Back pain and pregnancy: a review

Back pain and pregnancy: a review

Pain, 64 (1996) 405-414 405 © 1996 Elsevier Science B.V. All rights reserved 0304-3959/96/$27.00 PAIN 2973 Review Article Back pain and pregnancy:...

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Pain, 64 (1996) 405-414

405

© 1996 Elsevier Science B.V. All rights reserved 0304-3959/96/$27.00

PAIN 2973

Review Article Back pain and pregnancy: a review Myles MacEvilly * and Donal Buggy Pain Management Unit, Department of Anaesthesia, St. James" Hospital, Dublin 8 (Ireland) (Received 16 August 1994, revised version received 13 January 1995, accepted 2 August 1995)

Summary Back pain is a common symptom in association with pregnancy. This article reviews the pathogenesis of back pain during pregnancy (gestational back pain) and of new onset postpartum back pain. The studies implicating epidural analgesia and postpartum back pain are discussed. Possible physiological mechanisms contributing to gestational back pain are outlined. Guidelines are provided for the prevention and symptomatic management of the back pain syndromes of pregnancy. Key words: Back pain; Backache; Pregnancy; Epidural anaesthesia

Table of Contents Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

405

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

406

2. Gestational back pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

406

3. Postpartum back pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

406

4. Postpartum epidural-related backache . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

407

5. Physiological mechanisms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.1. Posture . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.2. Changes in total body water content . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.3. Endocrine changes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.4. Engorgement of epidural veins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

408 408 409 409 409

6. Pain of labour . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

409

7. Clinical syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

410

8. Management of back pain in pregnancy (Table V) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.1 Patient education . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.2 Physiotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.3 Physical treatments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.4 Management of labour . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.5 Drug therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

411 411 411 411 411 411

9. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

412

* Corresponding author: Dr. M. MacEvilly, Pain Management Unit, Department of Anaesthesia, St. James's Hospital, Dublin 8, Ireland. Tel.: (353) 1-453-7941, ext. 2516; FAX: (353) 1-454-9804.

SSDI 0 3 0 4 - 3 9 5 9 ( 9 5 ) 0 0 1 8 4 - 0

406

Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

412

References

412

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1. Introduction Back pain occurs at some time during pregnancy in almost every second woman. Retrospective studies indicate a prevalence of 48-56% (Mantle et al. 1977; Fast et al. 1987) while a prospective study, which followed pregnant women from week 12, found the overall 9-month period prevalence to be 49% (Ostgaard 1991a). Back pain in the parturient is so common it is often looked upon as a part of normal pregnancy. Yet, more than a third of pregnant women reported it as a severe problem, not only compromising their ability to work in gainful employment during pregnancy, but also interfering with normal daily life (Ostgaard 1991a). Furthermore, back pain occurs at night in over one-third of pregnant women, contributing significantly to insomnia (Fast 1987). Knowledge of the pathogenesis, physiology and management of this widespread problem is far from complete.

the adaptive capability of the trunk musculature in susceptible individuals. Work factors may be important. Ostgaard found a direct relationship between back pain in pregnancy and perceived monotonous work and fatigue at the end of the working day, but a negative correlation with work satisfaction, standing posture and facility to take rest breaks (Ostgaard et al. 1991). Hispanic women have a proportionally lower instance of back pain in pregnancy than Caucasian women. It is postulated that the latter group tend to have a higher socio-economic status, and are hence less likely to be engaged in manual work and so exercise their trunk and back musculature less (Fast et al. 1987). Younger age is also a risk factor, possibly due to higher sensitivity to hormonal changes induced by relaxin and oestrogens, or to more pronounced collagen laxity (Fast et al. 1987; Bookhout 1988; Ostgaard 1991).

