NEARLY ALL WOMEN HAVE MUSCULOSKELETAL complaints at some point during their pregnancy, including a significant portion with severe pain and/or disabling symptoms.^1,2 Unfortunately, women in this population may be counseled by well-intentioned family, friends, and care providers that their pain symptoms are a “normal” part of pregnancy and the postpartum period. Minimization of pain during pregnancy may lead to a delay in diagnosis of musculoskeletal pathology, or worse, a total lack of care. Consequently, this vulnerable patient population faces the potential for increased morbidity, development of chronic disease, decreased quality of life during pregnancy, and potential disability. The presence of severe pain during pregnancy may also lead women to refrain from future pregnancies due to fear-avoidance behaviors.³

There are a myriad of pathophysiologic diagnoses involving the neurologic and musculoskeletal systems that affect pregnant and postpartum women (Table 38–1). Although not covered in this chapter, it is important to also consider gynecologic, gastroenterologic, infectious, rheumatologic, and oncologic diagnoses since these can also present with neurologic and musculoskeletal symptoms. Pregnancy and lactation necessitate judicious use of imaging and medications. Conservative management including physical therapy and complementary medicine treatments that are typically viewed as benign must also be carefully considered and adjusted to reduce risk of harm to the mother and her child.

Rehabilitation of the pregnant and postpartum woman with pain is complex and requires close monitoring, supervision, and care coordination to ensure safe, effective care for the mother and baby. The goal of this chapter is to provide clinicians with tools to assist in diagnosis, treatment, and prevention of musculoskeletal or neuromuscular pain in the pregnant and postpartum patient.

Low Back Pain

Low back pain (LBP) is the most common musculoskeletal complaint in pregnancy. LBP is broadly reported to affect 45% to 75% of pregnant women at some point during their pregnancy and 30% to 45% of women in the postpartum period.^1,4–8 Up to 25% of women report severe pain, with 8% reporting severe disability due to low back pain.⁵ Likely, these statistics are underestimations. The rate of reporting LBP symptoms is low, estimated at 32%, possibly due to the belief that LBP in pregnancy is “normal” or “expected.”^1,3,5

The differential diagnosis for LBP in pregnancy is broad, and etiology ranges from benign to serious causes. Risk factors for development of LBP in pregnancy include prior back pain, multiparity, back pain in a prior pregnancy, joint hypermobility, and elevated body mass index (BMI).^1,5,8 Risk factors for persistent LBP in the postpartum period at 24 months include premorbid back pain, joint hypermobility, earlier onset of low back pain (first trimester), and persistently elevated BMI postpartum (above pre-pregnancy levels).^1,2 Exercise prior to pregnancy and during pregnancy are factors that have been shown to prevent the development of LBP during pregnancy and alleviate low back pain symptoms during pregnancy.¹

Common Causes of Musculoskeletal Low Back Pain

Benign LBP is the most common cause of LBP in pregnancy. The differential diagnosis of benign LBP in pregnancy is broad. Hormonal shifts, including increased relaxin and estrogen levels, are theorized to contribute to the development of benign LBP due to increased ligamentous laxity and subsequent changes in joint stability.^1,2,5,8,9 Relaxin levels peak around 12 weeks in pregnancy, but increased ligamentous laxity persists throughout pregnancy and into the postpartum period (Fig. 38–1).^1,10 Additional biomechanical changes associated with pregnancy, including weight gain, hyperlordosis, and anterior pelvic tilt (resulting in an anteriorly shifted center of gravity), also may contribute to LBP symptoms.^1,2,5,8,9 In addition to hormonal and biomechanical changes in pregnancy that lead to laxity and mechanical strain injuries, pregnant women are at risk, particularly at advanced maternal age, for other benign causes of low back pain. These include lumbar discogenic pain (degenerative disc disease, disc bulging, and disc herniation), lumbosacral radiculitis, degenerative disease (spondylosis, spondylolisthesis), and ischemia from vascular compression of the inferior vena cava by the gravid uterus.^1,5,11,12 Pain generators external to the lumbosacral spine, such as pelvic girdle pain (PGP) or hip pathology, must also be considered given similar pain referral patterns to the low back, but lumbar pain generators should be ruled out first. (Figs. 38–2 and 38–3)

