Reexamining the Oral Contraceptive Issues

Reexamining the Oral Contraceptive Issues

~~ ~~~ ~ ~~ principles and practice Reexamining the Oral Contraceptive Issues ROBERTA ORNE, RN, MS, AND JOELLEN W. HAWKINS, RNC, PHD, FAAN Oral co...

593KB Sizes 0 Downloads 24 Views

~~

~~~

~

~~

principles and practice Reexamining the Oral Contraceptive Issues ROBERTA ORNE, RN, MS, AND JOELLEN W. HAWKINS, RNC, PHD, FAAN Oral contraceptives have been in use since the 1960s. Over the past 20 plus years, the risks and benefits of oral contraceptives have captured the attention of the press and the public. According to current data, oral contraceptives seem to pose the greatest risk for women in their 40s who smoke cigarettes. They have the least risk and greatest benefit for young women, especially nonsmokers. This article focuses on a reexamination of the issues. Are oral contraceptives safe? If so, for whom? How can risk be predicted? What are noncontraceptive benefits? Implications for practice and for the future of oral contraceptives research are presented.

Oral contraceptives (OCs, the pill) are used by an estimated ten million women in the United States.’ The pill is now second only to sterilization in popularity among American women. About 70% of all women in the United States of reproductive age have, at some time in their lives, taken oral contraceptives.’ Over fifty million women around the world use oral contraceptives.’ After several years of bad press, oral contraceptives are now receiving recognition for their safety for low-risk young women as well as for noncontraceptive benefits. Are oral contraceptives really safe? If so, for whom? Can risk be predicted and, if so, how? Are there benefits beyond prevention of conception?

Submitted: October 1983. Accepted with revisions: April 1984.

30

RISKS: ARE ORAL CONTRACEPTIVES REALLY SAFE?

In the early 1960s an initial rush of optimism was felt that, at last, the perfect contraceptive method had been developed, but by the late 1960s problems began to surface. Oral contraceptives were not without life-threatening risks as well as annoying, although often transient, side effects. Data began to appear in the literature implicating oral contraceptives as contributing factors, if not causes, in heart disease, hypertension, cerebral vascular accidents, thrombus formation in the extremities, benign liver tumors, and gallbladder disease. Stadel provides an extensive and accurate review of the literature on the risks of oral contraceptives, taking care to provide both sides of controversial issue^.^,^

In 1961, a general practitioner in England reported a case of a woman on oral contraception who suffered a pulmonary e m b ~ l i s m . ~ Other case reports were made and epidemiologic studies undertaken. Stadel summarizes these reports by stating “current information suggests that oral contraceptives increase both the risk of overt venous thromboembolic disease and the occurrence of subclinical venous thromboembolic d i ~ e a s e . ” ~ In a study reported in 1982, the authors cite an association between venous thrombosis associated with oral contraceptive use and low levels of vascular plasminogen activator. The same association was not demonstrated for arterial thrombosis, h ~ w e v e r . ~ Deep vein and pulmonary embolism accounts for over 7000 hospitalizations among oral contraceptive users each year. The occurrence of superficial venous thrombosis. which seldom re-

January/February 1985 JOCNN

quires hospitalization and almost never causes death, affects approximately 11,800 oral contraceptive users each year.' Oral contraceptives are known to cause an increased risk of cardiovascular disease, particularly for women over 35 years of age and those who smoke.'