3. Postpartum back pain 2. Gestational back pain Pregnancy-related back pain is associated with a history of previous back pain; antegestational back pain is related to a greater intensity of back pain from week 12 until week 28, declining thereafter (Fast 1987; Bookhout 1988). Multiparity has been proposed as a contributory factor, but results are conflicting. A retrospective study of a cross-section of older women after their reproductive years (aged 38-64) found a lifetime incidence of low back pain (LBP) of 66% and 10% of these women indicated that their back pain began with pregnancy. This pregnancy-related back pain was associated with a higher number of subsequent abortions, either spontaneous or induced (Svensson 1990). This study suggested an association between back pain and parity, a conclusion consistent with other studies (Ostgaard 1991), but contrary to Fast et al. (1987). These authors found no relationship between the actual number of previous pregnancies and back pain but discovered more back pain-related disability in parous women compared with nulliparous women. It was suggested that this is due to weaker trunk muscles following the repeated posture alterations of pregnancy. However, abdominal muscle weakness per se caused by overstretch was, in a different study, not associated with back pain during pregnancy (Fast 1990). Weight gain, maternal obesity and foetal weight at term were not found to be related to gestational back pain (Fast 1987). After 30 weeks, a decrease in the prevalence and intensity of pregnancy-associated back pain is noted (Fast 1987; Ostgaard 1991). Perhaps the rapidity of weight gain between the 5th and 7th months of pregnancy exceeds

Women with a previous history of back pain have a significantly increased risk of postpartum back pain (MacArthur et al. 1990; Ostgaard et al. 1991) and back pain occurring during pregnancy is also associated with a postpartum back pain prevalence of about 40% (Grove 1973; MacArthur et al. 1990; Russell et al. 1993; Breen et al. 1994). Breen et al. 1994 noted also an association between new onset postpartum back pain with greater weight and shorter stature which suggests a musculoskeletal aetiology. While there was no difference in the incidence of back pain between those working inside and outside the home, several work factors had a bearing on postpartum back pain, such as the perceived heaviness of the work, frequency of twisting and bending forward, and constrained posture (Ostgaard and Andersson 1991). Younger maternal age was also a predisposing factor (Breen et al. 1994). Psychological factors were reported to be important (Russell et al. 1993). Of 156 patients who complained of new onset postpartum back pain who were asked to attend the outpatient clinic, 36 (23%) attended. Of these, 14 women were described as having possible psychological factors contributing to their back pain and 9 had scores outside the normal range on the evidence of a pain drawing (Ransford et al. 1976) and two psychological questionnaires: the Modified Somatic Perception Questionnaire (Main 1983) and the Modified Zung Depression Inventory (Waddell 1987). However, the presence of these psychological factors in this subgroup may of itself have contributed to their attendance at the clinic, with resultant sample bias.

407

4. Postpartum epidural-related backache The association between postpartum back pain and the use of epidural anaesthesia for delivery was reported by Massey Dawkins (1969) and Crawford (1972) with a quoted incidence of 30-4.5%. More recently, much attention has again focused on the role of epidural anaesthesia in contributing to new onset backache with conflicting results. In a retrospective study utilising a postal questionnaire, (MacArthur et al. 1990), 11,701 women who had delivered their most recent baby in a single maternity hospital between 1978 and 1985 were questioned subsequently. 18.9% of women who had epidural anaesthesia (n = 4766) during labour for vaginal delivery complained of new onset backache compared to 10.5% (n = 6935) who had not had an epidural ( P < 0.05). The authors concluded that the relationship between postpartum backache and epidural anaesthesia was probably causal and they speculated that it was postural due to a combination of stressed positions in labour, muscular relaxation and lack of mobility. They further analysed the same results for long-term problems and found that obstetric epidural anaesthesia was associated with several spinal axis symptoms as well as back pain (MacArthur et al. 1992). These included headache (as well as migraine), neckache and tingling in the hands and were considered to be part of an epidural-related symptom complex of which back pain is the prime component. These studies, however, are subject to recall bias in that data was obtained on deliveries occurring 1-9 years previously. A similarly designed study by Russell et al. (1993) of 1015 women between March 1990 and February 1991 had comparable results. Of 1the total sample, 612 received epidural analgesia and 403 did not. 17.8% of the epidural group (n = 109) reported new onset back pain, compared with 11.7% (n--47) of the patients who did not receive epidural analgesia ( P < 0.05). The results of this study were comparable to Mac,acthur et al. (1990) in stating that epidural anaesthesia was a strong predictive factor for the development of new long-term back pain. Russell et al. also investigated the nature of the postpartum backache