A thorough history and neurologic and musculoskeletal examination of the lumbosacral spine, pelvis, and hips is crucial in narrowing the diagnosis and guiding treatment. Dural tension testing, such as the seated slump and supine passive straight-leg raise tests, which place traction on the exiting spinal nerve roots, can help to diagnose the presence of lumbar disc herniation with nerve root involvement (Fig. 38–4).^13,14 In the absence of myelopathic signs, isolated single root-level radiculopathy is often managed conservatively.¹² Reflexes are typically easy to elicit in pregnancy; thus decreased or absent reflexes are usually quite significant. Reflex testing to this end remains an important part of the neurologic exam.

Low back pain severity does not always correlate with imaging findings. Because of this, the utility of routine imaging in the diagnosis of suspected benign musculoskeletal low back pain is low and has not been shown to change outcomes in the general population.¹² Magnetic resonance imaging (MRI) of the lumbosacral spine can be considered in patients whose pain does not improve with a 6-week course of conservative management, but should ideally be postponed to the postpartum period (if obtained at all), except in the presence of red flag symptoms, described in further detail later. A study evaluating MRI of the lumbosacral spine in healthy, asymptomatic women of childbearing age compared to pregnant women found no significant difference in disc bulges and herniations between groups.^1,2,8,15 Therefore, the use of ionizing or MRI in cases of musculoskeletal low back pain in the absence of red flag signs or symptoms (Table 38–2) is not recommended. Gadolinium contrast is contraindicated in pregnancy as well.

Musculoskeletal back pain in the absence of red flag signs or symptoms is typically self-limited with excellent response to conservative management. Initial treatment of musculoskeletal back pain in this population should be conservative. Physical therapy is recommended, preferably with a Women’s Health Certified Specialist (WCS) physical therapist (PT). Specialized evaluation with a PT who specializes in spine care with certification in mechanical diagnosis and treatment (MDT) can also be considered for patients with lumbosacral pain, but it should be noted that MDT therapy has not been studied or validated in pregnancy.

In general, the focus of physical therapy should be on active (rather than passive) patient-directed therapy with core and spinal stabilization, directional preference exercises (typically with an extension bias for discogenic pain), postural correction exercises, and progressive return to a therapeutic exercise program.^1,5,9 Careful consideration should be made for patients suffering from preeclampsia, and consultation with the obstetrician is ideal prior to beginning a rehabilitation program.

Lumbar and abdominal support binders for symptomatic care and external stabilization exercises can also be utilized for women with pain stemming from weakened core musculature—though it should be noted that binders will not be effective in instances of lumbar disc herniation or other focal pathology of the lumbosacral spine.^1,2,5,8 Complementary and alternative therapies, including acupuncture, osteopathic or chiropractic manipulation, massage, and yoga, are all thought to be safe and well-tolerated treatment options in pregnancy, but a risk/benefit discussion is warranted prior to considering their use in pregnancy, given the lack of clearly established evidence regarding safety and efficacy in this vulnerable population.¹ Oral analgesic medications may be recommended and will be described in greater detail later. Women should be counseled on red flag symptoms indicative of serious low back pain (noted next), which would prompt return for urgent/emergent evaluation.

Low Back Pain with Red Flag Signs and Symptoms

Serious causes of LBP (vertebral fractures, sacral insufficiency fractures, spinal cord compression, cauda equina syndrome) should be considered in pregnant and postpartum patients presenting with red flag symptoms (see Table 38–2).¹² In patients with identified red flag symptoms, referral to an emergency room for further risk stratification, consideration for urgent (within 48 hours) versus emergent (immediate) MRI of the lumbosacral spine, and neurologic/neurosurgical evaluation is recommended.¹²

