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What are contraindications to IUDs?
Based on limited evidence, use of intrauterine devices (IUDs) is not contraindicated for women with HIV/AIDS (strength of recommendation [SOR]: C), multiple sexual partners (SOR: C), previous actinomyces colonization (SOR: C), most types of fibroids (SOR: C), or previous ectopic pregnancy (SOR: C).
The risk to IUD users of pelvic inflammatory disease (PID) is similar to women using no contraception (SOR: B). Nulliparous women may experience increased insertion discomfort and higher rates of expulsion (SOR: B). IUD use of <3.5 years is not associated with decreased fertility (SOR: B).
IUDs are an excellent choice when estrogens are contraindicated or adherence is an issue
Shashi Mittal, MD
Baylor Family Medicine Residency at Garland, Garland, Tex
One percent of contraceptive users in the United States choose an IUD, compared with 25% in Europe. This is partly due to misinformation. An older IUD, the Dalkon shield, had a braided polyfilament tail that was associated with a higher risk of PID. People in the US still associate IUDs with this risk.
However, modern IUDs have a monofilament tail, which has not been linked to higher rates of PID. IUDs are an excellent alternative when estrogens are contraindicated, for prevention of pregnancy up to 5 days after unprotected sex, during lactation, and when adherence to a contraceptive has been difficult.
Evidence summary
IUDs are an effective and safe form of contraception. However, many clinicians have questions about the true contraindications to IUD use in the following situations.
Infection. IUDs do not increase the risk of complications among immunosuppressed HIV-positive women.1 IUD insertion does not increase the risk of PID for women with gonorrhea or chlamydia infection compared with infected nonusers.2 In one study, having multiple sexual partners was not associated with an increased risk of PID unless those partners carry specific infections, such as gonorrhea or chlamydia.3
In the US, approximately 1 in 1000 women develop PID after IUD insertion.3 Bacterial vaginosis may increase dysmenorrhea for women with IUDs (34.8 vs 13.9%, P=.03).4 In an observational study, all of 7 women with actinomyces who had IUDs removed remained negative for actinomyces after insertion of a new IUD.5
Nulliparity and infertility. Nulliparous women have increased rates of discomfort with IUD placement (17.8% vs 8.8%) and may have an increased risk of expulsion (up to 18.5% in one study, compared with less than 5.7% for all IUD users).6 Short-term (≤3.5 years) IUD use by nulliparous women was not associated with decreased fertility in a case-control study;7 however, 1 cohort study demonstrated lower fertility with use of a copper IUD for longer periods: hazard ratio (HR): 0.69 (95% confidence interval [CI], 0.497–0.97) for 42–78 months; HR=0.50 (95% CI, 0.34–0.73) for >78 months.8
Uterine anomalies. Significant uterine enlargement can increase the risk of IUD expulsion (0 vs 4 women [13%]; P=.04 in 1 retrospective cohort study).9 There are case reports of IUD failure and uterine perforation among women with anomalies that distort the uterine cavity.10,11
Other. Some contraindications to IUD use, such as concurrent pregnancy, are obvious. Other common sense contraindications might include insertion by patients with recent postpartum endometritis, gynecologic malignancy, genital bleeding of unknown cause, and gestational trophoblastic disease.
Recommendations from others
Manufacturer product labeling lists a number of contraindications. The American College of Obstetrics and Gynecology and the World Health Organization have similar but generally less restrictive lists of contraindications to IUD placement (TABLE).
TABLE
Contraindications to IUD placement
| ACOG | WHO* | MANUFACTURER | |
|---|---|---|---|
| Uterine anomaly (including distension of uterine cavity) | L, C | L, C | L, C |
| History of PID | L, C (past 3 mo only) | L, C (current PID only for both) | L (if no subsequent pregnancy), C |
| Postpartum endometritis or septic abortion in the past 3 months | L, C | L, C (immediately post-septic abortion for both) | L, C |
| Untreated cervicitis/vaginitis, including bacterial vaginosis | L, C | L, C (not bacterial vaginosis) | L, C (including genital actinomycosis) |
| Multiple sexual partners | L, C (increased STI risk is a relative contraindication for both) | L, C | |
| Immunosuppression | L, C (AIDS is a contraindication for both, unless clinically well on antiretroviral therapy) | L, C | |
| * Includes conditions rated as level 3 (risks usually outweigh benefits) or 4 (represents an unacceptable health risk) by WHO | |||
| L, levonorgestrel (Mirena) IUD; C, Copper T 380 (Paragard) IUD; IUD, intrauterine device; ACOG, American College of Obstetricians and Gynecologists; WHO, World Health Organization; PID, pelvic inflammatory disease; STI, sexually transmitted infection | |||
1. Sinei SK, Morrison CS, Sekadde-Kigondu C, Allen M, Kokonya D. Complications of use of intrauterine devices among HIV-1-infected women. Lancet 1998;351:1238-1241.
2. Ryden G, Fahraeus L, Molin L, Ahman K. Do contraceptives influence the incidence of acute pelvic inflammatory disease in women with gonorrhoea? Contraception 1979;20:149-157.
3. Steen R, Shapiro K. Intrauterine contraceptive devices and risk of pelvic inflammatory disease: standard of care in high STI prevalence settings. Reprod Health Matters 2004;12:136-143.
4. Ferraz do Lago R, Simoes JA, Bahamondes L, et al. Follow-up of users of intrauterine devices with and without bacterial vaginosis and other cervicovaginal infections. Contraception 2003;68:105-109.
5. Mao K, Guillebaud J. Influence of removal of intrauterine contraceptive devices on colonisation of the cervix by actinomyces-like organisms. Contraception 1984;30:535-544.
6. Weiner E, Berg AA, Johansson I. Copper intrauterine contraceptive devices in adolescent nulliparae. Br J Obstet Gynaecol 1978;85:204.-
7. Hubacher D, Lara-Richaldi R, Taylor DJ, Guerra-Infante F, Guzman-Rodriguez R. Use of copper intrauterine devices and the risk of tubal infertility among nulligravid women. N Engl J Med 2001;345:561-567.
8. Doll H, Vessey M, Painter R. Return of fertility in nulliparous women after discontinuation of the intrauterine device: comparison with women discontinuing other methods of contraception. BJOG 2001;108:304-314.
9. Ikomi A, Mansell E, Spence-Jones C, Singer A. Treatment of menorrhagia with the levonorgestrel intrauterine system: Can we learn from our failures? J Obstet Gynaecol 1998;20:630-631.
10. Seibel MM, Hann L. Pregnancy and an IUD in separate horns of a bicornate uterus. JAMA 1982;247:753-754.
11. Caspi B, Shoham Z, Barash A, Lancet M. Sonographic demonstration of an intrauterine device perforating a uterine myoma. J Clin Ultrasound 1989;17:535-537.
Based on limited evidence, use of intrauterine devices (IUDs) is not contraindicated for women with HIV/AIDS (strength of recommendation [SOR]: C), multiple sexual partners (SOR: C), previous actinomyces colonization (SOR: C), most types of fibroids (SOR: C), or previous ectopic pregnancy (SOR: C).
The risk to IUD users of pelvic inflammatory disease (PID) is similar to women using no contraception (SOR: B). Nulliparous women may experience increased insertion discomfort and higher rates of expulsion (SOR: B). IUD use of <3.5 years is not associated with decreased fertility (SOR: B).
IUDs are an excellent choice when estrogens are contraindicated or adherence is an issue
Shashi Mittal, MD
Baylor Family Medicine Residency at Garland, Garland, Tex
One percent of contraceptive users in the United States choose an IUD, compared with 25% in Europe. This is partly due to misinformation. An older IUD, the Dalkon shield, had a braided polyfilament tail that was associated with a higher risk of PID. People in the US still associate IUDs with this risk.
