Editorials - November 15, 2000 - American Family Physician

Editorials

Informed Consent and Emergency Contraception

ALAN L. MCGAUGHRAN, M.D.
Blairsville Family Health Center,
Blairsville, Pennsylvania

See article on page 2287.

Informed consent is a crucial concept connected with the prescription of any medical therapy. When it comes to the practice of emergency postcoital contraception, discussions about the expected outcomes, the potential side effects and the possible mechanisms of action are essential for patients to make an informed decision about its use. Without accurate information presented before prescribing, patients may experience emotional distress from an unanticipated result, an unforeseen side effect or the later discovery of a mechanism of action that is in conflict with their value system.

Discussion with patients about expected results should include the risk of pregnancy at the current stage of their menstrual cycle and the reduction of that risk. The likelihood of pregnancy with treatment is implied when discussing the topic of risk reduction. In an article in this issue of American Family Physician, Wertheimer¹ cites a pregnancy rate of 8 percent as a result of intercourse in the second or third week of the menstrual cycle. The risk reduction rate after emergency contraception treatment is approximately 75 percent; that is, the pregnancy rate is reduced from 8 percent to 2 percent. The number needed to treat (NNT) is a valuable concept to use in patient communications. With approximately 6 percent of treated women achieving an antigestational effect, the NNT means that 17 women would need to be treated to prevent one ensuing pregnancy. Likewise, one in 50 treated women can expect pregnancy despite treatment.

Wertheimer¹ mentions that the most common side effects of emergency contraception are nausea and vomiting. Mastalgia, fatigue and dizziness are also noted as adverse reactions.^2,3 Delayed onset of menstruation is more likely with mifepristone treatment.⁴ Headache is the symptom most commonly reported either with estrogen plus progestin treatment or with mifepristone alone.⁴ Pelvic infection is a risk with insertion of an intrauterine device (IUD). Discussion of these reactions constitutes a part of informed consent.

How these methods exert their antigestational effect is not known with certainty. Several mechanisms of action have been proposed for the various agents used to prevent the possible progression to fertilization and pregnancy after intercourse.² These mechanisms are summarized by Wertheimer.¹ Some of these proposed mechanisms involve effects that make fertilization less likely, such as inhibition of ovulation and toxicity to sperm. Others involve effects after fertilization, like reduction in progesterone secretion in the corpus luteum and inhibition of implantation. Effects on fallopian tube transport may occur before or after fertilization.

I would like to comment on the evidence for postfertilization effects. With regard to the corpus luteum, estrogen combined with progestin or high-dose estrogen can lower progesterone levels during the luteal phase. Whether the levels decrease to the point at which pregnancy is not sustained is not yet known. Mifepristone "induces regression of the corpus luteum in about 50 percent of women."² IUD insertion or mifepristone administration following ovulation may cause endometrial changes that could impede implantation of the conceptus in the endometrium.

Glasier² suggests that the changes noted in the endometrium after postovulatory use of high-dose estrogen or estrogen plus progestin "may not be sufficient to inhibit implantation." She also notes, however, that "the postovulatory administration of estrogen or levonorgestrel inhibits implantation in some animals."² Additionally, high doses of postcoital estrogen may lead to an "increased incidence of ectopic pregnancy."² This observation implies that some effect occurs after fertilization, because prefertilization mechanisms would be expected to correspond with an equal decrease in both tubal and intrauterine pregnancy rates. A proportionately increased rate of tubal pregnancy would be explained by decreased tubal motility or by inhibition of intrauterine implantation, or both.

Another observation relates to postfertilization action. As previously noted, postcoital use of mifepristone often causes a delay in the subsequent menstrual period, which is indicative of its suppression of ovulation.⁴ A delay was much less likely with high-dose estrogen and progestin (13 percent versus 42 percent). This effect would suggest that inhibition of ovulation is less a factor with the estrogen-progestin combination and that other mechanisms of action (e.g., postfertilization effects) are more responsible for the results of these particular agents. The evidence is certainly indicative of postfertilization effects at least some of the time.

For those who believe that human life begins with fertilization, these postfertilization effects are certainly of concern. The case has already been made--in detail--that adequate informed consent for users of oral contraceptives includes discussion of their postfertilization effects.⁵ Likewise, information about the antigestational effects after fertilization should be part of the information that is given to any patient who is considering the option of postcoital contraception. Patients will then be able to make informed choices that align with their values.