Interventional Procedures for Low Back Pain

The safety and efficacy of epidural steroid injections (without use of fluoroscopic guidance, since radiography is contraindicated) in pregnant women are unknown and therefore are not recommended.¹ Anatomic-guided (nonfluoroscopic) epidural steroid injections are theoretically thought to be safe when performed by an experienced interventional pain physician.¹ However, steroid exposure in pregnancy is not recommended and should be deferred until the postpartum period due to the concern for adverse fetal effects. Women who are lactating should be informed that high-dose glucocorticosteroids can suppress lactation for 24 to 48 hours.¹⁶ Orthopedic and neurosurgical spine interventions should be reserved for women with neurologic red flags (see Table 38–2) and high-risk diagnoses, including unstable vertebral fractures, cord compression, and cauda equina syndrome, as described earlier.^1,2,5,8,9

Pelvic Girdle Pain

Per the 2008 European guidelines, PGP is “defined by pain experienced between the posterior iliac crest and the gluteal fold, particularly in the vicinity of the sacroiliac joints (SIJ). The pain may radiate in the posterior thigh and can also occur in conjunction with/or separately in the [pubic] symphysis.”¹⁷ PGP is a diagnosis of exclusion, which can be made only after ruling out lumbar spine pain generators.^3,7,17–22 PGP is classically associated with pregnancy, trauma, and reactive arthritis.^3,7,17,18,22 As in LBP, pregnancy- and postpartum-related PGP is thought to arise due to hormonal factors and nonoptimal pelvic joint stability.^3,7,17,18,22 Pelvic joint stability can be affected by alterations in form closure of the bony joints; force closure of the musculotendinous, ligamentous, and fascial soft tissues; and alterations in motor control.²² Pregnancy-related PGP (PRPGP) is common, with a prevalence reported between 23% and 65% of women.^3,19,23 Postpartum PGP (PPPGP) is less common, but its prevalence has previously been reported at 8% to 20% in the first 3 years postpartum.^23–25 The majority of cases of PGP are self-limited and resolve within 12 weeks’ postpartum.²⁶ Risk factors for persistent PPPGP include older age (>30 years old), a moderate-high Oswestry Disability Index (ODI) during pregnancy, and the presence of concomitant PGP and lumbosacral pain during pregnancy.²⁴ Cesarean section has been independently associated with increased risk for persistent PGP.²⁷ Breastfeeding has not been associated with persistent PGP, and in fact a recent follow-up study of 10,603 women demonstrated that breastfeeding actually has a small positive effect on improvement in PGP symptoms, and thus should be encouraged.²⁸

Women with PGP report pain with transitional movements. Functional disability complaints, including decreased tolerance for prolonged sitting, standing, or walking, may also be reported.^17,19 PGP can be reproduced by specific physical examination provocative maneuvers.^3,7,17,22 In pregnant women, Vleeming et al’s European guidelines proposed validated maneuvers for diagnosis of PRPGP, including pain provocation tests (Posterior Pelvic Pain Provocation/P4/Thigh Thrust Test, Patrick’s/FABER Test, Gaenslen’s Test, Modified Trendelenburg Test) and pain palpation tests (pubic symphysis palpation, long dorsal ligament palpation) (Fig. 38–5).¹⁷ The P4 and Patrick’s/FABER tests are the most sensitive and specific tests for evaluation of PRPGP.^17,29 The classic Laslett provocative sacroiliac (SI) joint maneuvers (Sacral Thrust Test, Heel Drop Test, Gaenslen’s Test, P4/Thigh Thrust Test, Pelvic/Sacroiliac Joint Distraction Test, and Pelvic/Sacroiliac Joint Compression Test) have not been validated in pregnancy but can be used in postpartum patients (see Fig. 38–5).^{17,19,30–32} Based on Laslett’s criteria, three out of six positive tests are 91% specific for SI joint mediated pain.^30,31 Pubic symphysis pain provocation maneuvers include Patrick’s/FABER, Passive Straight-Leg Raise Pubic Symphysis Palpation, and modified Trendelenburg Test (Fig. 38–6).^17,31,33 Diagnosis of PGP can typically be made clinically, and imaging is recommended only if red flags are present (as described earlier).¹⁷

Sacroiliitis is largely a clinical diagnosis. A physical therapy program focusing on SI joint mobilization should be prescribed; an SI joint belt may also be considered. Steroid injection into the SI joints and radiofrequency ablation of the sacral nerves should be avoided if possible.