However, modern IUDs have a monofilament tail, which has not been linked to higher rates of PID. IUDs are an excellent alternative when estrogens are contraindicated, for prevention of pregnancy up to 5 days after unprotected sex, during lactation, and when adherence to a contraceptive has been difficult.
Evidence summary
IUDs are an effective and safe form of contraception. However, many clinicians have questions about the true contraindications to IUD use in the following situations.
Infection. IUDs do not increase the risk of complications among immunosuppressed HIV-positive women.1 IUD insertion does not increase the risk of PID for women with gonorrhea or chlamydia infection compared with infected nonusers.2 In one study, having multiple sexual partners was not associated with an increased risk of PID unless those partners carry specific infections, such as gonorrhea or chlamydia.3
In the US, approximately 1 in 1000 women develop PID after IUD insertion.3 Bacterial vaginosis may increase dysmenorrhea for women with IUDs (34.8 vs 13.9%, P=.03).4 In an observational study, all of 7 women with actinomyces who had IUDs removed remained negative for actinomyces after insertion of a new IUD.5
Nulliparity and infertility. Nulliparous women have increased rates of discomfort with IUD placement (17.8% vs 8.8%) and may have an increased risk of expulsion (up to 18.5% in one study, compared with less than 5.7% for all IUD users).6 Short-term (≤3.5 years) IUD use by nulliparous women was not associated with decreased fertility in a case-control study;7 however, 1 cohort study demonstrated lower fertility with use of a copper IUD for longer periods: hazard ratio (HR): 0.69 (95% confidence interval [CI], 0.497–0.97) for 42–78 months; HR=0.50 (95% CI, 0.34–0.73) for >78 months.8
Uterine anomalies. Significant uterine enlargement can increase the risk of IUD expulsion (0 vs 4 women [13%]; P=.04 in 1 retrospective cohort study).9 There are case reports of IUD failure and uterine perforation among women with anomalies that distort the uterine cavity.10,11
Other. Some contraindications to IUD use, such as concurrent pregnancy, are obvious. Other common sense contraindications might include insertion by patients with recent postpartum endometritis, gynecologic malignancy, genital bleeding of unknown cause, and gestational trophoblastic disease.
Recommendations from others
Manufacturer product labeling lists a number of contraindications. The American College of Obstetrics and Gynecology and the World Health Organization have similar but generally less restrictive lists of contraindications to IUD placement (TABLE).
TABLE
Contraindications to IUD placement
| ACOG | WHO* | MANUFACTURER | |
|---|---|---|---|
| Uterine anomaly (including distension of uterine cavity) | L, C | L, C | L, C |
| History of PID | L, C (past 3 mo only) | L, C (current PID only for both) | L (if no subsequent pregnancy), C |
| Postpartum endometritis or septic abortion in the past 3 months | L, C | L, C (immediately post-septic abortion for both) | L, C |
| Untreated cervicitis/vaginitis, including bacterial vaginosis | L, C | L, C (not bacterial vaginosis) | L, C (including genital actinomycosis) |
| Multiple sexual partners | L, C (increased STI risk is a relative contraindication for both) | L, C | |
| Immunosuppression | L, C (AIDS is a contraindication for both, unless clinically well on antiretroviral therapy) | L, C | |
| * Includes conditions rated as level 3 (risks usually outweigh benefits) or 4 (represents an unacceptable health risk) by WHO | |||
| L, levonorgestrel (Mirena) IUD; C, Copper T 380 (Paragard) IUD; IUD, intrauterine device; ACOG, American College of Obstetricians and Gynecologists; WHO, World Health Organization; PID, pelvic inflammatory disease; STI, sexually transmitted infection | |||
Based on limited evidence, use of intrauterine devices (IUDs) is not contraindicated for women with HIV/AIDS (strength of recommendation [SOR]: C), multiple sexual partners (SOR: C), previous actinomyces colonization (SOR: C), most types of fibroids (SOR: C), or previous ectopic pregnancy (SOR: C).
The risk to IUD users of pelvic inflammatory disease (PID) is similar to women using no contraception (SOR: B). Nulliparous women may experience increased insertion discomfort and higher rates of expulsion (SOR: B). IUD use of <3.5 years is not associated with decreased fertility (SOR: B).
IUDs are an excellent choice when estrogens are contraindicated or adherence is an issue
Shashi Mittal, MD
Baylor Family Medicine Residency at Garland, Garland, Tex
One percent of contraceptive users in the United States choose an IUD, compared with 25% in Europe. This is partly due to misinformation. An older IUD, the Dalkon shield, had a braided polyfilament tail that was associated with a higher risk of PID. People in the US still associate IUDs with this risk.
However, modern IUDs have a monofilament tail, which has not been linked to higher rates of PID. IUDs are an excellent alternative when estrogens are contraindicated, for prevention of pregnancy up to 5 days after unprotected sex, during lactation, and when adherence to a contraceptive has been difficult.
Evidence summary
IUDs are an effective and safe form of contraception. However, many clinicians have questions about the true contraindications to IUD use in the following situations.
Infection. IUDs do not increase the risk of complications among immunosuppressed HIV-positive women.1 IUD insertion does not increase the risk of PID for women with gonorrhea or chlamydia infection compared with infected nonusers.2 In one study, having multiple sexual partners was not associated with an increased risk of PID unless those partners carry specific infections, such as gonorrhea or chlamydia.3
In the US, approximately 1 in 1000 women develop PID after IUD insertion.3 Bacterial vaginosis may increase dysmenorrhea for women with IUDs (34.8 vs 13.9%, P=.03).4 In an observational study, all of 7 women with actinomyces who had IUDs removed remained negative for actinomyces after insertion of a new IUD.5
Nulliparity and infertility. Nulliparous women have increased rates of discomfort with IUD placement (17.8% vs 8.8%) and may have an increased risk of expulsion (up to 18.5% in one study, compared with less than 5.7% for all IUD users).6 Short-term (≤3.5 years) IUD use by nulliparous women was not associated with decreased fertility in a case-control study;7 however, 1 cohort study demonstrated lower fertility with use of a copper IUD for longer periods: hazard ratio (HR): 0.69 (95% confidence interval [CI], 0.497–0.97) for 42–78 months; HR=0.50 (95% CI, 0.34–0.73) for >78 months.8
Uterine anomalies. Significant uterine enlargement can increase the risk of IUD expulsion (0 vs 4 women [13%]; P=.04 in 1 retrospective cohort study).9 There are case reports of IUD failure and uterine perforation among women with anomalies that distort the uterine cavity.10,11
Other. Some contraindications to IUD use, such as concurrent pregnancy, are obvious. Other common sense contraindications might include insertion by patients with recent postpartum endometritis, gynecologic malignancy, genital bleeding of unknown cause, and gestational trophoblastic disease.
Recommendations from others
Manufacturer product labeling lists a number of contraindications. The American College of Obstetrics and Gynecology and the World Health Organization have similar but generally less restrictive lists of contraindications to IUD placement (TABLE).