and found that epidural-related back pain was postural and not severe. Data was obtained within 18 months of delivery and thus was not subject to recall bias. Patients with prolonged labour and complicated deliveries did not require more epidurals than other patients in each of these studies. A more recent study by Breen et al. (1994) of 1042 patients looked at the incidence of new onset back pain 1-2 months after delivery and at likely predisposing factors including epidural anaesthesia for labour and delivery. Epidural administration was not associated with the development of new onset postpartum back pain, the incidence of the latter being 44% in the group having had an epidural compared to 45% in those who had not. Epidural-related back pain is thought to be initiated by the loss of normal joint protective reflexes with consequent immobility, poor posture and stressed positions during labour. Interestingly, ambulatory epidural anaesthesia which, of necessity, avoids motor blockade is associated with a trend towards less back pain than a similar epidural regimen in patients confined to bed (Collis et al. 1994). The discrepancy between the early studies of MacArthur et al. (1990), Russell et al. (1993) and Breen et al. (1994) seems to relate to the extent and degree of motor blockade (Table I). A further small (n--77) retrospective study comparing the incidence of long-term backache after epidural anaesthesia or general anaesthesia specifically for manual removal of the placenta found a significantly higher incidence of back pain after epidural anaesthesia (Vickers and May 1993). This small review requires a large prospective controlled investigation to confirm a cause and effect association. In addition, the type of local anaesthetic injected into the epidural space also seems important in the genesis of back pain. Fibbuch and Opper (1989) and, later, Stevens et al. (1991) and Hynson (1991) reported the immediate onset of back pain after regression of chloroprocaine epidural anaesthesia. Levy et al. (1989) confirmed the findings of Fibbuch and Opper (1989) and also implicated adrenaline as a contributory factor - - the incidence being 55% without adrenaline, as compared to 65% with it ( P < 0.05). Stevens et al. (1993) in a prospective randomized study of

TABLE I NEW ONSET POST PARTUM BACKACHE

Study

MacArthur et al. (1990) (n = 11,701) Russell et al. (1993) (n = 1015) Breen et al. (1994) (n = 1042)

Number (%)

P

Local anaesthetic used

With epidural

Without epidural

19

11

P < 0.05

Bupivacaine 0.25-0.5% a

18

12

P < 0.05

Bupivacaine O.25-0.5% ~

44

45

NS b

Bupivacaine 0.04-0.125% (infusion)

a Likely bolus concentration in current use at time of these studies. b NS, not significant.

408 TABLE II POSSIBLE RISK FACTORS FOR THE DEVELOPMENTOF EPIDURAL-RELATEDBACKACHE Reference

Factor

Comment

MacArthur et al. (1990) Russell et al. (1993)

Sensory and/or motor block Correlation between epidural analgesia and backache Degree of motor block

Induces immobility and stressed position during labour New onset postpartum backache related to epidural analgesia is postural and not severe

Collis et al. (1994) Stevens et al. (1993) Levy et al. (1989) Scott and Hibbard (1990) Seeberger and Orwyler (1992) Schmidt and Nolte (1992)

Type and volume of local anaesthetic agent Adrenaline in association with local anaesthetic agent Epidural abscess Epidural blood patch Epidural haematoma

day case knee surgery patients, implicated the preservative disodium E D T A in chloroprocaine solutions and concluded that higher total injected volumes of chloroprocaine ( > 25 ml) influenced the character, incidence, severity and duration of epidural-related back pain. Back pain is the usual presenting symptom in association with an epidural haematoma, either spontaneous in origin or associated with spinal or epidural procedures (Scott 1990; Sage 1990; Schmidt 1992). Epidural abscesses may also give rise to back pain, but are uncommon (Scott 1990), as indeed may epidural bloodpatch treatment for inadvertent post dural puncture headache (Seeberger 1992). TABLE III POSITIVEASSOCIATIONSFOR BACK PAIN AND PREGNANCY Study