Treatment of PGP focuses primarily on pelvic stabilization. The active straight-leg raise test (ASLR) is a functional test used in the assessment of PGP, and is helpful for predicting response to stabilization exercises if the patient experiences improvement of her pain/symptoms when the examiner provides manual external compression of the pelvic ring (Fig. 38–7).^17,32 Pelvic stabilization can be active and patient-directed through the use of pelvic stabilization exercises, or passive with the use of external pelvic stabilization belts. Prescription of an active, individualized exercise program (under the guidance of an American Physical Therapy Association (APTA)–certified WCS PT) focusing on pelvic stabilization exercises to enhance motor control/muscular force closure of the pelvis is recommended.^17,34 Because of the conflicting evidence behind the use of pelvic stabilization exercises alone, the addition of physical therapy exercises promoting muscular strengthening of the entire spine is also recommended.³⁴ Use of pelvic stabilization belts to provide passive external force closure of the pelvis is frequently prescribed for PGP, but there is a lack of established evidence to support their efficacy.^7,22,26 Patients with improvement of symptoms on functional ASLR testing may have greater benefit from the prescription of pelvic stabilization belts. Ideally, pelvic stabilization belts should be used in concert with active patient-directed PT. Pelvic stabilization belts have been shown to have highest efficacy when placed directly below the anterior superior iliac spines (ASIS).³⁵ Importantly, pelvic stabilization belts should be distinguished from abdominal binders and lumbar braces, which are not of benefit in the management of PGP. Use of complementary therapies such as acupuncture and chiropractic manipulation lacks established evidence but can also be considered as adjunctive therapy if benefit outweighs risk.^7,22,26

Pubic Symphysis Separation

In healthy, nonpregnant women, the pubic symphysis measures about 3 to 6 mm in width.⁹ Pubic symphysis widening up to 10 mm is a normal part of pregnancy.³⁵ This widening begins around 10 to 12 weeks’ gestation, and is promoted by hormonal changes (increased relaxin/estrogen), as well as structural changes with the growing gravid uterus and pregnancy-related weight gain.^{1,2,5,8,9,17,33} As the pubic symphysis widens, pain can develop, but notably the degree of widening or separation on imaging does not correlate with symptoms.^1,5 Pubic symphysis pain is more common in the second and third trimesters as pregnancy progresses.⁵ In contrast to physiologic pubic symphyseal widening, pathophysiologic true separation, or “rupture” of the pubic symphysis (beyond 10 mm), is rare and is considered a postpartum diagnosis that typically arises from traumatic injury to the pubic symphysis during delivery, such as forceful fetal descent or excessive abducted positioning of the maternal hips.^1,2,5,8,9 The prevalence of pubic symphysis separation (also seen in the literature as pubic symphysis diastasis, symphysiolysis, and pubic symphysis rupture) is estimated at 1:3,000 to 1:30,000 pregnant women.^1,9,35 Pubic symphysis separation is considered a traumatic pelvic injury affecting the stability of the pelvic ring.^9,35 In pubic symphysis separation, patients report symptoms worse with transitional movements and exercise, and may have an antalgic “waddling” gait.^5,8,9 Physical examination reveals focal tenderness, difficulty with single-leg stance, and occasionally palpable widening over the pubic symphysis.^9,33 Similar to PGP, special exam tests for pubic symphysis pain include Trendelenburg test, passive straight-leg raise test, and Patrick’s/FABER Test (see Figs. 38–5 and 38–6).^17,31,33 The ASLR test without and with compression is helpful to determine if patients will respond to external pelvic compression devices (see Fig. 38–7).³²