TABLE
Contraindications to IUD placement
| ACOG | WHO* | MANUFACTURER | |
|---|---|---|---|
| Uterine anomaly (including distension of uterine cavity) | L, C | L, C | L, C |
| History of PID | L, C (past 3 mo only) | L, C (current PID only for both) | L (if no subsequent pregnancy), C |
| Postpartum endometritis or septic abortion in the past 3 months | L, C | L, C (immediately post-septic abortion for both) | L, C |
| Untreated cervicitis/vaginitis, including bacterial vaginosis | L, C | L, C (not bacterial vaginosis) | L, C (including genital actinomycosis) |
| Multiple sexual partners | L, C (increased STI risk is a relative contraindication for both) | L, C | |
| Immunosuppression | L, C (AIDS is a contraindication for both, unless clinically well on antiretroviral therapy) | L, C | |
| * Includes conditions rated as level 3 (risks usually outweigh benefits) or 4 (represents an unacceptable health risk) by WHO | |||
| L, levonorgestrel (Mirena) IUD; C, Copper T 380 (Paragard) IUD; IUD, intrauterine device; ACOG, American College of Obstetricians and Gynecologists; WHO, World Health Organization; PID, pelvic inflammatory disease; STI, sexually transmitted infection | |||
1. Sinei SK, Morrison CS, Sekadde-Kigondu C, Allen M, Kokonya D. Complications of use of intrauterine devices among HIV-1-infected women. Lancet 1998;351:1238-1241.
2. Ryden G, Fahraeus L, Molin L, Ahman K. Do contraceptives influence the incidence of acute pelvic inflammatory disease in women with gonorrhoea? Contraception 1979;20:149-157.
3. Steen R, Shapiro K. Intrauterine contraceptive devices and risk of pelvic inflammatory disease: standard of care in high STI prevalence settings. Reprod Health Matters 2004;12:136-143.
4. Ferraz do Lago R, Simoes JA, Bahamondes L, et al. Follow-up of users of intrauterine devices with and without bacterial vaginosis and other cervicovaginal infections. Contraception 2003;68:105-109.
5. Mao K, Guillebaud J. Influence of removal of intrauterine contraceptive devices on colonisation of the cervix by actinomyces-like organisms. Contraception 1984;30:535-544.
6. Weiner E, Berg AA, Johansson I. Copper intrauterine contraceptive devices in adolescent nulliparae. Br J Obstet Gynaecol 1978;85:204.-
7. Hubacher D, Lara-Richaldi R, Taylor DJ, Guerra-Infante F, Guzman-Rodriguez R. Use of copper intrauterine devices and the risk of tubal infertility among nulligravid women. N Engl J Med 2001;345:561-567.
8. Doll H, Vessey M, Painter R. Return of fertility in nulliparous women after discontinuation of the intrauterine device: comparison with women discontinuing other methods of contraception. BJOG 2001;108:304-314.
9. Ikomi A, Mansell E, Spence-Jones C, Singer A. Treatment of menorrhagia with the levonorgestrel intrauterine system: Can we learn from our failures? J Obstet Gynaecol 1998;20:630-631.
10. Seibel MM, Hann L. Pregnancy and an IUD in separate horns of a bicornate uterus. JAMA 1982;247:753-754.
11. Caspi B, Shoham Z, Barash A, Lancet M. Sonographic demonstration of an intrauterine device perforating a uterine myoma. J Clin Ultrasound 1989;17:535-537.
1. Sinei SK, Morrison CS, Sekadde-Kigondu C, Allen M, Kokonya D. Complications of use of intrauterine devices among HIV-1-infected women. Lancet 1998;351:1238-1241.
2. Ryden G, Fahraeus L, Molin L, Ahman K. Do contraceptives influence the incidence of acute pelvic inflammatory disease in women with gonorrhoea? Contraception 1979;20:149-157.
3. Steen R, Shapiro K. Intrauterine contraceptive devices and risk of pelvic inflammatory disease: standard of care in high STI prevalence settings. Reprod Health Matters 2004;12:136-143.
4. Ferraz do Lago R, Simoes JA, Bahamondes L, et al. Follow-up of users of intrauterine devices with and without bacterial vaginosis and other cervicovaginal infections. Contraception 2003;68:105-109.
5. Mao K, Guillebaud J. Influence of removal of intrauterine contraceptive devices on colonisation of the cervix by actinomyces-like organisms. Contraception 1984;30:535-544.
6. Weiner E, Berg AA, Johansson I. Copper intrauterine contraceptive devices in adolescent nulliparae. Br J Obstet Gynaecol 1978;85:204.-
7. Hubacher D, Lara-Richaldi R, Taylor DJ, Guerra-Infante F, Guzman-Rodriguez R. Use of copper intrauterine devices and the risk of tubal infertility among nulligravid women. N Engl J Med 2001;345:561-567.
8. Doll H, Vessey M, Painter R. Return of fertility in nulliparous women after discontinuation of the intrauterine device: comparison with women discontinuing other methods of contraception. BJOG 2001;108:304-314.
9. Ikomi A, Mansell E, Spence-Jones C, Singer A. Treatment of menorrhagia with the levonorgestrel intrauterine system: Can we learn from our failures? J Obstet Gynaecol 1998;20:630-631.
10. Seibel MM, Hann L. Pregnancy and an IUD in separate horns of a bicornate uterus. JAMA 1982;247:753-754.
11. Caspi B, Shoham Z, Barash A, Lancet M. Sonographic demonstration of an intrauterine device perforating a uterine myoma. J Clin Ultrasound 1989;17:535-537.
Evidence-based answers from the Family Physicians Inquiries Network
What is the appropriate evaluation and treatment of children who are “toe walkers”?
The evaluation of toe-walking focuses on differentiating normal children from those with mild cerebral palsy. Gait analysis may be a useful diagnostic tool, but further investigation is needed to confirm its reliability (strength of recommendation [SOR]: C, based on case series).
Observation alone is generally as successful as serial casting and surgery in decreasing the frequency of toe-walking at follow-up (SOR: C, based on case series).
Avoid overmedicalizing a problem that appears to run a benign course
Vince Winkler-Prins, MD
Michigan State University, East Lansing
The challenge with idiopathic toe-walking appears to be how to discriminate it from the more serious entities of cerebral palsy and muscular dystrophy. Idiopathic toe-walking should be evident in an otherwise healthy child as he or she begins to walk. It should be bilateral, there should be no spasticity and reflexes should not be overly brisk. A few follow-up visits at 3- or 6-month intervals should reassure all that this problem is nonprogressive. I have seen many toe-walking children over the years but no toe-walking adults without cerebral palsy or muscular dystrophy. This seems to confirm this review’s findings that observation appears to be as useful as casting or surgery. Until there is a natural history study of toe-walking, we need to be watchful to not overmedicalize a problem that appears to run a benign course.
Evidence summary
Idiopathic toe-walking is a childhood condition of unknown cause characterized by persistence of a tiptoe gait pattern without evidence of neurologic, orthopedic, or psychiatric disease.1 The incidence in the general population is not known. Children with idiopathic toe-walking usually have limited ankle dorsiflexion and are able to walk with a heel-strike for short periods when asked to do so. Longitudinal data is lacking to determine whether ankle equinus is the primary cause of idiopathic toe-walking or is a consequence of chronically walking on tiptoes. A family history of toe-walking ranges from 30% to 71% in the literature and is considered a characteristic of idiopathic toe walking.2-4
Evaluation. An important element of the evaluation of idiopathic toe-walking is to distinguish it from neuromuscular disorders associated with toe-walking, such as mild cerebral palsy. Case series with small numbers of subjects (range=27–41) have used gait electromyography (EMG) to distinguish cerebral palsy from idiopathic toe-walking.4-6 The overlap in gait EMG values in cerebral palsy and idiopathic toe-walking precludes its use as a differentiating diagnostic test.
