilage. Primary innervation to this joint is thought to be from S1. Sturesson, in 1989, described true movement of the SIJ measuring approximately 1–3° of rotation.¹² The sacroiliac joint has also been shown to be a potential generator of low back pain.¹³ In the pregnant patient, the potential for dysfunction is increased secondary to pregnancy-related hormone-induced ligamentous laxity and resultant asymmetry. It is thought that the laxity prepares for and facilitates delivery of the baby at term.¹⁴ Ostgaard, in a prospective study of back pain in 855 pregnant women, found an incidence of 19% with sacroiliac pain in week 30 of gestation.¹⁵ Additionally, Damen showed that in pregnant patients who were evaluated by Doppler imaging of vibrations there was found to be a definite relationship between asymmetric laxity of the sacroiliac joints and pregnancy-related pelvic pain.⁸ Patients typically report pain over the sacrum or the sacral sulcus. Transitional motions, particularly while turning in bed and arising from the seated to the standing position frequently triggers or exacerbates the presenting symptoms. Physical examination maneuvers will be discussed later, but posterior pelvic pain provocation test and active straight leg raise testing are well-documented, reliable diagnostic tests to assess pregnancy-related sacroiliac joint pain.

The relationship between pelvic obliquity and sacroiliac joint dysfunction is somewhat intuitive. Typically, when a persistent pelvic obliquity exists there is associated SIJ pain and dysfunction due to the anatomic relationship between these structures. The pelvic obliquity, which is secondary to ligamentous laxity, is thought to create the SIJ dysfunction and change in joint mechanics.

PELVIC FLOOR MYOFASCIAL PAIN

The pelvic floor is made up of two layers of muscles. The superficial layer of muscles including the ischiocavernosus, bulbocavernosus, and transverse perinei muscles make up the urogenital diaphragm. These superficial muscles provide uretheral support and may be superficial pelvic pain generators. The deep pelvic floor musculature is made up of two large muscles, the levator ani and the coccygeus. The levator ani is actually made up of a combination of three muscles, specifically the pubococcygeus, the puborectalis, and the iliococcygeus. A firm understanding of the anatomy of this region is paramount to fully appreciating the functional significance of these muscles. They are appropriately named for their attachments at the level of the coccyx and hence should be considered as potential sources of coccygeal pain, especially when the muscles are in a shortened state.

All of these muscles together form the pelvic floor which provides support for the intra-abdominal organs and prevents prolapse. Their combined optimal function as a neuromuscular unit is integral to maintaining urinary, flatal, and fecal continence. They also contract during orgasm to provide sexual appreciation. The pelvic floor muscles have a heightened role during pregnancy in maintaining functional support of the changing body habitus. They can be damaged at the time of labor and delivery and remain a persistent cause of pain.

When a pelvic obliquity is present, the resulting asymmetry affects the pelvic floor muscles that originate from and that are attached to the pelvic bones. With a pelvic obliquity, the attaching muscles will be either abnormally shortened or lengthened. A force–tension curve of these muscles will be shifted, thereby demonstrating their disadvantageous biomechanical state. As well, it is known that muscle injury and soreness are more selectively associated with eccentric contraction.15a-c An inherently lengthened muscle must also work harder to function properly, and if the external force on the muscular floor is greater than the force the muscles can generate, weakness may eventually develop in addition to or in conjunction with pain.

COCCYDYNIA

Coccydynia (synonymous with coccygodynia and coccyodynia) is defined as pain in and around the coccyx without significant symptom referral. Sitting or arising from the seated to standing position are common exacerbating influences. A prepartum history of coccyx pain or complaints of very low back pain or tailbone pain warrant consideration of this diagnosis in pregnancy. The coccyx is heavily supported by ligamentous structures and serves as the attachment point for pelvic floor musculature. The combination of laxity and asymmetry can create abnormal motion at the level of the coccyx similar to that of the SIJ. It is important to note that coccygeal pain may be secondary to pelvic floor muscle myofascial pain and dysfunction.

There is a blatant absence of literature guiding the evaluation of the coccyx in pregnancy; however, it can be easily done via rectal examination. A study by Maigne ¹⁶ found that body mass index determines the manner by which a subject sits down and that pathologies were different in obese, normal weight, and thin patients. For a detailed description of the analyses in the nonpregnant patient the reader is referred to Chapter 120 by Yves Maigne. Hypermobility of the coccyx defined as coccygeal flexion exceeding 25° when the patient is in the sitting position as evaluated on plain radiograph was also a cause of coccydynia. The pregnant state lends itself to the potential of coccygeal dysfunction and pain with the acute increase of BMI over 9 months as well as ligamentous laxity that accompanies pregnancy as a result of relaxin and estrogen.