Mild cases typically improve with rest and ice.¹ Conservative treatment is first line with an initial period of rest (particularly in the lateral decubitus position) and use of a pelvic binder (placed below the ASIS) to help maintain reduction of the pubic symphysis, followed by progressive weight bearing as tolerated (with or without an assistive device) and physical therapy with a focus on external pelvic stabilization exercises.^1,5,9,33,35 Pubic symphysis diameter typically returns to baseline within 5 months as pelvic floor muscle strength is regained.³³ Recalcitrant cases may require surgical fixation (open reduction, internal fixation).^9,35 Subsequent vaginal deliveries are felt to be safe.^9,35 Regardless of management, risk for recurrence in future pregnancies is high.^5,9,35

Osteitis Pubis

Osteitis pubis is a separate entity from pubic symphysis separation but may represent sequelae of widening of fibrocartilaginous pubic symphysis.³⁶ Imbalance of the abdominal muscles and hip adductors are thought to contribute to the development of osteitis pubis.³⁶ Osteitis pubis is an aseptic inflammatory process that presents with focal pain at the pubic symphysis with radiation into the medial groin and thigh, as well as exacerbation with Valsalva maneuver and transitional movements, and may be accompanied by a “clicking” sensation in the pubic region.⁸ The onset of pain is typically insidious with rapid progression over days.¹ Imaging demonstrates bony resorption around the pubic symphysis with subsequent re-ossification on serial exams.^1,8,36 The course is typically self-limited with good response to conservative management, including a short period of rest, protected weight bearing, oral analgesic medications, and ice, followed by physical therapy with a WCS-certified PT and progression of activity level.³⁶ Symptoms usually resolve with conservative management in days to weeks as re-ossification occurs.^1,8,36 However, a subset of patients will develop chronic pain related to osteitis pubis.³⁶ In postpartum patients with recalcitrant osteitis pubis who have failed conservative management, diagnostic/therapeutic corticosteroid and anesthetic injection of the pubic symphysis under fluoroscopic guidance can be considered.³⁶ However, in a retrospective cohort study the long-term therapeutic benefit was questionable.³⁷

Pelvic Floor Myofascial Pain and Dysfunction

Pelvic floor myofascial pain (PFMP) and pelvic floor myofascial dysfunction (PFMD) are distinct but overlapping entities. Pelvic floor dysfunction arises from abnormal activity of the pelvic floor muscles, including overactive (i.e., high tone, “spastic” pelvic floor) and underactive (i.e., low tone pelvic floor).^7,38 Pelvic floor dysfunction is an umbrella term that broadly covers a spectrum of disorders, including voiding/defecatory dysfunction (urinary incontinence, anal/fecal incontinence, retention, urgency), constipation, pelvic pain syndrome, pelvic organ prolapse (POP), and sexual dysfunction.^7,38 Pelvic floor dysfunction with increased pelvic floor muscle activity has been demonstrated in 52% of patients with pregnancy-related low back and pelvic pain.⁷ PGP has been associated with urinary incontinence (UI), and UI has been associated with pelvic floor muscle (PFM) weakness.^3,18 Hormonal changes during pregnancy (including increased relaxin) are thought to alter muscle length, thereby causing PFMD via altered contraction and relaxation patterns and subsequent changes in muscle strength.^3,18,39 These muscle contraction/relaxation pattern alterations may lead to pelvic girdle pain through joint instability, as described earlier, though this has not been conclusively demonstrated.^{3,7,17,18,22,39} There is also evidence that dysfunction of the pelvic floor muscles leads to PFMP with palpable tender points on digital vaginal exam.³ Of note, vaginal pelvic floor examination is not routinely recommended in pregnant patients but is readily done in postpartum women. Lumbosacral radiculopathy, SI joint dysfunction, and hip joint pathology can all refer pain to the pelvic floor or create a compensatory pelvic floor (PF) response and hence should be considered in a comprehensive musculoskeletal diagnosis.³⁹ Direct sources for PFMP in pregnancy and peripartum include weight bearing of the gravid uterus, labor and delivery, and any obstetric complications of delivery affecting pelvic floor muscle integrity.³ Levator ani avulsion has been documented in 20% of primiparous women and has been found in association with pelvic floor disorders, yet it is not known how this injury might influence persistent musculoskeletal pain in women.^40–42