The only aspect of EMG testing that has been useful in differentiating cerebral palsy from idiopathic toe-walking is gastrocnemius coactivation during resisted knee extension—a finding indicative of neurologic pathology.5,6 Kinematic analysis and observation of gait and measurement of ankle range of motion have been studied as diagnostic tools to differentiate idiopathic toe-walking from cerebral palsy.5-8 In the largest of these 4 studies (23 children with mild cerebral palsy and 22 with idiopathic toe-walking), maximal knee extension occurred at ground contact in the idiopathic toe-walking group whereas in the mild cerebral palsy group, the knee was flexed at ground contact.7 Measurement of ankle range of motion is not reliable in distinguishing between idiopathic toe-walking and cerebral palsy groups.5-7
Treatment. Simple observation, physical therapy, serial casting, and Achilles tendon lengthening surgery have been studied in the treatment of idiopathic toe-walking.2,3,9-11 In the largest case series (n=136),10 the frequency of toe-walking decreased in 51% of those in both the observation and casted groups. In this same study, the surgical group had lower rates of toe-walking, but no direct comparisons could be made to the nonsurgical groups because the patients in the surgical group were older and had longer follow-up than the other groups.
In a retrospective comparison3 of observation (which included physical therapy and special shoes), casting, and surgery among 80 children with idiopathic toe-walking, surgery resulted in significantly higher parental satisfaction (satisfied was defined as “child rarely walks on tiptoe”), 67% vs 25% and 24% for observation and casting groups respectively (P<.05). Three smaller studies (from 13 to 18 subjects) also showed decreased toe-walking at follow-up, regardless of treatment.2,9,11
There is no convincing evidence that treatment is necessary for this condition. We found no randomized trials of treatment for idiopathic toe-walking and no follow-up studies of sufficient size and duration that evaluate long-term effects of toe walking on the patient later in life.
Recommendations from others
No recommendations or guidelines were found.
1. Hall JE, Salter RB, Bhalla SK. Congenital short tendo calcaneus. J Bone Joint Surg Br 1967;49B:695-697.
2. Hirsch G, Wagner B. The natural history of idiopathic toe-walking: a long-term follow-up of fourteen conservatively treated children. Acta Paediatr 2004;93:196-199.
3. Stricker SJ, Angulo JC. Idiopathic toe walking: a comparison of treatment methods. J Pediatr Orthop 1998;18:289-293.
4. Kalen V, Adler N, Bleck EE. Electromyography of idiopathic toe walking. J Pediatr Orthop 1986;6:31-33.
5. Policy JF, Torburn L, Rinsky LA, Rose J. Electromyographic test to differentiate mild diplegic cerebral palsy and idiopathic toe-walking. J Pediatr Orthop 2001;21:784-789.
6. Rose J, Martin JG, Torburn L, Rinsky LA, Gamble JG. Electromyographic differentiation of diplegic cerebral palsy from idiopathic toe walking: involuntary coactivation of the quadriceps and gastrocnemius. J Pediatr Orthop 1999;19:677-682.
7. Kelly IP, Jenkinson A, Stephens M, O’Brien T. The kinematic patterns of toe-walkers. J Pediatr Orthop 1997;17:478-480.
8. Hicks R, Durinick N, Gage JR. Differentiation of idiopathic toe-walking and cerebral palsy. J Pediatr Orthop 1988;8:160-163.
9. Stott NS, Walt SE, Lobb GA, Reynolds N, Nicol RO. Treatment for idiopathic toe-walking: results at skeletal maturity. J Pediatr Orthop 2004;24:63-69.
10. Eastwood DM, Menelaus MB, Dickens DR, Broughton NS, Cole WG. Idiopathic toe-walking: does treatment alter the natural history. J Pediatr Orthop B 2000;9:47-49.
11. Brouwer B, Davidson LK, Olney SJ. Serial casting in idiopathic toe-walkers and children with spastic cerebral palsy. J Pediatr Orthop 2000;20:221-225.
The evaluation of toe-walking focuses on differentiating normal children from those with mild cerebral palsy. Gait analysis may be a useful diagnostic tool, but further investigation is needed to confirm its reliability (strength of recommendation [SOR]: C, based on case series).
Observation alone is generally as successful as serial casting and surgery in decreasing the frequency of toe-walking at follow-up (SOR: C, based on case series).
Avoid overmedicalizing a problem that appears to run a benign course
Vince Winkler-Prins, MD
Michigan State University, East Lansing
The challenge with idiopathic toe-walking appears to be how to discriminate it from the more serious entities of cerebral palsy and muscular dystrophy. Idiopathic toe-walking should be evident in an otherwise healthy child as he or she begins to walk. It should be bilateral, there should be no spasticity and reflexes should not be overly brisk. A few follow-up visits at 3- or 6-month intervals should reassure all that this problem is nonprogressive. I have seen many toe-walking children over the years but no toe-walking adults without cerebral palsy or muscular dystrophy. This seems to confirm this review’s findings that observation appears to be as useful as casting or surgery. Until there is a natural history study of toe-walking, we need to be watchful to not overmedicalize a problem that appears to run a benign course.
Evidence summary
Idiopathic toe-walking is a childhood condition of unknown cause characterized by persistence of a tiptoe gait pattern without evidence of neurologic, orthopedic, or psychiatric disease.1 The incidence in the general population is not known. Children with idiopathic toe-walking usually have limited ankle dorsiflexion and are able to walk with a heel-strike for short periods when asked to do so. Longitudinal data is lacking to determine whether ankle equinus is the primary cause of idiopathic toe-walking or is a consequence of chronically walking on tiptoes. A family history of toe-walking ranges from 30% to 71% in the literature and is considered a characteristic of idiopathic toe walking.2-4
Evaluation. An important element of the evaluation of idiopathic toe-walking is to distinguish it from neuromuscular disorders associated with toe-walking, such as mild cerebral palsy. Case series with small numbers of subjects (range=27–41) have used gait electromyography (EMG) to distinguish cerebral palsy from idiopathic toe-walking.4-6 The overlap in gait EMG values in cerebral palsy and idiopathic toe-walking precludes its use as a differentiating diagnostic test.
The only aspect of EMG testing that has been useful in differentiating cerebral palsy from idiopathic toe-walking is gastrocnemius coactivation during resisted knee extension—a finding indicative of neurologic pathology.5,6 Kinematic analysis and observation of gait and measurement of ankle range of motion have been studied as diagnostic tools to differentiate idiopathic toe-walking from cerebral palsy.5-8 In the largest of these 4 studies (23 children with mild cerebral palsy and 22 with idiopathic toe-walking), maximal knee extension occurred at ground contact in the idiopathic toe-walking group whereas in the mild cerebral palsy group, the knee was flexed at ground contact.7 Measurement of ankle range of motion is not reliable in distinguishing between idiopathic toe-walking and cerebral palsy groups.5-7
Treatment. Simple observation, physical therapy, serial casting, and Achilles tendon lengthening surgery have been studied in the treatment of idiopathic toe-walking.2,3,9-11 In the largest case series (n=136),10 the frequency of toe-walking decreased in 51% of those in both the observation and casted groups. In this same study, the surgical group had lower rates of toe-walking, but no direct comparisons could be made to the nonsurgical groups because the patients in the surgical group were older and had longer follow-up than the other groups.
In a retrospective comparison3 of observation (which included physical therapy and special shoes), casting, and surgery among 80 children with idiopathic toe-walking, surgery resulted in significantly higher parental satisfaction (satisfied was defined as “child rarely walks on tiptoe”), 67% vs 25% and 24% for observation and casting groups respectively (P<.05). Three smaller studies (from 13 to 18 subjects) also showed decreased toe-walking at follow-up, regardless of treatment.2,9,11
There is no convincing evidence that treatment is necessary for this condition. We found no randomized trials of treatment for idiopathic toe-walking and no follow-up studies of sufficient size and duration that evaluate long-term effects of toe walking on the patient later in life.
Recommendations from others
No recommendations or guidelines were found.
The evaluation of toe-walking focuses on differentiating normal children from those with mild cerebral palsy. Gait analysis may be a useful diagnostic tool, but further investigation is needed to confirm its reliability (strength of recommendation [SOR]: C, based on case series).