~~ The overwhelming majority of the estimated 500 deaths each year associated with the use of the pill are caused by stroke and heart attack. In addition, perhaps 1070 hospitalizations each year of pill users are due to these causes. Risk is closely tied to age: women under 25 have a risk of heart attack and stroke of approximately 4/100,000, and under 20 probably even less; women 25 to 34, a risk of 13/100,000; and 35 and older, 54/100,000.' If no women over 35 took the pill and no users of any age smoked, the death rate associated with pill has been estimated to be as low as 70 per year.' Numerous articles have appeared in the professional literature on the adverse effects of oral contraceptive use on lipoprotein triglyceride and cholesterol levels believed to be related to cardiovascular risk through acceleration of atherosclerosis. Knopp and colleagues demonstrated an increase in total plasma triglyceride concentrations and high density lipids (HDL) with a concurrent increase in the estrogen potency of the oral contraceptive used.6 It is important to acknowledge here the role of high density lipoprotein in removing cholesterol from tissues. Since a low HDL concentration is associated with atherogenesis, a protective role for HDL can be hypothesized. The low density lipid (LDL) cholesterol/triglyceride ratio decreased for five of the six oral contraceptive products in the study (exception OvralB), regardless of estrogen potency.6 These same investigators also found that although estrogen

January/February 1985 JOCNN

tends to increase HDL levels (high density lipoprotein cholesterol), high potency progestins, norgestrel, and norethindrone acetate overcome this tendency.6 Their findings are corroborated by Wynn and N i t h t h ~ a n a n t h a n . ~ These findings mediate for choosing the lowest possible potency level of estrogen and progestins other than norgestrel and norethindrone acetate, especially for women at risk for cardiovascular The effects of oral contraceptives on metabolism are not well understood, but are described by the authors of several clinical studies. Spellacy asserts that synthetic estrogens seem to produce few adverse effects on carbohydrate metabolism. His work implicates the 19-norprogestin norgestrel, rather than estrogens, as causing alterations in carbohydrate metabolism resulting in elevations of blood glucose and plasma insulin." With an oral contraceptive containing 30 to 35 micrograms of estrogen and norgestrel as the progestin, some negative changes in carbohydrate metabolism are evident. Substituting norethindrone for norgestrel eliminated these changes in Spellacy's work." In a study with oral contraceptives containing 30 micrograms of ethinyl estradiol and 150 micrograms of levonorgestrel, a progressive deterioration in glucose tolerance and an initial rise in insulin secretion were demonstrated. N o such changes were demonstrated with norethindrone." A study of mean conception time for women revealed a conception interval of 13 months or more for women discontinuing use of oral contraceptives and attempting pregnancy. The interval was somewhat longer than for other method^.'^ The authors of this study propose 15 months

rather than 12 as the period for trying to conceive before seeking fertility advice.I3 Benign liver tumors, known as hepatocellular adenomas, occur as a rare but serious complication of the use of oral contraceptives. The rate of occurrence is 3/100,000 users, accounting for about 300 hospitalizations a year. Most of those affected are 30 years of age and older and are long-term users. The tumors are fatal in approximately 10% of cases."' Gallbladder disease is a complication for pill users, the risk being limited to the first year of use. Oral contraceptives seem to precipitate clinical symptoms in women at risk for developing gallbladder disease and in women with the disease already present. This complication accounts for hospitalization of 860 women a year.',' In a study reported in 1983, the investigators state that their data support a relationship between long-term oral contraceptive use and the risk of cervical ne0p1asia.I~ These data must be viewed with caution, since the control group is limited to users of intrauterine devices rather than the general p0pu1ation.l~ Furthermore, assessing cervical cancer is very difficult because of the possibility of so many confounding variables.16 Further studies must be performed to confirm or refute this important finding. Another important investigation was reported in 1983 that suggests an association between breast cancer and the long-term use of combination-type oral contraceptives with a progestogen potency five or more before age 25. The authors state that this finding is not confounded by known breastcancer risk factors. Little or no risk is demonstrated with pill use with a low progestogen component.17 Caution must again prevail in interpreting these findings.