Uncommoncause; MRI required Uncommoncause Uncommoncause: back pain primary presenting symptom: asssociated with periop, anticoagulation. Specific nociceptors are found in intramuscular (Mense 1993) or periosteal (Gronblad et al. 1984) tissues. An additional possible cause of epidural-related back pain may be the activation by small haematomas of these nociceptors associated with epidural needle insertion. In summary, possible risk factors (Table II) for the development of epidural-related back pain includes the degree of motor blockade, chloroprocaine (with or without adrenaline), epidural haematomas, epidural abscesses, epidural blood patch and possibly small haematomas in the integuments. Persistent, severe postpartum back pain requires urgent investigation by computed tomography (CT) or magnetic resonance imaging (MRI), and surgery, if indicated by these tests (Shapira et al. 1991). The pathogenesis of back pain in pregnancy thus remains obscure, but the variety of associated features suggests a multifactorial aetiology (Table III).

Association

Gestational back pain Fast et al. (1987)

Past history back pain; Caucasian race Svensson et al. (1990) Parity; abortion (spontaneous or induced) Ostgaard et al. (1991) Parity Bookhout and Boissonault (1988) Younger age Breen (1994)

Postpartum back pain Ostgaard et al. (1991a) MacArthur et al. (1990) Breen and Oriol (1992) Breen et al. (1994) Russell et al. (1993) MacArthur et al. (1990)

Ambulatory epidural analgesia for labour may reduce both labour and postpartum backache Chloroprocaine associated with back pain: preservative implicated Adjunctive use of adrenaline associated with back pain

Previous back pain Gestational back pain Short stature Psychologicalfactors Epidural analgesia in labour Nulliparity Asian race No episiotomy Spinal anaesthesia Prolonged second stage of labour Spontaneous onset of labour Lower social class

5. Physiological mechanisms The normal physiological changes of pregnancy may induce mechanical and structural changes in the spine and neuraxis contributing to gestational and possibly postpartum back pain. These include posture, changes in total body water content, endocrine changes and engorgement of epidural veins. 5.1. Posture Postural alterations characterised by an increase in lumbar lordosis may contribute to the development of LBP. Most of the weight gain is concentrated low in the pelvis, with anterior abdominal protuberance. There is thus a tendency to fall forward, hence the woman unconsciously shifts her upper body back 'over the pelvis' to restore her centre of gravity (Bookhout 1988). Fahrni (1975) concluded that this lordotic posture predisposed to excessive

409 disc herniation after finding a lower incidence of LBP in primitive societies whose lumbar spine was kept straight for prolonged periods every day. Higher back pain may result from compensatory thoracic kyphosis and forward head posture (Bookhout 1988). Hasson (1985) denied an association between lumbar lordosis and LBP, having found no difference in the occurrence of lordosis in individuals with and without acute or chronic LBP. However, the subjects in this study were not pregnant, and over one-half were male, thus the study population is not applicable to pregnancy. In the non-pregnant patient, abnormal posture resulting in stress on synovial facet joints and ligaments may produce joint inflammation. Consequently, there will be increased synovial fluid production, with distention of the joint capsule, giving rise to pain. Inflammation, of itself, increases spontaneous activity in joint afferent nerves, heightening sensitivity to movement (McLain 1993). Joint motion may also induce release of noxious neuropeptides, kinins and other mediators of inflammation that act on receptors in the joint capsule and periosteum, further increasing afferent nociceptive input (Baiter 1992). It is possible that in susceptible individuals, the increased lordotic posture in the parturient accentuates the shearing forces on lumbar intervertebral discs and increases compression on the zygopophyseal joints, with subsequent long-term degeneration ot! articular cartilage.