Attention should also be paid to the language used in such discussions with patients. The terms "conception," "contraception," "abortion" and "beginning of pregnancy" may have different meanings to patients compared with the definitions that have evolved in medical practice. "Conception" in current medical usage is sometimes used as a synonym for fertilization. However, more often it is used to indicate implantation. This trend is not necessarily reflected in the general public's usage and understanding of this term.

Many lay persons would consider the terms "conception" and "fertilization" to be synonymous. For many lay persons, "contraception" would be thought of as something that prevented fertilization; abortion would refer to any interruption after fertilization; and the beginning of pregnancy would be at fertilization. Wertheimer¹ acknowledges this in the statement, "Some individuals may consider these hormones to be abortifacients if they interfere with implantation." Effective and truthful communication with our patients depends on language that is mutually understood. Such communication is necessary for informed consent and is one of the foundations of quality medical practice.

REFERENCES

Wertheimer RE. Emergency postcoital contraception. Am Fam Physician 2000;62:2287-92.

Glasier A. Emergency postcoital contraception. N Engl J Med 1997;337:1058-64.

Wellbery C. Emergency contraception. Arch Fam Med 2000;9:642-6.

Glasier A, Thong KJ, Dewar M, Mackie M, Baird DT. Mifepristrone (RU 486) compared with high-dose estrogen and progestogen for emergency postcoital contraception. N Engl J Med 1992;327: 1041-4.

Larimore WL, Stanford JB. Postfertilization effects of oral contraceptives and their relationship to informed consent. Arch Fam Med 2000;9:126-33.

Dr. McGaughran is a faculty member of the Latrobe Area Hospital Family Practice Residency, Latrobe, Pa.

Address correspondence to Alan McGaughran, M.D., Blairsville Family Health Center (associated with Latrobe Area Hospital), 56 Club Lane, Blairsville, PA 15717.

Emergency Contraception: Still Not Too Late

CAROLINE WELLBERY, M.D.
Georgetown University School of Medicine
Washington, D.C.

See article on page 2287.

Emergency contraception is an effective, if underused, means of preventing pregnancy when unprotected intercourse has occurred. Why should physicians know about emergency contraception? Unwanted pregnancies exact a high price emotionally and economically.¹ Inconsistent use of contraceptives, contraceptive accidents and sexual assault are all situations one wishes would never occur, but do. Emergency contraception offers a cost-effective chance to intervene in response to such unanticipated exposures. A major public health advantage of emergency contraception is that its appropriate use decreases reliance on abortion: it is estimated that emergency contraception would prevent one half of all unintended pregnancies, another one half of which would have ended in abortion.²

The underuse of emergency contraception may be related to a lack of marketing. Although the most common type of emergency contraception is nothing more than oral contraceptives given in high doses, manufacturers cannot promote their products for emergency use without specific labeling by the U.S. Food and Drug Administration (FDA). Now that there are two FDA-labeled, dedicated products, Preven (an emergency contraception kit with levonorgestrel 0.25 mg/ethinyl estradiol 50 µg [4 tablets]) and Plan B (levonorgestrel 0.75 mg [two tablets]), it is possible that physician and public awareness of emergency contraception will increase. Plan B appears to be even more effective than the Yuzpe regimen (the combined estrogen-progestin approach) and is significantly better tolerated.³Change occurs slowly, however, and the politics of contraception may force the discussion and distribution of emergency contraception to maintain a low public profile. Preven and Plan B may not be universally available in pharmacies for some time.

Easy access to postcoital contraception is important because the first dose of emergency hormone must be taken within 72 hours after unprotected intercourse. Studies have shown that emergency contraception can be self-administered. In one study,⁴ women who used emergency contraception at home were more likely to use it than those who had received instructions about it but had to call a physician to obtain it. During the 12-month study period, the treatment group did not use emergency contraception more than once, suggesting that it was used appropriately--as an emergency measure, not as the sole method of contraception.

Physicians should do their part to ensure knowledge and to facilitate access to emergency contraception. Ideally, emergency contraception should be available without a prescription. In a pilot program in Washington state, women could obtain emergency contraception directly from pharmacists. During its implementation, almost 12,000 prescriptions were filled (personal communication, Kristin Marciante, March 15, 2000).

Although more like programs may be established in the future, what can physicians tell their patients in the meantime? First, physicians should incorporate education about emergency contraception into routine office visits--advising all patients of reproductive age about the available options, offering patients a prescription or a ready-made packet from the office so that they will have emergency contraception available if they need it.