Observation alone is generally as successful as serial casting and surgery in decreasing the frequency of toe-walking at follow-up (SOR: C, based on case series).
Avoid overmedicalizing a problem that appears to run a benign course
Vince Winkler-Prins, MD
Michigan State University, East Lansing
The challenge with idiopathic toe-walking appears to be how to discriminate it from the more serious entities of cerebral palsy and muscular dystrophy. Idiopathic toe-walking should be evident in an otherwise healthy child as he or she begins to walk. It should be bilateral, there should be no spasticity and reflexes should not be overly brisk. A few follow-up visits at 3- or 6-month intervals should reassure all that this problem is nonprogressive. I have seen many toe-walking children over the years but no toe-walking adults without cerebral palsy or muscular dystrophy. This seems to confirm this review’s findings that observation appears to be as useful as casting or surgery. Until there is a natural history study of toe-walking, we need to be watchful to not overmedicalize a problem that appears to run a benign course.
Evidence summary
Idiopathic toe-walking is a childhood condition of unknown cause characterized by persistence of a tiptoe gait pattern without evidence of neurologic, orthopedic, or psychiatric disease.1 The incidence in the general population is not known. Children with idiopathic toe-walking usually have limited ankle dorsiflexion and are able to walk with a heel-strike for short periods when asked to do so. Longitudinal data is lacking to determine whether ankle equinus is the primary cause of idiopathic toe-walking or is a consequence of chronically walking on tiptoes. A family history of toe-walking ranges from 30% to 71% in the literature and is considered a characteristic of idiopathic toe walking.2-4
Evaluation. An important element of the evaluation of idiopathic toe-walking is to distinguish it from neuromuscular disorders associated with toe-walking, such as mild cerebral palsy. Case series with small numbers of subjects (range=27–41) have used gait electromyography (EMG) to distinguish cerebral palsy from idiopathic toe-walking.4-6 The overlap in gait EMG values in cerebral palsy and idiopathic toe-walking precludes its use as a differentiating diagnostic test.
The only aspect of EMG testing that has been useful in differentiating cerebral palsy from idiopathic toe-walking is gastrocnemius coactivation during resisted knee extension—a finding indicative of neurologic pathology.5,6 Kinematic analysis and observation of gait and measurement of ankle range of motion have been studied as diagnostic tools to differentiate idiopathic toe-walking from cerebral palsy.5-8 In the largest of these 4 studies (23 children with mild cerebral palsy and 22 with idiopathic toe-walking), maximal knee extension occurred at ground contact in the idiopathic toe-walking group whereas in the mild cerebral palsy group, the knee was flexed at ground contact.7 Measurement of ankle range of motion is not reliable in distinguishing between idiopathic toe-walking and cerebral palsy groups.5-7
Treatment. Simple observation, physical therapy, serial casting, and Achilles tendon lengthening surgery have been studied in the treatment of idiopathic toe-walking.2,3,9-11 In the largest case series (n=136),10 the frequency of toe-walking decreased in 51% of those in both the observation and casted groups. In this same study, the surgical group had lower rates of toe-walking, but no direct comparisons could be made to the nonsurgical groups because the patients in the surgical group were older and had longer follow-up than the other groups.
In a retrospective comparison3 of observation (which included physical therapy and special shoes), casting, and surgery among 80 children with idiopathic toe-walking, surgery resulted in significantly higher parental satisfaction (satisfied was defined as “child rarely walks on tiptoe”), 67% vs 25% and 24% for observation and casting groups respectively (P<.05). Three smaller studies (from 13 to 18 subjects) also showed decreased toe-walking at follow-up, regardless of treatment.2,9,11
There is no convincing evidence that treatment is necessary for this condition. We found no randomized trials of treatment for idiopathic toe-walking and no follow-up studies of sufficient size and duration that evaluate long-term effects of toe walking on the patient later in life.
Recommendations from others
No recommendations or guidelines were found.
1. Hall JE, Salter RB, Bhalla SK. Congenital short tendo calcaneus. J Bone Joint Surg Br 1967;49B:695-697.
2. Hirsch G, Wagner B. The natural history of idiopathic toe-walking: a long-term follow-up of fourteen conservatively treated children. Acta Paediatr 2004;93:196-199.
3. Stricker SJ, Angulo JC. Idiopathic toe walking: a comparison of treatment methods. J Pediatr Orthop 1998;18:289-293.
4. Kalen V, Adler N, Bleck EE. Electromyography of idiopathic toe walking. J Pediatr Orthop 1986;6:31-33.
5. Policy JF, Torburn L, Rinsky LA, Rose J. Electromyographic test to differentiate mild diplegic cerebral palsy and idiopathic toe-walking. J Pediatr Orthop 2001;21:784-789.
6. Rose J, Martin JG, Torburn L, Rinsky LA, Gamble JG. Electromyographic differentiation of diplegic cerebral palsy from idiopathic toe walking: involuntary coactivation of the quadriceps and gastrocnemius. J Pediatr Orthop 1999;19:677-682.
7. Kelly IP, Jenkinson A, Stephens M, O’Brien T. The kinematic patterns of toe-walkers. J Pediatr Orthop 1997;17:478-480.
8. Hicks R, Durinick N, Gage JR. Differentiation of idiopathic toe-walking and cerebral palsy. J Pediatr Orthop 1988;8:160-163.
9. Stott NS, Walt SE, Lobb GA, Reynolds N, Nicol RO. Treatment for idiopathic toe-walking: results at skeletal maturity. J Pediatr Orthop 2004;24:63-69.
10. Eastwood DM, Menelaus MB, Dickens DR, Broughton NS, Cole WG. Idiopathic toe-walking: does treatment alter the natural history. J Pediatr Orthop B 2000;9:47-49.
11. Brouwer B, Davidson LK, Olney SJ. Serial casting in idiopathic toe-walkers and children with spastic cerebral palsy. J Pediatr Orthop 2000;20:221-225.
1. Hall JE, Salter RB, Bhalla SK. Congenital short tendo calcaneus. J Bone Joint Surg Br 1967;49B:695-697.
2. Hirsch G, Wagner B. The natural history of idiopathic toe-walking: a long-term follow-up of fourteen conservatively treated children. Acta Paediatr 2004;93:196-199.
3. Stricker SJ, Angulo JC. Idiopathic toe walking: a comparison of treatment methods. J Pediatr Orthop 1998;18:289-293.
4. Kalen V, Adler N, Bleck EE. Electromyography of idiopathic toe walking. J Pediatr Orthop 1986;6:31-33.
5. Policy JF, Torburn L, Rinsky LA, Rose J. Electromyographic test to differentiate mild diplegic cerebral palsy and idiopathic toe-walking. J Pediatr Orthop 2001;21:784-789.
6. Rose J, Martin JG, Torburn L, Rinsky LA, Gamble JG. Electromyographic differentiation of diplegic cerebral palsy from idiopathic toe walking: involuntary coactivation of the quadriceps and gastrocnemius. J Pediatr Orthop 1999;19:677-682.
7. Kelly IP, Jenkinson A, Stephens M, O’Brien T. The kinematic patterns of toe-walkers. J Pediatr Orthop 1997;17:478-480.
8. Hicks R, Durinick N, Gage JR. Differentiation of idiopathic toe-walking and cerebral palsy. J Pediatr Orthop 1988;8:160-163.
9. Stott NS, Walt SE, Lobb GA, Reynolds N, Nicol RO. Treatment for idiopathic toe-walking: results at skeletal maturity. J Pediatr Orthop 2004;24:63-69.
10. Eastwood DM, Menelaus MB, Dickens DR, Broughton NS, Cole WG. Idiopathic toe-walking: does treatment alter the natural history. J Pediatr Orthop B 2000;9:47-49.