5.2. Changes in total body water content Mean total body water increases by an equal amount in primigravida and multiparous women, by up to 8.5 1. This is more than is accounted for in the foetal amniotic fluid and placenta, and is reflected in increased hydration of macromolecules in connective tissue ground substance (MacFayden 1989). Its occurrence may stem initially from the natriuretic effect of oestrogens which increase in early pregnancy. The negative sodium balance induces renin and isorenin release (from the uterus), resulting in production of angiotensin II and subsequent increase in aldosterone and antidiuretic hormone levels, which resorb sodium and conserve water. Fluid retention, particularly of connective tissues around the vertebral column and pelvis, increases laxity around these joints 5.3. Endocrine changes The effect of fluid retention is augmented by endocrine changes of pregnancy, particularly the influence of relaxin. A two-chain polypeptide 'with a molecular weight of 6500, it is not unlike insulin and regulates collagen physiology. Secreted by the corpus luteum, it softens the ligaments around the pelvic joints and cervix, possibly by enhancing fluid retention in these tissues. This laxity, necessary to accommodate the developing foetus and to facilitate delivery at birth, may also cause pain by distention and by an exaggerated range of movement in these joints (MacFayden 1989).

Endogenous neuropeptides, such as enkephalin, dynorphin (Sander et al. 1989), neuropeptide-Y and substances P and K, have been identified in the dorsal horn of the spinal cord and are thought to act as modulators of afferent pain impulses or as descending attenuators of pain impulses (McLain 1993). Substance P levels are decreased in pregnancy (Mouton et al. 1992). While there is some evidence that an increase in pain threshold occurs in pregnancy, this is likely to be maximal towards the end of the gestational period, possibly related to enhanced opioid activity in the spinal cord at term (Cogan and Spinnato 1986; Whipple et al. 1990). Pain in the middle trimester, consequently, may be less modulated. Progesterone levels are raised during pregnancy: animal studies show that progesterone sensitises nerves to some local anaesthetic agents (probably by a latent hormonal effect on protein synthesis) and selectively increases the cardiac membrane depressant effect of bupivacaine (Bader et al. 1990; Moiler and Covino 1992). It is possible to speculate that increased hormonal activity in pregnancy may also influence pain neuropeptides and specifically those in the spinal cord and in synovial fluid; this is a source of possible investigation.

5.4. Engorgement of epidural veins Since 67% of women in the second half of pregnancy reported nocturnal back pain, it has been suggested that hypervolaemia, combined with obstruction of the inferior vena cava by the enlarging uterus could result in engorgement of the venous system, especially the extradural veins distal to the occluded zone. This may result in hypoxia and metabolic disturbance of unmyelinated nerves, leading to back pain (Fast et al. 1979). In a later study, the same author suggested that the explanation lay in the inability of pregnant women to turn in bed as frequently as non-gravid individuals (Fast et al. 1987).

6. Pain of labour

Back pain in pregnancy will predictably be at its most intense during labour. Back pain in labour results from the rich sensory innervation of the uterus and cervix, which pass through Frankenhauser's plexus, located bilaterally on the lateral aspect of the cervix. These fibres pass through the hypogastric plexus and reach the spinal cord at T l l , T12 and L1. Back pain is particularly associated with cervical dilatation and is transmitted by sensory fibres which pass within the sympathetic nerves to the lateral horn of the cord at L1/2. Pain of the second stage of labour is localised to the perineum in most cases, but may extend to the coccygeal area, mediated by the perineal nerves which enter the cord at S 2, S 3 and S 4 (LlewellynJones 1986). A study by Melzack and Belanger (1989) found that the intensity of labour pain is significantly correlated with back pain during menstruation, suggesting that they both

410 share the same mechanisms. Episodic LBP before pregnancy, on the contrary, was not associated with labour pain; rather, it correlates with back pain during pregnancy. They postulate that the strain on back musculoskeletal structures induced by pregnancy activates the mechanisms that underlie non-pregnancy associated LBP. Additional work by Melzack (1993) found that women in early labour who are in a vertical position, sitting or standing, have an 83% reduction in continuous back pain and a 50% reduction in back pain associated with contractions. This may contribute to the reported efficacy of ambulatory epidural analgesia (Breen and Oriol 1992; Collis et al. 1993). Recumbent positions were more comfortable in the later first stage and second stage of labour, however (Melzack 1993).