During pregnancy, 24% to 60% of women report UI symptoms and up to 10% report flatulence/anal incontinence (AI) symptoms, with most cases resolving within 3 months postpartum.^43,44 Approximately 21% of women experience UI within 10 weeks of vaginal delivery, and an estimated 15% to 30% have UI symptoms at 5 years after their first vaginal delivery.⁴⁵ Furthermore, women with stress UI (SUI) at 3 months postpartum are reported to have a 91% increased risk of SUI symptoms at 12 years postpartum. Risk factors for the development of UI include nulliparity, vaginal delivery, and obstetric surgical delivery.⁴⁴ Risk factors for prolonged UI symptoms postpartum include incontinence during pregnancy, vaginal delivery, use of forceps, tobacco use, prolonged breastfeeding, and elevated BMI.⁴⁴ Risk factors for AI include vaginal delivery, use of instrumentation, episiotomy, increased birth weight (>4 kg), and prolonged second stage of labor.^46–48 The etiologies for UI and AI are typically a result of delivery with trauma to the bladder or urethra, anal sphincter, pelvic nerves, or pelvic floor muscles.⁴⁴

Birth-related trauma to the perineum and pelvic floor is known to occur in the setting of vaginal delivery, which poses inherent risk for perineal trauma. Perineal tears are graded from first through fourth degrees, in order of severity and structures affected (Table 38–3).⁴⁹ Obstetric repair of first- and second-degree lacerations has not been shown to positively affect postpartum pelvic floor function, and suturing of second-degree lacerations has actually been associated with an increase in postpartum PFMP.⁵⁰ Therefore, it is recommended that first- and second-degree lacerations be allowed to heal by secondary intent. In contrast, third- and fourth-degree perineal injuries (involving the anal sphincter), also known as obstetric anal sphincter injuries (OASIS), which are estimated at 2.1% of vaginal deliveries, have been implicated in the development of urinary retention, UI, AI, pelvic floor myofascial pain, and sexual dysfunction.^{45,47,49,51,52} Risk factors leading to OASIS include nulliparity and operative vaginal delivery (forceps assist, episiotomy).^49,51,53,54 Forceps delivery poses a greater risk for OASIS than both vacuum-assisted delivery and normal vaginal delivery.^49,51,55 Vaginal deliveries with or without OASIS have been implicated in the development of PFMD with AI in the postpartum period, with symptoms often persisting for years.⁴⁵ Without OASIS, 5% of women after vaginal delivery experience AI symptoms.⁴⁵ With OASIS, the prevalence of AI is estimated at 11%.⁴⁶ According to the most recent Society of Obstetricians & Gynaecologists of Canada (SOGC) OASIS guidelines, providers should follow a policy of “restricted episiotomy” and recommended obstetric slowing of the fetal head at crowning to decrease the risk of OASIS.^47,49,56 The SOGC Guidelines also note that women with OASIS can safely deliver vaginally in future pregnancies but do have a 4% to 8% risk of recurrent OASIS (which is lower than the maternal risk of cesarean section).⁴⁹

Unfortunately, the acute and chronic UI/AI symptoms described earlier may be viewed by patients as a “normal” part of pregnancy. Consequently, women often avoid seeking professional help for AI/UI symptoms, which obscures the true prevalence.⁴⁵ It is important to ask patients in the pregnancy and postpartum period about incontinence symptoms and pelvic pain with sexual intercourse, as these symptoms may not be easily proffered and thus may be easily missed.³⁹ Once identified, management of PFMP and PFMD should be interdisciplinary and can include obstetric repair of third- and fourth-degree perineal tears (including urinary and/or anal sphincter repair as needed), physiatry evaluation, women’s health/pelvic floor physical therapy referral (with an APTA WCS-certified PT with Certificate of Achievement in Pelvic Physical Therapy [CAPP] certification, if possible), therapeutic exercise, biofeedback, pain psychology, sexual counseling, and oral medications (nonsteroidal anti-inflammatory drugs [NSAIDs], Tylenol, bladder medications, laxatives in the acute setting, antidiarrheals in the chronic setting, neuropathic agents, sleep aids).^39,46,49 Knowing when to refer patients with ongoing symptoms for further gynecologic, urologynecologic, urologic, colorectal, gastroenterologic, and psychiatric evaluation is crucial in ensuring adequate management of these patients.³⁹ In recalcitrant cases of UI/AI, secondary elective surgical repair and sacral nerve stimulation can also be considered.⁴⁶