31

PREDICTING RISK

In a sense, dosage levels for oral contraceptives are at a crossroads. Estrogen levels have been reduced to the lowest level possible to still maintain contraceptive efficacy. At 20 micrograms of estrogen, some women ovulate but do not necessarily become pregnant due to cervical mucus changes, endometrial alterations, and effects on tuba1 mobility. On the progestin-only pill, approximately 40% of women will ovulate regularly and another 20% will ovulate occasionally." Methods of identifying women at risk through use of oral contraceptives beyond the methods currently in use (history, physical examination, and conventional laboratory studies such as LDL levels) need to be developed. Measuring plasminogen activator levels5 is one test for those women at risk for venous thrombosis (women with a history of varicose veins, thromboembolic episodes, strong family history). Correlating carbohydrate (CHO) metabolism alterations with progestogen potency prior to and upon initiation of use of oral contraceptives is another method. Measurement of plasma levels of estrogen and progestogen may be a predictor of cardiovascular risk and may provide guidelines for adjustment of dosage if, in fact, a correlation between specific plasma levels and risk can be a~certained.'~-" Stadel suggests that evaluation of the extent to which women vary in absorption, distribution, and elimination of oral contraceptive steroids may lead to new strategies for clinical management. If variation is substantial, procedures could be developed to titrate steroid dosage to achieve similar plasma levels in women whose absorption, distribution, and elimination vary.4

32

In examining the risks of oral contraceptive use, it is important to put them in perspective in relation to other risks experienced by women in their childbearing years. The risk of death for the pill user is lower than the risk of not using a method of contraception, except for older women who smoke.' The risk of death for all methods is lower than risk of unintended pregnancy and birth when no method is used, except for women 40 and older on the pill and women 35 and over who smoke. For the woman under 35 who does not smoke, taking the pill is safer than driving a car.' As Stubblefield states, the risk for oral contraceptive use is low for young women.z2 Since fertility is high in this group, providers may be doing these clients a disservice by discouraging use of the most effective contraceptive they have to offer.22Also, the risks of some of the life-threatening conditions are greater in pregnancy than while taking oral contraceptives.' Potential benefits are greatest and potential risks the least for these young women.22 BENEFITS

Rosenberg and colleagues report a reduction in risk for ovarian cancer noted for women taking oral contraceptives that persists as long as 10 years after use ceases.z3 They estimate a 40% to 50% decrease in risk and speculate that perhaps, as with the lowered risk correlated with high parity, suppression of ovulation in some way is the factor in risk reduct i ~ nCramer . ~ ~ and coinvestigators corroborate the findings of Rosenberg el al. They found a decreased risk of ovarian cancer for women who were between 40 and 59 years of age at the time of the study and for women who had discontinued use of oral contraceptives more

than ten years p r e v i ~ u s l yHulka .~~ and associates note, from their retrospective studies, a risk of endometrial cancer less than onehalf of that for n o n u s e ~ s . Five ~~'~~ years or more of oral contraceptive use reduced the risk to onethird of that for nonusers. Those oral contraceptives with predominantly progestational effects offered greater protection. Although controversial reports exist concerning the role of oral contraceptives and breast cancer, current data do not support a relationship between the two, with the exception of one study.I6A retrospective study by the Centers for Disease Control indicates a 0.96 relative risk of developing breast cancer for women who are users of oral contraceptives compared to nonuser~.~~ Burkman's work suggests that oral contraceptives may reduce the risk of pelvic inflammatory disease.z8 The work of Rubin and colleagues supports that of Burkman.29 The protective effects of oral contraceptives against pelvic inflammatory disease exist for women using oral contraceptives for longer than 12 months. These authors estimate that 50,000 initial cases of the disease are saved each year by oral contraceptive^.'^ Mishell, in a review of health benefits of oral contraceptives, included decreased risk of iron deficiency anemia by 50%; decreased incidence of menorrhagia, irregular menses, and intermenstrual bleeds: a 50% decrease in the risk of endometrial cancer; reduction in various types of benign breast diseases; a decrease in the occurrence of ovarian cysts; decrease in premenstrual tension and dysmenorrhea; and a decrease in ovarian cancer, rheumatoid arthritis, and ~alpingitis.~" Scrimshaw heralds the social impact of oral contraceptives: freedom, and supreme confidence in the ability to postpone ~ r e g n a n c y . ~ '