7. Clinical syndromes Clinical entities implicated as causes of back pain in pregnancy include pelvic insufficiency, sacro-iliac joint (SIJ) subluxation, sciatica, lumbosacral disc pathology, spondylolisthesis, postural back pain and lumbar lordosis, thoracic back pain and coccydynia (Table IV). Pelvic insufficiency is defined as pain at the pubic symphysis a n d / o r the SIJ developing in connection with pregnancy or delivery (Ostergaard et al. 1992). On examination, there is tenderness at the pubic bone and the SIJ, waddling gait, pain on posture change, and a positive Trendelenburg and sacral pressure test. Its incidence is 7 . 6 - 1 8 / 1 0 0 0 deliveries and is associated with multiparity and physical work, and peaks in the 5th to 8th months. It is

TABLE IV CLINICAL SYNDROMES OF BACK PAIN IN PREGNANCY Study

Clinical syndrome

Ostergaard et al. (1992) Daly et al. (1991) Bookhout and Boissonault (1988)

Pelvic insufficiency Sacroiliac joint subluxation Sciatica Postural back pain Thoracic back pain Lumbosacral disc pathology Spondylisthesis Coccodynia

LaBan et al. (1993) Kelsey et al. (1975) Whitehead (1986)

usually self-terminating after delivery, and may be alleviated by physiotherapy and a trochanteric belt (Ostergaard et al. 1992). Sacro-iliac joint subluxation occurs when certain criteria are present including pain in the sacral region; the absence of lumbar spine and hip disease; a positive Piedallu's sign (asymmetrical movement of the posterior superior iliac spine on anterior flexion, with asymmetry of the anterior superior iliac spine (Daly et al. 1991); a positive pelvic compression test and asymmetry of the anterior superior iliac spines. Its incidence in pregnancy is about 28%, and therapeutic rotational manipulation of the SIJ reportedly results in relief of pain in 91% of cases (Daly et al. 1991). The duration of analgesia was not reported, however. Pain over this joint is not always synonymous with purely SIJ dysfunction - - it may also reflect referred pain from the lumbar spine and hip, or a combination of these conditions.

TABLE V MANAGEMENT OF BACK PAIN IN PREGNANCY Reference

Treatment

Comment

Bookhout and Boissonault (1988)

Patient education

Bookhout and Boissonault (1988) Thomas et al. (1989)

Bundsen et al. (1981)

Physiotherapy Ozzlo pillow: wedge-shaped, supporting the abdomen when in lateral recumbent position Trochanteric belt: a pelvic girdle support TENS

Early childbirth training classes (even in first trimester), given by physiotherapist with special interest in obstetrics. Emphasis on informing patients on physiological changes of pregnancy, and self-relief exercises. SLI subluxation, pelvic insufficiency, lordosis, spondylolisthesis. Controlled study of Ozzlo versus ordinary pillow: third trimester night back pain reduced although ordinary pillow was also beneficial. Sleep perceived to be improved.

Ernst (1993)

Avoid smoking

Aselton et al. (1985) CLASP (1994) Streissguth (1987) Briggs (1994) Heinonen et al. (1977) Gilstrap and Little (1992) Witter (1993)

Low-dose aspirin ( < 300 mg/day) Low-dose aspirin ( < 300 mg/day) Paracetarnol

Empirical evidence that pelvic insufficiency is relieved: no controlled studies on efficacy available. Useful for pain of labour. Middle and third trimester pain: no study on efficacy available. Causal relationship between smoking and LBP in non-pregnant patients. Therapeutic doses safe: not hazardous with epidural analgesia for labour. Commonly used. Apparently safe for short-term use.

Codeine NSAIDs

Useful in therapeutic dose in first and second trimester. Commonly used. Probably pose little risk in middle trimester.