11. Brouwer B, Davidson LK, Olney SJ. Serial casting in idiopathic toe-walkers and children with spastic cerebral palsy. J Pediatr Orthop 2000;20:221-225.
Evidence-based answers from the Family Physicians Inquiries Network
What are the risks to the fetus associated with diagnostic radiation exposure during pregnancy?
There is no evidence of significant risk to the developing fetus from any single diagnostic x-ray exposure (strength of recommendation: C, based on non-homogenous case-control studies). No studies were found on fetal exposure risks from other forms of diagnostic radiation such as computed tomography (CT) scans, fluoroscopy, or mammography. Prudent clinicians should order only those studies that result in clinically important information and efforts should be made to minimize fetal exposure.
Communication with the patient can go a long way to alleviate concerns regarding effects of radiation
Timothy Huber, MD
Oroville, Calif
The lack of high-quality research coupled with a general societal fear of radiation during pregnancy can create tension between the physician and the patient who needs diagnostic studies during pregnancy. This review reassures the conscientious practitioner that there is little to fear from the prudent use of routine studies. There is less clarity when a woman needs multiple or higher-dose radiation studies, especially in the first trimester.
Patients need our best estimates regarding the medical necessity, diagnostic benefit, and overall risk in these situations. Open communication with the patient can go a long way to alleviate concerns regarding the possible teratogenic or carcinogenic effects of radiation. Working more closely with our radiology colleagues to determine the best set of studies for a particular situation can help reduce the overall total radiation exposure. I refer patients who are Internet-savvy to www.familydoctor.org for more information about diagnostic radiation exposure in pregnancy.
Evidence summary
Clinicians have been concerned about x-ray exposure during pregnancy since the 1950s. Much of this concern was based on the Oxford Survey of Childhood Leukemia, as well as other early case-control studies.1-3 These studies reported an approximate 40% increase in the risk of childhood leukemia among offspring of women who received diagnostic x-rays in pregnancy. However, by modern standards, these studies are of poor quality as they are limited by reliance on maternal recall of prenatal x-ray exposure, lack of consideration for multiple confounding factors, lack of blinding in determination of exposure and outcome status, limitations in selection of both cases and controls, and other significant methodological flaws.
Modern, well-designed studies have failed to replicate the association between in utero radiation and childhood malignancies found in the early studies. We found 1 good-quality and 5 fair-quality case-control studies examining the association between in utero x-ray exposure and childhood leukemia, as well as 6 fair-quality case-control studies examining the association with other childhood malignancies. These studies found no significant association between in utero exposure to any x-ray in general, or to abdominal or pelvic x-rays and development of subsequent childhood leukemia, central nervous system tumors or other malignancies (TABLE).
No meta-analyses, randomized controlled trials, cohort studies or good- or fair-quality case-control studies were found examining in utero x-rays and decreased head circumference, congenital malformations, spontaneous abortion, low birth weight, or developmental problems. One recent, fair-quality case-control study found an association between prenatal dental x-rays and low birth weight (odds ratio [OR]=1.8 [95% confidence interval, 1.09–1.36]) for radiation exposures above 0.4 Gy.4 However, this study has been criticized for several reasons, including lack of biological plausibility and failure to control for dental disease.5
There does not appear to be an increased risk of adverse pregnancy outcomes with prenatal endoscopic retrograde cholangiopancreaticogram (ERCP), though this conclusion is based on 2 incomplete case series reports with no follow-up of the infants after delivery.6,7 No good- or fair-quality studies were found examining the association between other diagnostic radiation exposures (CT scan, mammography, positron emission tomography scan, dual-energy x-ray absorptiometry [DEXA]) with adverse pregnancy outcomes.
TABLE
Risk of childhood malignancy after in utero diagnostic X-ray studies1
| OUTCOME | TYPE OF STUDY | ODDS RATIO [95% CI] |
|---|---|---|
| Leukemia9-14 | Any x-ray | 0.8–1.8 [0.5–3.6] |
| Pelvic x-ray | 0.7–3.4 [0.4–12.9] | |
| CNS tumor12,15 | Any x-ray | 0.78 [0.44–1.36] |
| Abdominal x-ray | 1.5 [0.5–4.2] | |
| Any cancer12,13,16,17 | Any x-ray | 0.92–1.2 [0.47–2.4] |
| Abdominal x-ray | 1.4 [0.8–2.5] |
Recommendations from others
The American College of Obstetricians and Gynecologists recommends that women be counseled that x-ray exposure from a single diagnostic procedure does not result in harmful fetal effects. Concern about possible effects of ionizing radiation exposure should not prevent medically indicated diagnostic x-ray procedures from being performed on a pregnant woman.8
1. Fattibene P, Mazzei F, Nuccetelli C, Risica S. Prenatal exposure to ionizing radiation: sources, effects and regulatory aspects. Acta Paediatr 1999;88:693-702.
2. Bross ID, Natarajan N. Risk of leukemia in susceptible children exposed to preconception, in utero and postnatal radiation. Prev Med 1974;3:361-369.
3. Stewart A, Webb J, Hewitt D. A survey of childhood malignancies. BMJ 1958;1:1495-1508.
4. Hujoel PP, Bollen AM, Noonan CJ, del Aguila MA. Antepartum dental radiography and infant low birth weight. JAMA 2004;291:1987-1993.
5. Brent RL. Commentary on JAMA article by Hujoel et al. Health Phys 2005;88:379-381.
6. Kahaleh M, Hartwell GD, Arseneau KO, et al. Safety and efficacy of ERCP in pregnancy. Gastrointest Endosc 2004;60:287-292.
7. Tham TC, Vandervoort J, Wong RC, et al. Safety of ERCP during pregnancy [see comment]. Am J Gastroenterol 2003;98:308-311.
8. ACOG Bulletins. ACOG Committee Opinion No. 299: Guidelines for diagnostic imaging during pregnancy. Obstet Gynecol 2004;104:647-651.
9. Roman E, Ansell G, Bull D. Leukaemia and non-Hodgkin’s lymphoma in children and young adults: are prenatal and neonatal factors important determinants of disease? Br J Cancer 1997;76:406-415.
10. Shu XO, Potter JD, Linet MS, et al. Diagnostic X-rays and ultrasound exposure and risk of childhood acute lymphoblastic leukemia by immunophenotype. Cancer Epidemiol Biomarkers Prev 2002;11:177-185.
11. McKinney PA, Cartwright RA, Saiu JM, et al. The inter-regional epidemiological study of childhood cancer (IRESCC): a case control study of aetiological factors in leukaemia and lymphoma. Arch Dis Child 1987;62:279-287.
12. Rodvall Y, Pershagen G, Hrubec Z, Ahlbom A, Pedersen NL, Boice JD. Prenatal X-ray exposure and childhood cancer in Swedish twins. Int J Cancer 1990;46:362-365.
13. Shu XO, Jin F, Linet MS, et al. Diagnostic X-ray and ultrasound exposure and risk of childhood cancer. Br J Cancer 1994;70:531-536.
14. Naumburg E, Bellocco R, Cnattingius S, Hall P, Boice JD, Ekbom A. Intrauterine exposure to diagnostic X rays and risk of childhood leukemia subtypes. Radiat Res 2001;156:718-723.
15. Schuz J, Kaletsch U, Kaatsch P, Meinert R, Michaelis J. Risk factors for pediatric tumors of the central nervous system: results from a German population-based case-control study. Med Pediatr Oncol 2001;36:274-282.
16. Shiono PH, Chung CS, Myrianthopoulos NC. Preconception radiation, intrauterine diagnostic radiation, and childhood neoplasia. J Natl Cancer Inst 1980;65:681-686.
