Lumbopelvic pain (LPP) during pregnancy has traditionally been an area where health care providers have instructed patients that their symptoms are a part of pregnancy and they should improve with time. It is now becoming increasingly apparent that these conditions cause significant negative impact during pregnancy¹ and in some cases pregnancy can be the initiation of chronic pain.² Here we will highlight the epidemiology, risk factors, suggested causes, diagnosis, and treatment of LPP in pregnancy. LPP can be divided into lumbar pain (LP) and pelvic girdle pain (PGP) although the two disorders can coincide and it is important to keep a broad differential in mind when caring for pregnant women.

LPP during pregnancy is the most common musculoskeletal complaint during pregnancy. In various populations, around 50% of women have complaints of LPP with most articles reporting a range between 34% and 90%.^{3,4,5,6,7,8,9} LPP is more common in pregnant women than in the general population. Many women who experience LPP do not report their symptoms or seek treatment for their pain. Chang et al found that only 12% of Taiwanese women studied sought treatment for their pain.¹⁰ These numbers are similar to an American study where of the 599 women followed up, 67% reported pain and 75% of those reporting pain took pain medication during their pregnancy. Yet, 85% reported they had not been offered treatment for their pain.¹¹

PGP, in particular, has been shown to significantly impact everyday life and quality of life.^12,13 A study from Sweden suggests PGP is more than four times as frequently encountered as LP during pregnancy.¹⁴ In spite of this frequency, only 25% of pregnant women and 5% postpartum women will seek medical care.¹⁵ Of women reporting LPP, most had mild to moderate pain and 9% to 20% had pain that was so severe it was completely disabling.^4,16,17 The onset of pain is generally around the 22nd week of gestation with a range between the 5th and 7th months, but can occur within the first month and 20% of women experience pain prior to the 16th week.^6,16 Risk factors identified for the development of LPP included back pain prior to pregnancy and during menstruation, increased body mass index (BMI), older and younger age, multiparous, high stress, low job satisfaction, trauma to the back or pelvis, smoking, depression, not exercising prior to pregnancy, and poor sleep.^{5,16,18,19,20,21,22,23} The impact of developing LPP in a Norwegian study showed that 75% of their working pregnant women were placed on sick leave at some point in the pregnancy and LPP was a major contributing cause.^16,23,24 In addition to missed work, LPP also affected domains of sleep quality, fear of movement, and body perception.²⁵ Postpartum depression was noted to be three times more common in women who experienced LPP.¹⁴

Most women have symptom resolution by 3 to 6 months postpartum, but as many as 10% of women with pregnancy-associated LPP continue to have symptoms to 2 years.²⁰ Postpartum LPP can affect women of all ages, races, and activity levels. A 2007 study from Norway showed that even elite athletes experience LPP during and post pregnancy at the same rates as controls.²⁶ Studies have revealed that mode of delivery affects postpartum LPP. Women who underwent cesarean delivery were two to four times more likely to have LPP.^27,28 Similar to those who develop LPP during pregnancy, those with postpartum LPP are more likely to have LP prepregnancy.²⁹ Other risk factors for persistent LPP were earlier onset of LPP, a greater number of pain-provoking tests being positive (in particular, the active straight leg raise [ASLR]), belief that symptoms would persist, weak back flexors, older age, higher BMI, pain that improved with increasing time spent in bed, and dissatisfaction with work.^{5,14,29,30,31} In another study from Sweden, 40% stated their symptoms were moderately to severely disabling.³² A more recent study from Norway showed that most women made recovery from their LPP at 1 year with improvements in pain and physical functioning.³³ Primiparous women often describe having a lack of knowledge with regard to what to expect with LPP and do not anticipate the impact that it will have on their daily life.³⁴ This highlights the need for health care providers to give information to their pregnant patients about what to expect with LPP in pregnancy and thereafter.

Numerous physiologic changes happen to a woman’s body during pregnancy. It is normal during pregnancy to experience an increase in weight gain of 25 to 35 lb. This in combination with the gravid uterus leads to anterior displacement of the center of gravity and can result in a significant increase in force on
the lumbar spine.^16,19,20,35 It is thought that there is an increase in lordosis of the lumbar spine because of pregnancy, but there is literature that suggests that this does not occur and that instead increased thoracic kyphosis, thoracic lordosis, lumbar kyphosis, and sacral posterior inclination describe the typical postural changes of pregnancy.^{6,16,19,20,36,37,38,39} This cloudy literature is further muddied by the absence of a clear link between postural changes and the development of LPP. These do contribute to increased anterior pelvic tilt, which serves to increase sacroiliac ligament load.²⁰ Ligamentous laxity increases during pregnancy and it is thought that estrogen, progesterone, and relaxin all contribute to this increase. Relaxin is believed to be a key driver to this laxity via its collagenolytic effect.⁴⁰ It peaks at the end of the first trimester and remains at an elevated level throughout pregnancy. Some have suggested that relaxin plays a role in the LPP of pregnancy, but recent studies fail to make a clear relationship between these two.^{6,16,19,20,40,41,42,43} Decreased bone mineral density can occur during pregnancy and can compound the negative effects of changes in body mechanics and posture.^42,44 Other theories on the development of LPP in pregnancy are that prolonged supine positioning leads to vena cava compression, venous stasis, relative hypoxemia, and neural tissue with insufficient supply for metabolic requirements.^16,45,46 Another contributing cause to LPP is asymmetric loading of the spine and pelvis, which likely contribute to imbalance in these regions in addition to the increase in laxity.^6,20,47 Deep tissue hypersensitivity, altered pelvic mobility and motor control, and increased pelvic floor muscle function may all play a role in the experience of LPP.^{48,49,50,51,52,53,54} In general, it would seem that PGP seems to be more influenced by pregnancy than LP, but one could see how these changes could lead to both.