Ostergaard et al. (1992)

411 Sciatica commonly oo~"urs in association with SIJ dysfunction. The L4-L5 component of the sciatic nerve runs anterior to the SIJ, thus ligamentous relaxation of the joint may affect this nerve, giving rise to neuronal dysfunction. Lumbosacral disc pathology, which has an incidence of 2.5/1000 live births, may be worsened by pregnancy. There is evidence that pregnancy itself may be an independent risk factor for ,mbsequent development of disc herniation (Kelsey et al. 1975; LaBan et al, 1983). In spondylolisthesis ( < 1/1000 live births) there is anterior slippage of the upper vertebral body on the lower one, especially at L5-S1, which may be more likely to occur in pregnancy as a result of musculoskeletal stresses, as described above (Kelsey el: al. 1975; LaBan et al. 1983). Coccydynia is a rare form of LBP in pregnancy, except where previous injury to this bone has occurred (Whithead 1986). Postural back pain of pregnancy may be a nonspecific 'tired ache' towards evening or after sustained effort, while lumbar lordosis is a major component of LBP in pregnancy, as mentioned previously. Thoracic back pain may occur following thoracic kyphosis and flaring of ribs at term, with stretching of costovertebral and costotransverse joints and stretching of thoracic muscles and ligaments around the vertebrae (Bookhout and Boissonault 1988). The differential diagnosis of back pain in pregnancy (other than musculoskeletal disorders) includes obstetric complications: spontaneous abortion and antepartum haemorrhage; infections such as bacterial or tuberculous osteomyelitis, as well as urinary tract infections including pyelonephritis (which may present as renal angle pain); and renal colic secondary' to ureterolithiasis. The inflammatory conditions of ankylosing spondylitis and, uncommonly, rheumatoid or osteoarthritis are also possibilities. Neoplasms should be ruled out, especially lymphoma, secondary neoplasia from breast, ovary or thyroid primary carcinoma and, rarely, multiple myeloma. Metabolic bone disease, such as osteoporosis and osteomalacia are also uncommon causes of back pain in women of childbearing age. In certain tropical regions, sickle-cell disease may be relevant. While there is no data on the specific incidence of back pain in these conditions, back pain may present as the primary symptom.

8. Management of back pain in pregnancy (Table V) 8.1. Patient education Back pain in pregnancy is under-emphasised. Education about the due emergence of back pain in pregnancy should be an integral part of early childbirth training courses, which should be supervised by a physiotherapist with a special interest in obstetrics. Advice to stop smoking should be given early in pregnancy, not only for its effects on foetal growth patterns, but also because of its causal

relationship with prolapsed intervertebral discs and the severity of LBP in the non pregnant patient (Ernst 1993).

8.2. Physiotherapy In the third trimester, physiotherapy is beneficial for SIJ subluxation and also for many of the other back pain conditions, such as pelvic insufficiency, postural back pain and lordosis and spondylolisthesis, by a combination of information, education and instruction in self-relief exercises (Bookhout and Boissonault 1988). These exercises are designed to increase the strength of the lumbosacral and pelvic girdle muscles and require daily repetition to be fully effective (Bookout and Boissonault 1988). 8.3. Physical treatments Mechanical supports are also useful. The Ozzlo pillow, a wedgeshaped pillow to support the abdomen of a pregnant woman lying on her side, alleviates pain and aids sleep (Thomas et al. 1989). The trochanteric belt, a pelvic girdle support worn around the lower back was found to be helpful in cases of pelvic insufficiency associated with pregnancy (Ostergaard et al. 1992). Transcutaneous electrical nerve stimulation (TENS) has been advocated for the pain of labour (Bundsen et al. 1981), but no trial of its use in intractable back pain in pregnancy has been described. Acupuncture may have a useful role but we are not aware of any scientific study examining its effects in this setting. To our knowledge myofascial pain syndromes which are amenable to simple needling techniques (Chan Gunn 1990) have not been described in association with the clinical conditions of pack pain in pregnancy. 8.4. Management of labour The vertical position has been shown to reduce back pain in early labour (2-5 cm servical dilation) by as much as 83% (Melzack 1993) and this may contribute to the efficacy of mobile epidural analgesia in labour, which is currently the focus of much attention. Its reported efficacy may be due to the absence of motor block which increases maternal satisfaction and to the vertical position which it encourages (Breen et al. 1992; Collis et al. 1994). 8.5. Drug therapy Low-dose aspirin has a major preventative role in the development of pregnancy-induced hypertension (Fitzgerald et al. 1990), and in the prevention of recurrent abortion and intra-uterine growth retardation (Uzan et al. 1991). Both aspirin and the NSAIDs contribute to dysfunction of platelet aggregation and might be responsible for prolonged bleeding during the epidural insertion, if a vessel is punctured. However, haemorrhagic complications following epidural injections in hundreds of such patients was rare (Benzon et al. 1983). Provided the bleeding time and platelet count parameters are maintained, low-dose aspirin therapy is compatible with the safe administration of regional analgesia in labour (O'Sullivan 1990). More-