Diastasis Recti Abdominis

Diastasis recto abdominis (DRA; seen also in the literature as rectus diastasis and rectus diastasis separation) is a separation of the two muscle bellies of the rectus abdominis due to weakening of the linea alba, particularly near the level of the umbilicus, related to the widening of the abdomen due to the growing gravid uterus, displacement of abdominal organs, and hormonal changes of pregnancy.^57–60 Cesarean section has been proposed to pose a higher risk for DRA than vaginal delivery, although more recent evidence has shown no difference between method of delivery.⁶⁰ Regular exercise prior to and during pregnancy is felt to decrease the risk for development of DRA.⁵⁸ The exact incidence of DRA is unknown but is thought to start around week 14 of gestation, peaks in the third trimester of pregnancy (reported in 66% to 100% of women), and persists immediately after delivery (reported in 53% of immediate postpartum women).^57–59 Typically, there is partial resolution of DRA at 1 to 8 weeks’ postpartum, but many women have persistent DRA for months or years.^58,59 The clinical implications of DRA are unknown, but it has been proposed that DRA may lead to lumbopelvic pain and instability due to changes in posture and core muscle stability.⁵⁷ DRA can be evaluated by palpation on physical examination (Fig. 38–8).⁵⁷ A diagnosis of DRA is made when widening is greater than two fingerbreadths (mild: two to three fingerbreadths, moderate: three to four fingerbreadths, and severe: more than four fingerbreadths).⁵⁷ Treatment with core-strengthening and stabilization exercises is the usual recommendation, though evidence regarding efficacy of various exercises has been mixed.⁶⁰ Activation of the internal/external obliques and transversus abdominis muscles via a “drawing-in” maneuver has been classically recommended both to narrow the inter-rectus distance (IRD) via horizontal force closure and to prevent and treat concomitant low back pain.⁶⁰ Isometric abdominal “crunch” maneuvers have classically been thought to provoke DRA (hence the use of this maneuver to diagnose DRA), though recent ultrasound studies of postpartum women have demonstrated the opposite effects, with imaging evidence of IRD narrowing with abdominal crunch maneuvers in postpartum women over time.^59,60 In addition to physical therapy exercises to promote core and lumbar stabilization, the use of abdominal binders for additional support can be considered.⁵⁸ Surgical referral for abdominoplasty in women with persistent lumbopelvic symptoms that are recalcitrant to conservative management can be considered but should be a last resort.⁵⁸ Overall, further evidence is needed to understand the prevalence, clinical implications, and treatment of DRA.⁵⁸