January/February 1985 JOCNN

WHAT’S NEW

In 1982, Ortho Pharmaceutical Company introduced the biphasic pill, Ortho-Novum lO/llB. This combination pill contains 35 micrograms of ethinyl estradiol in each of the 21 pills. The first 10 pills contains 0.5 milligrams of progestogen (norethindrone) and the last 11 1.0 milligrams of the same. The theoretical basis, according to the manufacturer, is to emulate the normal ovarian cycle: estrogen domination in the first half and progesterone in the second.32.33In fact, this rationale is more myth than fact; the cycles are anovulatory and, therefore, cannot be compared with the complex ovarian-endometrial interaction of ovulating women. The manufacturer’s literature describes a lower incidence of breakthrough bleeding because the estrogen is relatively unopposed.33 In the same year, Wyeth introduced NordetteB to the U.S. market after a decade of use in other countries. Touted as an ultra lowdose pill, it contains 30 micrograms of ethinyl estradiol (comparable to other oral contraceptives) and 0.15 milligrams of levonorgestrel, a progestogen with a high progesterone potency. Wyeth states that this product produces minimal bleeding irregularities and cases of amenorrhea.32,34 A triphasic pill (TriphasilB) is now available in the United States; it is already marketed in Europe. The manufacturer is Wyeth and Schering. This pill contains varying amounts of estrogen and progestogen. The first six pills have 30 micrograms of ethinyl estrodiol and 0.05 milligrams of levonorgestrel; the next five contain 40 micrograms of ethinyl estrodiol and 0.075 milligrams of levonorgestrel; and the last 10 contain 30 micrograms of

January/February 1985 JOCNN

ethinyl estrodiol and 0.125 milligrams of levonorgestrel. Progressive increase in dose of progestin seems to reduce the incidence of breakthrough b l e e d i r ~ g . ~ ~ . ~ ~ Two triphasic oral contraceptives appeared on the market in 1984. The first, Ortho-Novum 7/7/ 7 8 , contains 35 micrograms of ethinyl estradiol in each pill; in the first seven, there are 0.5 milligrams of norethindrone, in the next seven, 0.75 milligrams, and in the last seven, 1.0 milligrams. Tri-NorinylB (Syntex) also has 35 micrograms of ethinyl estradiol in each pill; the first seven have 0.5 milligrams of norethindrone; the next nine, 1.0 milligrams, and the last five, 0.5 milligrams.

NURSING IMPLICATIONS

Unless the perfect contraceptive method is discovered tomorrow, practitioners will be working with many women using oral contraceptives for a long time to come. To that end, management strategies designed to provide for safe use, detection of risk, and prompt handling of problems a r e essential. Whereas data a r e far from absolute and conclusive, it is encouraging to realize that not all effects associated with oral contraceptive use aside from protection from pregnancy a r e negative. Nurses must continue to ponder questions confronting them as providers. Trends in birth control methods are changing. Nurses need to keep informed about oral contraceptives and estrogen/progestogen levels (Appendix A). Pill use is still very high, although sterilization is now the leading method used by women in the United States.’ Barrier methods are increasing in popularity. Safety versus convenience a s a trade-off is a real issue. Nurses must be involved in o r at least aware of

research on risk detection and reduction for oral contraceptives. SUMMARY