17. Meinert R, Kaletsch U, Kaatsch P, Schuz J, Michaelis J. Associations between childhood cancer and ionizing radiation: results of a population-based case-control study in Germany. Cancer Epidemiol Biomarkers Prev 1999;8:793-799.
There is no evidence of significant risk to the developing fetus from any single diagnostic x-ray exposure (strength of recommendation: C, based on non-homogenous case-control studies). No studies were found on fetal exposure risks from other forms of diagnostic radiation such as computed tomography (CT) scans, fluoroscopy, or mammography. Prudent clinicians should order only those studies that result in clinically important information and efforts should be made to minimize fetal exposure.
Communication with the patient can go a long way to alleviate concerns regarding effects of radiation
Timothy Huber, MD
Oroville, Calif
The lack of high-quality research coupled with a general societal fear of radiation during pregnancy can create tension between the physician and the patient who needs diagnostic studies during pregnancy. This review reassures the conscientious practitioner that there is little to fear from the prudent use of routine studies. There is less clarity when a woman needs multiple or higher-dose radiation studies, especially in the first trimester.
Patients need our best estimates regarding the medical necessity, diagnostic benefit, and overall risk in these situations. Open communication with the patient can go a long way to alleviate concerns regarding the possible teratogenic or carcinogenic effects of radiation. Working more closely with our radiology colleagues to determine the best set of studies for a particular situation can help reduce the overall total radiation exposure. I refer patients who are Internet-savvy to www.familydoctor.org for more information about diagnostic radiation exposure in pregnancy.
Evidence summary
Clinicians have been concerned about x-ray exposure during pregnancy since the 1950s. Much of this concern was based on the Oxford Survey of Childhood Leukemia, as well as other early case-control studies.1-3 These studies reported an approximate 40% increase in the risk of childhood leukemia among offspring of women who received diagnostic x-rays in pregnancy. However, by modern standards, these studies are of poor quality as they are limited by reliance on maternal recall of prenatal x-ray exposure, lack of consideration for multiple confounding factors, lack of blinding in determination of exposure and outcome status, limitations in selection of both cases and controls, and other significant methodological flaws.
Modern, well-designed studies have failed to replicate the association between in utero radiation and childhood malignancies found in the early studies. We found 1 good-quality and 5 fair-quality case-control studies examining the association between in utero x-ray exposure and childhood leukemia, as well as 6 fair-quality case-control studies examining the association with other childhood malignancies. These studies found no significant association between in utero exposure to any x-ray in general, or to abdominal or pelvic x-rays and development of subsequent childhood leukemia, central nervous system tumors or other malignancies (TABLE).
No meta-analyses, randomized controlled trials, cohort studies or good- or fair-quality case-control studies were found examining in utero x-rays and decreased head circumference, congenital malformations, spontaneous abortion, low birth weight, or developmental problems. One recent, fair-quality case-control study found an association between prenatal dental x-rays and low birth weight (odds ratio [OR]=1.8 [95% confidence interval, 1.09–1.36]) for radiation exposures above 0.4 Gy.4 However, this study has been criticized for several reasons, including lack of biological plausibility and failure to control for dental disease.5
There does not appear to be an increased risk of adverse pregnancy outcomes with prenatal endoscopic retrograde cholangiopancreaticogram (ERCP), though this conclusion is based on 2 incomplete case series reports with no follow-up of the infants after delivery.6,7 No good- or fair-quality studies were found examining the association between other diagnostic radiation exposures (CT scan, mammography, positron emission tomography scan, dual-energy x-ray absorptiometry [DEXA]) with adverse pregnancy outcomes.
TABLE
Risk of childhood malignancy after in utero diagnostic X-ray studies1
| OUTCOME | TYPE OF STUDY | ODDS RATIO [95% CI] |
|---|---|---|
| Leukemia9-14 | Any x-ray | 0.8–1.8 [0.5–3.6] |
| Pelvic x-ray | 0.7–3.4 [0.4–12.9] | |
| CNS tumor12,15 | Any x-ray | 0.78 [0.44–1.36] |
| Abdominal x-ray | 1.5 [0.5–4.2] | |
| Any cancer12,13,16,17 | Any x-ray | 0.92–1.2 [0.47–2.4] |
| Abdominal x-ray | 1.4 [0.8–2.5] |
Recommendations from others
The American College of Obstetricians and Gynecologists recommends that women be counseled that x-ray exposure from a single diagnostic procedure does not result in harmful fetal effects. Concern about possible effects of ionizing radiation exposure should not prevent medically indicated diagnostic x-ray procedures from being performed on a pregnant woman.8
There is no evidence of significant risk to the developing fetus from any single diagnostic x-ray exposure (strength of recommendation: C, based on non-homogenous case-control studies). No studies were found on fetal exposure risks from other forms of diagnostic radiation such as computed tomography (CT) scans, fluoroscopy, or mammography. Prudent clinicians should order only those studies that result in clinically important information and efforts should be made to minimize fetal exposure.
Communication with the patient can go a long way to alleviate concerns regarding effects of radiation
Timothy Huber, MD
Oroville, Calif
The lack of high-quality research coupled with a general societal fear of radiation during pregnancy can create tension between the physician and the patient who needs diagnostic studies during pregnancy. This review reassures the conscientious practitioner that there is little to fear from the prudent use of routine studies. There is less clarity when a woman needs multiple or higher-dose radiation studies, especially in the first trimester.
Patients need our best estimates regarding the medical necessity, diagnostic benefit, and overall risk in these situations. Open communication with the patient can go a long way to alleviate concerns regarding the possible teratogenic or carcinogenic effects of radiation. Working more closely with our radiology colleagues to determine the best set of studies for a particular situation can help reduce the overall total radiation exposure. I refer patients who are Internet-savvy to www.familydoctor.org for more information about diagnostic radiation exposure in pregnancy.
Evidence summary
Clinicians have been concerned about x-ray exposure during pregnancy since the 1950s. Much of this concern was based on the Oxford Survey of Childhood Leukemia, as well as other early case-control studies.1-3 These studies reported an approximate 40% increase in the risk of childhood leukemia among offspring of women who received diagnostic x-rays in pregnancy. However, by modern standards, these studies are of poor quality as they are limited by reliance on maternal recall of prenatal x-ray exposure, lack of consideration for multiple confounding factors, lack of blinding in determination of exposure and outcome status, limitations in selection of both cases and controls, and other significant methodological flaws.
Modern, well-designed studies have failed to replicate the association between in utero radiation and childhood malignancies found in the early studies. We found 1 good-quality and 5 fair-quality case-control studies examining the association between in utero x-ray exposure and childhood leukemia, as well as 6 fair-quality case-control studies examining the association with other childhood malignancies. These studies found no significant association between in utero exposure to any x-ray in general, or to abdominal or pelvic x-rays and development of subsequent childhood leukemia, central nervous system tumors or other malignancies (TABLE).
No meta-analyses, randomized controlled trials, cohort studies or good- or fair-quality case-control studies were found examining in utero x-rays and decreased head circumference, congenital malformations, spontaneous abortion, low birth weight, or developmental problems. One recent, fair-quality case-control study found an association between prenatal dental x-rays and low birth weight (odds ratio [OR]=1.8 [95% confidence interval, 1.09–1.36]) for radiation exposures above 0.4 Gy.4 However, this study has been criticized for several reasons, including lack of biological plausibility and failure to control for dental disease.5
There does not appear to be an increased risk of adverse pregnancy outcomes with prenatal endoscopic retrograde cholangiopancreaticogram (ERCP), though this conclusion is based on 2 incomplete case series reports with no follow-up of the infants after delivery.6,7 No good- or fair-quality studies were found examining the association between other diagnostic radiation exposures (CT scan, mammography, positron emission tomography scan, dual-energy x-ray absorptiometry [DEXA]) with adverse pregnancy outcomes.