Transient Osteoporosis of Pregnancy

Transient osteoporosis of pregnancy (TOP; also seen in the literature as bone marrow edema syndrome, regional migratory osteoporosis, Sudeck’s atrophy, and regional algodystrophy) is a rare but serious orthopedic complication of pregnancy that can predispose pregnant and postpartum women to the development of insufficiency fractures. TOP is a self-limited disease classically described in women in their third trimester of pregnancy and middle-aged men.^61–63 TOP typically presents during the third trimester or the immediate postpartum period.⁶⁴ The incidence has been reported at 0.4/100,000 pregnant women.⁶⁵ TOP is characterized by acute progressive pain, antalgic gait, and severe functional disability.^66–68 It has classically been demonstrated in load-bearing joints such as the vertebral bodies of the spine, sacrum, hips, knees, and ankles.^{61–63,69,70} TOP involving the hips (TOH) has been the variant most commonly reported in the literature. TOP is self-limited, usually resolving within 2 to 12 months of symptom onset, though healing may be prolonged by fracture development.^66–68 The greatest risk for development of a fracture is 2 months after symptom onset.⁶⁸ The exact pathophysiology of TOP is unknown, but proposed mechanisms include abnormal mechanical stress, history of osteopenia/osteoporosis, microvascular injury, reversible ischemia due to venous stasis, maternal calcium demands, and hormonal factors.^71,72 Risk factors for TOP include primigravida (particularly “elderly” primigravida), poor nutritional status, low calcium intake, and family history of osteoporosis.⁷² In order to prevent morbidity and functional disability associated with fracture development, women presenting with severe lumbosacral or pelvic girdle pain concerning for TOP should undergo noncontrast MRI to assess for TOP and possible insufficiency fracture. Noncontrast MRI is the gold standard for diagnosis.^64,73,74 MRI findings demonstrate osteopenia and bone marrow edema with decreased T1 signal intensity and increased T2 signal intensity.⁷³ Treatment of TOP is conservative and includes physical therapy, protected weight bearing, and analgesic medications.^72,75,76 Early protected weight bearing provides the benefit of stimulation of osteoblastic activity to promote bone healing.⁷⁷ There is little evidence to support the use of bisphosphonates, calcitonin, calcium/vitamin D supplementation, or steroids.^72,76 Surgical intervention may be warranted in the case of displaced fractures.⁷²

Avascular Necrosis

The exact cause of avascular necrosis (AVN; also seen in the literature as femoral osteonecrosis and osteonecrosis of the femoral head) in pregnant women is unknown but is postulated to be due to elevated levels of unbound cortisol with increased adrenocortical activity, increased female hormones (estrogen/progesterone), and biomechanical loading forces on the hip joints.^1,2,8 The highest risk for development of hip AVN is during the third trimester.⁸ Symptom onset is typically insidious.⁹ Patients typically present with deep groin pain that radiates to the back, thigh, and ipsilateral knee; pain with weight bearing; and antalgic gait.^1,2,8 The diagnosis is easily missed, as symptoms can mimic PGP. AVN may be evident on plain films, but MRI is the test of choice for diagnosis (and is also helpful to distinguish TOP from AVN, given the similar clinical presentation).^2,5,8,9 AVN is low intensity on T1 MRI and moderate intensity on T2 MRI, with a pathognomonic “double line sign” (Fig. 38–9).⁹ Treatment of AVN in pregnancy mimics that in nonpregnant patients. Due to the high risk for development of compression fracture, surgical intervention (including core decompression with bone graft placement) is typically recommended.⁹

Insufficiency Fractures

One of the most concerning orthopedic complications in pregnancy are fractures. Clinically, a pregnant patient with antalgic gait and pain with weight bearing must be fully evaluated, and fracture must be ruled out.

Hormonal changes leading to joint instability of the pelvic ring cause pregnant women to be at increased vulnerability for fracture development.⁶⁴ Pelvic and acetabular fractures in pregnancy are rare but are associated with increased maternal (9%) and fetal (35%) mortality, including increased risk for preterm birth and placental abruption.^64,78–80 Women with sacral fractures may present with symptoms of radiculopathy due to nerve root compression by the fractured bone, which may be confused for more benign lumbosacral radiculitis.⁷⁷ Stress fractures are defined by two categories: fatigue fractures (fracture of normal bone exposed to abnormal/repetitive stress) and insufficiency fractures (fracture of abnormal bone exposed to normal stress).^74,81 Pregnant and postpartum women are at risk for fatigue fractures due to excess weight gain, hyperlordosis, fetal macrosomia, and vaginal delivery.⁸² Despite these biomechanical changes, pelvic stress fractures are mostly due to insufficiency fractures.⁷⁴ One proposed risk factor for pelvic girdle insufficiency fractures in peripartum women is the presence of TOP, as described earlier.⁶⁴