Until a contraceptive method that is cheap, 100% effective, reversible, easily available and accessible, easy to use, acceptable to clients and their partners, and without side effects and contraindications is developed, oral contraceptives are here to stay. Practitioners must remain current and present clients with unbiased information about all contraceptive options. Careful screening, evaluating the likelihood of proper use and motivation, educating clients in a way that encourages their questions, frequent monitoring, and seeking consultation when appropriate can minimize risks. Providers must avoid the temptation to prescribe “for clients.” Clients must make their own informed choice in collaboration with providers; they should feel supported in their right to choose. Providers must recognize that they can err by being overcautious as well as undercautious in prescribing oral contraceptives in an effort to reduce risk to the lowest possible level. REFERENCES 1. Ory HW, Forrest JW, Lincoln R. Making choices: evaluating the health risks and benefits of birth control methods. New York: The Alan Guttmacher Institute, 1983:lO. 2. Kols A, Reinhart W, Piotrow PT, Doucette L, Quillin WF. Oral contraceptives in the 1980s. Population Reports 1982;10(3):A189. 3. Stadel BV. Oral contraceptives and cardiovascular risk. New Engl J Med 1981;305:612-8. 4. Stadel BV. Oral contraceptives and cardiovascular risk. New Engl J Med 1981;305:672-8. 5. Miller KE, Pizzo SV. Venous and

arterial thromboembolic disease in women using oral contracep-

33

tives. Am J Obstet Gynecol 1982;144(7):24-7. 6. Knopp RH, Walden CE, Wahl PW, Hoover JJ. Effects of oral contraceptives on lipoprotein triglyceride and cholesterol: relationships to estrogen and progestin potency. Am J Obstet Gynecol 1982;142 (6)Part 2:725-31. 7. Wynn V, Niththyananthan R. The effect of progestins in combined oral contraceptives on serum lipids with special reference to highdensity lipoproteins. Am J Obstet Gynecol 1982;142:766-71. 8. Kay CR. Progestogens and arterial disease-Evidence from the Royal College of General Practitioners’ Study. ACOG 1982;142:762-5. 9. Plunkett ER. Contraceptive steroids, age, and the cardiovascular system. ACOG 1982;142:747-51. 10. Mann JI. Progestogens in cardiovascular disease: an introduction to the epidemiologic data. Am J Obstet Gynecol 1982;142(6)Part 2~752-7. 11. Spellacy WN. Carbohydrate metabolism during the treatment with estrogen, progestogen and lowdose oral contraceptives. Am J Obstet Gynecol 1983;142(6):Part 2:732-4. 12. Wynn V. Effect of duration of lowdose oral contraceptive administration on carbohydrate metabolism. Am J Obstet Gynecol 1982;142(6)Part 2:739-46. 13. Linn S, Schoenbaum SC, Monson RR, et al. Delay in conception for former “pill” users. JAMA 1982;247(5):629-32. 14. Vessey MP, Lawless M, McPherson K, Yeates D. Neoplasia of the cervix uteri and contraception: a possible adverse effect of the pill. Lancet 1983:2(8356):930-4. 15. Randall KJ. Oral contraceptives and cancer. Letters to the editor. Lancet 1983;2(8357): 1018. 16. Kay CR. Oral contraceptives and cancer. Letters to the editor. Lancet 1983;2(8357): 1018. 17. Pike MC, Henderson BE, Krailo MD, Duke A. Breast cancer in young women and use of oral con-

34

traceptives: possible modifying effect of information and age at use. Lancet 1983;2(8356):926-9. 18. Sondheimer S. Contraception. Unpublished speech given at the 8th Annual Post-Graduate Seminar Nurse Practitioner in Family Planning. Philadelphia, February 8, 1984. 19. Goldzieher JW, Dozier TS, d e la Pena A. Plasma levels and pharmacokinetics of ethinyl estrogens in various populations. 1. Ethinylestradiol. Contraception 1980; 21:1-16. 20. Goldzieher JW, Dozier TS, d e la Pena A. Plasma levels and pharmacokinetics of ethinyl estrogens in various populations. 11. Mestranol. Contraception 1980;21: 17-27. 21. Stadel BV, Sternthal PM, Schlesselman JJ. Variation of ethinylestradiol blood levels among healthy women using oral contraceptives. Fertil Steril 1980;33: 257-60. 22. Stubblefield PG. Editorial JOGN News 1983;12:7. 23. Rosenberg L, Shapiro S, Slone D, et al. Epithelial ovarian cancer and combination oral contraceptives. JAMA 1982;247:3210-2. 24. Cramer DW, Hutchison GB, Welch WR, et al. Factors affecting the association of oral contraceptives and ovarian cancer. New Engl J Med 1982;307( 17):1047-51. 25. Hulka BS, Chambless LE, Kaufman DG, et al. Protection against endometrial carcinoma by combination-product oral contraceptives. JAMA 1982;247:475-7. 26. OCs protect against endometrial cancer, study shows. Contraceptive Technology Update 1982;3(3): 29-30. 27. Ory HW, Layde PM, Webster LA, Wingo PA. Long-term oral contraceptive use and the risk of breast cancer. Presented at the 31st Annual Epidemic Intelligence Service (EIS) Conference, Atlanta, Georgia, April 19-23, 1982. 28. Burkman RT. The women’s health study. Association between intra-

29.