STRESS FRACTURE

Stress fracture is defined as fracture due to repetitive cyclic loading on normal bone, whereas insufficiency fracture occurs when normal forces are applied to abnormal bone. Stress insufficiency fracture occurs when repetitive cyclic loading occurs in the setting of abnormal bone. Any of these fractures at the level of the sacrum, pelvis, or hip may be the cause of back pain in the pregnant patient, similar to the nonpregnant patient. Fractures should be considered in a patient diagnosed with sacroiliac dysfunction which is not improving with medical rehabilitation and interventional spine techniques; in the case of known trauma; or in a patient with a prepartum history of amenorrhea, eating disorder, or known osteopenia (female athletic triad).¹⁷

Risk factors specific to pregnancy that predispose for sacral fatigue fractures include rapid or excessive weight gain in the third trimester, increased lumbar lordosis, pelvic instability due to relaxin effect, rapid vaginal delivery, and prolactin-induced transient osteopenia. These injuries should also be considered immediately postpartum in the breastfeeding patient. Polatti showed evidence of a progressive decline in bone mineral density (BMD) in lactating women over the first 6 months with increase in BMD following a 1-month weaning period.^17a Calcium supplementation during lactation had only a transient effect in minimizing bone loss.

The imaging study of choice in pregnancy after the first trimester when there is a high suspicion of stress fracture is magnetic resonance imaging. A comprehensive literature review revealed several reported sacral fractures associated with pregnancy.^18,^19,^19a

PUBIC SYMPHYSIS

Symphysitis and symphyseal separation

Pubic symphysis motion and asymmetry is seen during pregnancy. Anterior pain can be associated with this increased motion and simultaneously precipitate posterior pelvic or low back pain. Maximum widening of the pubic symphysis during pregnancy is considered to be 10 mm. By definition, pubic symphysis separation is a width greater than 10 mm and is usually seen after a traumatic labor and delivery. Bjorklund et al., in 2000, studied the association between symphyseal distention and pelvic pain and circulating relaxin levels in the pregnant patient.²⁰ They found that severe pelvic pain during pregnancy was strongly associated with an increased symphyseal distention; however, relaxin levels were not associated with the degree of distention or with pelvic pain in pregnancy. Another study showed that the majority of pregnant women with symphyseal pain had an average pubic symphysis width of 9.5 mm or more via sonographic measurement. In comparison, the asymptomatic pregnant patient had an average width of 6.3 mm.²¹

Osteitis pubis

Acute pubic symphysis inflammation, which can begin in pregnancy in association with a pelvic obliquity, can often lead to a chronic, painful, noninfectious inflammatory condition known as osteitis pubis. Osteitis pubis has been described as a complication of various obstetrical and gynecological procedures, including vaginal deliveries.²² Periosteal trauma seems to be part of the initiating event, although there is controversy regarding the true pathophysiological nature of the disorder. One of the first cases cited in the obstetrical literature was a report of a patient with osteitis pubis after a traumatic forceps vaginal delivery. Wiltse and Frantz reported 10 cases associated with the pregnant state.²³ As the pubic symphysis becomes more lax to allow passage of the fetus, there is potential for excess movement and trauma. Plain films are the imaging method of choice; however, radiographic findings often lag behind clinical symptoms. Typically, X-ray changes can be seen 4 weeks after the traumatic event, and include loss of smooth cortical bone and reactive sclerosis. Treatment needs to be initiated based on physical examination in the peripartum period to prevent chronic postpartum pain.

LUMBAR DISC HERNIATION

Although early studies by LaBan et al. in 1983 ²⁴ suggested that pregnancy was an independent risk factor for the development of a herniated disc, it has been proven in subsequent studies that the actual incidence of lumbar herniated disc is no greater for pregnant women than for the general population.^2,⁴ It is an uncommon etiology of low back pain in pregnancy with an incidence of 1:10 000.²⁴ Risk factors include prior history of low back pain, increased body mass index, and lower socioeconomic status. Advanced maternal age, birth weight, and primiparity are controversial risk factors. In the last 20 years, the incidence of women aged 30 years and older at delivery has increased from 17.7% to 30.2%.^24a Since the inexorable alterations that occur as the degenerative disc cascade proceeds²⁵ will be more prominent as a female ages, it is expected that the probability of pain emanating from degenerative disc disease will be higher in this group. Pain from lumbar degenerative disc disease should be considered in the pregnant and nonpregnant patient alike who complains of back pain, numbness and tingling, or with neurologic findings on examination. A thorough examination is critical to differentiate the symptoms of degenerative disc disease from the radicular pain of a herniated disc from SIJ dysfunction. It is important to note that patients can have SIJ dysfunction concurrently with an S1 radiculopathy. If there is progressive weakness or bowel or bladder incontinence in pregnancy associated with back pain, cauda equina syndrome must be ruled out. Immediate imaging with MRI and surgical referral, even in pregnancy, is warranted.