TABLE
Risk of childhood malignancy after in utero diagnostic X-ray studies1
| OUTCOME | TYPE OF STUDY | ODDS RATIO [95% CI] |
|---|---|---|
| Leukemia9-14 | Any x-ray | 0.8–1.8 [0.5–3.6] |
| Pelvic x-ray | 0.7–3.4 [0.4–12.9] | |
| CNS tumor12,15 | Any x-ray | 0.78 [0.44–1.36] |
| Abdominal x-ray | 1.5 [0.5–4.2] | |
| Any cancer12,13,16,17 | Any x-ray | 0.92–1.2 [0.47–2.4] |
| Abdominal x-ray | 1.4 [0.8–2.5] |
Recommendations from others
The American College of Obstetricians and Gynecologists recommends that women be counseled that x-ray exposure from a single diagnostic procedure does not result in harmful fetal effects. Concern about possible effects of ionizing radiation exposure should not prevent medically indicated diagnostic x-ray procedures from being performed on a pregnant woman.8
1. Fattibene P, Mazzei F, Nuccetelli C, Risica S. Prenatal exposure to ionizing radiation: sources, effects and regulatory aspects. Acta Paediatr 1999;88:693-702.
2. Bross ID, Natarajan N. Risk of leukemia in susceptible children exposed to preconception, in utero and postnatal radiation. Prev Med 1974;3:361-369.
3. Stewart A, Webb J, Hewitt D. A survey of childhood malignancies. BMJ 1958;1:1495-1508.
4. Hujoel PP, Bollen AM, Noonan CJ, del Aguila MA. Antepartum dental radiography and infant low birth weight. JAMA 2004;291:1987-1993.
5. Brent RL. Commentary on JAMA article by Hujoel et al. Health Phys 2005;88:379-381.
6. Kahaleh M, Hartwell GD, Arseneau KO, et al. Safety and efficacy of ERCP in pregnancy. Gastrointest Endosc 2004;60:287-292.
7. Tham TC, Vandervoort J, Wong RC, et al. Safety of ERCP during pregnancy [see comment]. Am J Gastroenterol 2003;98:308-311.
8. ACOG Bulletins. ACOG Committee Opinion No. 299: Guidelines for diagnostic imaging during pregnancy. Obstet Gynecol 2004;104:647-651.
9. Roman E, Ansell G, Bull D. Leukaemia and non-Hodgkin’s lymphoma in children and young adults: are prenatal and neonatal factors important determinants of disease? Br J Cancer 1997;76:406-415.
10. Shu XO, Potter JD, Linet MS, et al. Diagnostic X-rays and ultrasound exposure and risk of childhood acute lymphoblastic leukemia by immunophenotype. Cancer Epidemiol Biomarkers Prev 2002;11:177-185.
11. McKinney PA, Cartwright RA, Saiu JM, et al. The inter-regional epidemiological study of childhood cancer (IRESCC): a case control study of aetiological factors in leukaemia and lymphoma. Arch Dis Child 1987;62:279-287.
12. Rodvall Y, Pershagen G, Hrubec Z, Ahlbom A, Pedersen NL, Boice JD. Prenatal X-ray exposure and childhood cancer in Swedish twins. Int J Cancer 1990;46:362-365.
13. Shu XO, Jin F, Linet MS, et al. Diagnostic X-ray and ultrasound exposure and risk of childhood cancer. Br J Cancer 1994;70:531-536.
14. Naumburg E, Bellocco R, Cnattingius S, Hall P, Boice JD, Ekbom A. Intrauterine exposure to diagnostic X rays and risk of childhood leukemia subtypes. Radiat Res 2001;156:718-723.
15. Schuz J, Kaletsch U, Kaatsch P, Meinert R, Michaelis J. Risk factors for pediatric tumors of the central nervous system: results from a German population-based case-control study. Med Pediatr Oncol 2001;36:274-282.
16. Shiono PH, Chung CS, Myrianthopoulos NC. Preconception radiation, intrauterine diagnostic radiation, and childhood neoplasia. J Natl Cancer Inst 1980;65:681-686.
17. Meinert R, Kaletsch U, Kaatsch P, Schuz J, Michaelis J. Associations between childhood cancer and ionizing radiation: results of a population-based case-control study in Germany. Cancer Epidemiol Biomarkers Prev 1999;8:793-799.
1. Fattibene P, Mazzei F, Nuccetelli C, Risica S. Prenatal exposure to ionizing radiation: sources, effects and regulatory aspects. Acta Paediatr 1999;88:693-702.
2. Bross ID, Natarajan N. Risk of leukemia in susceptible children exposed to preconception, in utero and postnatal radiation. Prev Med 1974;3:361-369.
3. Stewart A, Webb J, Hewitt D. A survey of childhood malignancies. BMJ 1958;1:1495-1508.
4. Hujoel PP, Bollen AM, Noonan CJ, del Aguila MA. Antepartum dental radiography and infant low birth weight. JAMA 2004;291:1987-1993.
5. Brent RL. Commentary on JAMA article by Hujoel et al. Health Phys 2005;88:379-381.
6. Kahaleh M, Hartwell GD, Arseneau KO, et al. Safety and efficacy of ERCP in pregnancy. Gastrointest Endosc 2004;60:287-292.
7. Tham TC, Vandervoort J, Wong RC, et al. Safety of ERCP during pregnancy [see comment]. Am J Gastroenterol 2003;98:308-311.
8. ACOG Bulletins. ACOG Committee Opinion No. 299: Guidelines for diagnostic imaging during pregnancy. Obstet Gynecol 2004;104:647-651.
9. Roman E, Ansell G, Bull D. Leukaemia and non-Hodgkin’s lymphoma in children and young adults: are prenatal and neonatal factors important determinants of disease? Br J Cancer 1997;76:406-415.
10. Shu XO, Potter JD, Linet MS, et al. Diagnostic X-rays and ultrasound exposure and risk of childhood acute lymphoblastic leukemia by immunophenotype. Cancer Epidemiol Biomarkers Prev 2002;11:177-185.
11. McKinney PA, Cartwright RA, Saiu JM, et al. The inter-regional epidemiological study of childhood cancer (IRESCC): a case control study of aetiological factors in leukaemia and lymphoma. Arch Dis Child 1987;62:279-287.
12. Rodvall Y, Pershagen G, Hrubec Z, Ahlbom A, Pedersen NL, Boice JD. Prenatal X-ray exposure and childhood cancer in Swedish twins. Int J Cancer 1990;46:362-365.
13. Shu XO, Jin F, Linet MS, et al. Diagnostic X-ray and ultrasound exposure and risk of childhood cancer. Br J Cancer 1994;70:531-536.
14. Naumburg E, Bellocco R, Cnattingius S, Hall P, Boice JD, Ekbom A. Intrauterine exposure to diagnostic X rays and risk of childhood leukemia subtypes. Radiat Res 2001;156:718-723.
15. Schuz J, Kaletsch U, Kaatsch P, Meinert R, Michaelis J. Risk factors for pediatric tumors of the central nervous system: results from a German population-based case-control study. Med Pediatr Oncol 2001;36:274-282.
16. Shiono PH, Chung CS, Myrianthopoulos NC. Preconception radiation, intrauterine diagnostic radiation, and childhood neoplasia. J Natl Cancer Inst 1980;65:681-686.
17. Meinert R, Kaletsch U, Kaatsch P, Schuz J, Michaelis J. Associations between childhood cancer and ionizing radiation: results of a population-based case-control study in Germany. Cancer Epidemiol Biomarkers Prev 1999;8:793-799.
Evidence-based answers from the Family Physicians Inquiries Network