30.

31.

32. 33.

34. 35.

36.

uterine device and pelvic inflammatory disease. Obstet Gynecol 1981;57:269-76. Rubin GL, Ory HW, Layde PM. Oral contraceptives and pelvic inflammatory disease. Am J Obstet Gynecol 1982;144(6):630-5. Mishell DR. Noncontraceptive health benefits of oral steroidal contraceptives. Am J Obstet Gynecol 1982;142(6)Part 2:809- 16. Scrimshaw SCM. Women and the pill: from panacea to catalyst. Fam Plann Perspect 1981;13(6):254-6, 260-2. Bartosch JC. Oral contraception: selection and management. Nurse Prac 1983;8:56, 58, 60, 62-3, 79. Ortho-Novum 10/11 Tablets. Manufacturer’s literature. Raritan, New Jersey: Ortho Pharmaceutical Corporation, 1982. NordetteB-28 Tablets. Package insert. Philadelphia: Wyeth Laboratories, Inc., 1982. Upton GV. The normal menstrual cycle and oral contraceptives: the physiological basis for a triphasic approach. In: Greenblatt RB, ed. The development of a new triphasic oral contraceptive. Proceedings of a special symposium held at the 10th World Congress of Fertility and Sterility. Lancaster, England: MTP Press, Ltd., 1980. Kols A, Rinehart W, Piotrow PT, et al. Oral contraceptives in the 1980s. Population Reports 1982; 10(3):A189-A224.

Address for correspondence: Joellen W. Hawkins, RNC, PhD, 151 Stanton Ave, Newton, MA 02166.

Roberta Orne is an assistant professor in the School of Nursing at the University of Connecticut in Storrs. Ms. Orne is a member of NAACOG, Sigma Theta Tau, and ANA. Joellen Hawkins is a professor at Boston College School of Nursing in Chestnut Hill, Massachusetts. Dr. Hawkins is a member of NAACOG, Sigma Theta Tau, and ANA.