412

over, the recent randomised, multi-centre clinical trial of the role of aspirin in prevention of pre-eclamptic toxaemia of pregnancy (CLASP 1994) found that epidural analgesia could be safely administered to parturients receiving lowdose aspirin. Low-dose aspirin therapy for back pain in pregnancy is thus an option in low or therapeutic doses (Aselton 1985; Gilstrap and Little 1992). Paracetamol (Acetominophen USP) crosses the placenta easily (Levy et al. 1975) and is commonly used in pregnancy (Streissguth et al. 1987) with 41% of women admitting to its use. It is stated not to be associated with foetal malformations (Jick 1981; Aselton 1985) nor with a decrease in the IQ of offspring at 4 years of age (Streissguth 1987). In therapeutic doses it is apparently safe for shortterm use (Briggs et al. 1994). Codeine does not seem to be associated with foetal abnormalities (Heinonen et al. 1977) but when used in larger doses in late pregnancy, it may result in drug withdrawal symptoms in the neonate (Mangurten and Benowna 1980). Concern in regard to the use of non-steroidal anti-inflammatory drugs in pregnancy is related to the risks of congenital malformations when prescribed in early pregnancy and with the premature closure of the foetal ductus arteriosus due to the inhibition of cyclo-oxygenase (Waldman and Kilbride 1992). Although commonly used, Kean and Buchanan (1990) suggest that, in general, drugs should be avoided in pregnancy; but they do state that simple NSAIDs in low doses are probably safe, i.e., no major problems. For example, the short-term use of Ibuprofen and Naproxen is alleged not to be associated with teratogenicity (Botogol 1994). In the rheumatic diseases such as rheumatoid arthritis, the use of NSAIDs in pregnancy is a balance between the risks of foetal abnormality (Witter 1993) and preventing re-activation of the disease (Brooks and Needs 1990). The normal physiological changes of pregnancy relating to the gastrointestinal tract can affect the disposition of drugs. Changes in gastric mucus and acid production and delayed gastric emptying may affect absorption. Alkalis influence the absorption of NSAIDs (Kean and Buchanan 1987).

9. Conclusion Evidence suggests that the impact of back pain in pregnancy is substantial. Yet, gestational back pain is often dismissed as trivial and not readily amenable to treatment. This is a widespread and probably erroneous opinion. While it is true that the state of pregnancy per se limits the scope for intervention by diagnostic imaging, pharmacology or surgery, simple treatment measures, as outlined (Table V) can be effective. Both basic and clinical research needs to be focused on the mechanisms contributing to back pain in pregnancy.

Isokinetic evaluation of trunk musculature in the isometric mode in the neutral position (Lorren 1990; Newton et al. 1993), at least in the puerperium, should be considered as an aid in this research. Additional outcome studies on the physical medicine aspects of treatment of LBP in pregnancy need to be conducted. Further elucidation of the physiology of pain in pregnancy, particularly the role of neuropeptides and the question of whether they are significantly modified by pregnancy hormones, is required. The growing use of ambulatory epidurals may reduce back pain associated with labour; whether it would reduce the incidence of long-term postpartum back pain awaits further study. Future prospective randomised trials of the effect of epidural analgesia on postpartum back pain will establish if the association is truly causal. On the other hand, section scan sonography - B image method (Haerten 1994) - with higher frequencies (5-10 MHz), or enhanced musculoskeletal MRI may quantify the degree of soft tissue haematoma formation associated with epidural needle insertion. Substantive prospects exist therefore for the expansion of the emergent field of research into back pain and pregnancy.

Acknowledgements The authors wish to thank Professor J. Bonnar and Dr. E. McGuinness, Department of Gynaecology, University of Dublin, Trinity College, for reviewing the manuscript.

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