January/February 1985 JOCNN

Appendix A. Oral Contraceptives: Formula and Dosage

Progestogen Content (rng)

Brevicon-21 Brevicon-28 Demulen 1/35-21 & 28 Dernulen-21 Demulen-28 Enovid 5 Enovid E Loestrin 1/20 Loestrin 1 5/30 Lo/Ovral Lo/OvraC28 Modicon-21 Modicon-28 Nordette 21 & 28 Norinyl 2 rng Norinyl 1 50/21 Norinyl 1 50/28 Norinyl 1 80/21 Norinyl 1 80/28 Norinyl 2 Norlestrin 2 5/50-21 Norlestrin 2 5/50-FE Norlestrin 1/50-21 Norlestrin 1/50-28 Norlestrin 1/50-FE Ortho-Novurn 1/35/28 Ortho-Novurn 1/35/ 21 Ortho-Novurn 2 rng Ortho-Novurn 10 rng Ortho-Novurn 10/11/ 21 white tablets peach tablets Ortho-Novurn 10/11/ 28 white tablets peach tablets Ortho-Novurn 1/50-21 Ortho-Novum 1/50-28 Ortho-Novurn 1/80-21 Ortho-Novurn 1/80-28 Ovcon-35 Ovcon-50 Ovral Ovral-28 Ovulen 21 Ovulen 28 ' MINI" Micronor Nor-Q-D

Estrogen Content (rncg)

0.5 0.5

35 35 35 50 50

1.o 1.o 1.o 5.0 2.5

+ + + +

75 100 1.o 1.5

20 30 30 30 35 35 30

0.3 0.3 0.5 0.5 0.1 5 2.0 1.o 1 .o 1.o 1.o 2.0

100 50 50

80 80 100 2.5 2.5 1.o 1.o 1.o

50 50 50 50 50 35

1.o

1.o 2.0 19.0

35 100 60

0.5 1.o

21 21 21 21 21 20 21 21 21 21 21 21 21 21 20 21 21 21 21 21 21 21 21 21 21 21

7 Inert 7 Inert

7 Inert

7 Iron 7 Iron 7 Inert 7 Inert 7 Inert

7 Inert 7 Inert

7 Iron 7 Inert 7 Iron 7 Inert

21 21 20

35

0.5 1.o 1.o 1 .o 1 .o 1.o 0.4 1.o

35 50 50

80 80 35 50 50 50

0.5 0.5 1.o 1.o

100 100

7 Inert

21 21 21 21 21 21 21 21 21 21

7 Inert 7 inert 7 Inert 7 Inert 7 Inert

7 Inert

.35

.35 (Continued)

January/February 1985 JOCNN

35

Appendix A (Continued)

Progestogen Content (mg)

Estrogen Content (mcg)

075

Ovrette Triphasil

0 050 (6) 0 075 (5) 0 125 (10)

Ortho-Novum 7 7/7/21

30 40 30 35

0 5 (7) 0 75 (7) 1 0 (7) Tri Norinyl 21 0 5 (7) 35 1 0 (9) 28 0 5 (5) Adapted from Erickson A, ed Pharmacy newsletter Boston Boston Hospital for Women 1977 2 Gyn Family Planning Nurse Practitioners A manual of standard practice procedures and policies Storrs, CT University of Connecticut Women s Health Clinic, 1980 Hatcher RA, et a/ Contraceptive technology 1980-1981 10th ed New York Irvington, 1980, 24, 25, 27, 28 Ory HW, Forrest JD Lincoln R Making choices New York Guttrnacher Institute, 1983 64-5 Adapted from and used with permission Hawkins JM, Higgins LP Health care of women gynecological assessment Monterey, CA Wadsworth, 1982 28

I

7 Inert

7 Inert

" -

1 1 1

Certification Program for Childbirth Educators Atlanta Mar. 18-20

Los A n g e l e s

A c o m p r e h e n s i v e professional development seminar l e a d i n g tc Certification a s a Childbirth Educator in Family C e n t e r e d Childbirth P r e p a r a t i o n a n d Psychoprophylaxis.

Apr. 1-3 N o r w i c h , Ct. Apr. 15-17 Seattle J u n e 24-26

Burlington, Vt. J u l y 17-19

In addition, on-site programs are a v a i l a b l e for hospital sponsorship. Details a v a i l a b l e from Registrar.

*

4

Major teaching hospitals, community hospitals a n d childbirth education groups have discovered the advantages of sponsoring on-site certification seminars. The Council of Childbirth Education Specialists will conduct a program for your staff nurses a n d other area nurses. We would be pleased to send you details.

W a s h i n g t o n DC AUg. 12-14 T a r r y t o w n , NY S e p t . 9-11 Den v er OCt. 16-18

Council of

ChilCbirth Education Specialists Write: REGISTRAR,P a t r i c i a H a s s i d , RN 168 W. 86 S t r e e t N.Y., N.Y.10024 January/February 1985 JOGNN