Physicians can create emergency contraception packets by using the options listed in Table 2 of the accompanying article.⁵Preven and Plan B can be obtained through federally funded clinics and college health centers and can also be ordered from a drug distribution house or over the telephone by qualified providers (to obtain Plan B, telephone 800-330-1271 or fax 877-407-3801).

An excellent Web site (http://ec.princeton.edu/) is available, and there is also an information line that will answer questions from physicians and patients (888-NOT-2-LATE). Emergency contraception is not an effective method of ongoing birth control. However, when used as indicated, it may prevent unintended pregnancies and reduce the number of abortions.

REFERENCES

Trussell J, Ellertson C, Stewart F, Koenig J, Raymond EG, Shochet T. Emergency contraception: a cost-effective approach to preventing unintended pregnancy. Women's Health Prim Care 1998;1:55-69.

Henshaw SK. Unintended pregnancy in the United States. Family Plann Perspect 1998;30:24-9,46.

Task Force on Postovulatory Methods of Fertility Regulation. Randomised controlled trial of levonorgestrel versus the Yuzpe regimen of combined oral contraceptives for emergency contraception. Lancet 1998;352:428-33.

Glasier A, Baird D. The effects of self-administering emergency contraception. N Engl J Med 1998; 339:1-4.

Wertheimer RE. Emergency postcoital contraception. Am Fam Physician 2000;62:2287-92.

Dr. Wellbery is an assistant professor in the Department of Family Medicine at Georgetown University School of Medicine, Washington, D.C. She is also assistant deputy editor of American Family Physician.

Address correspondence to Caroline Wellbery, M.D., 3800 Reservoir Rd., NW, 212 Kober-Cogan, Georgetown University, Washington, DC 20007.

Acute Venous Thromboembolism: Diagnostic Guidelines

VICTOR TAPSON, M.D.
Duke University Medical Center
Durham, North Carolina

The diagnostic difficulty associated with acute venous thromboembolism (i.e., deep venous thrombosis, pulmonary embolism, or both) is underscored by the frequency with which patients die before the diagnosis is made.¹ Pulmonary embolism (PE) occurs in hundreds of thousands of patients in the United States each year and frequently occurs in patients with cancer, chronic cardiopulmonary disease or trauma, or in postoperative patients, particularly those who are nonambulatory. Multiple risk factors involving venous stasis, thrombophilia and venous injury (Virchow's triad) significantly increase the risk of acute venous thromboembolism.

Patients may present with PE (even massive PE) without any antecedent symptoms or signs of deep venous thrombosis (DVT), even though the vast majority of cases of acute PE result from DVT in the proximal veins of the lower extremities (above the knee). Unfortunately, the symptoms and signs associated with DVT and with PE are nonspecific. Thus, a high index of suspicion is crucial for patients who are deemed to be at risk. Because of the magnitude of this problem and the varying diagnostic approaches available, the American Thoracic Society (ATS) developed a consensus statement to outline appropriate strategies to consider in patients with suspected DVT and PE. Importantly, the medical literature was reviewed and an evidence-based approach was devised,² with recommendations made based on available data.

In September 1999, the ATS Consensus Statement and Clinical Practice Guidelines were published.³ Although the guidelines were developed by the ATS, the majority of patients with suspected DVT and PE do not initially present to pulmonologists but instead visit other subspecialists, emergency department physicians, surgeons, internists and family physicians. Thus, it would appear prudent to briefly outline some important issues regarding management of acute venous thromboembolism.

The diagnostic approach to DVT and PE requires careful attention to the presence of risk factors. Although a patient who develops shortness of breath during bedrest for a hip fracture might have aspiration pneumonia, a flare of obstructive lung disease or atelectasis causing dyspnea, PE should always be included in the differential diagnosis. Even when a patient is admitted to the hospital with community-acquired pneumonia, congestive heart failure or emphysema, the development of worsening dyspnea always merits consideration of PE despite another strong explanation for the symptoms. The presence of symptoms such as leg pain or swelling, dyspnea, chest pain, syncope or hemoptysis, particularly in the setting of risk factors for DVT, should always lead to suspicion of DVT and PE.

What should be the initial diagnostic approach to patients with suspected DVT? In most hospitals in the United States and Europe, compression ultrasound (often with Doppler and color-flow) is the most common initial approach. The sensitivity and specificity of this test are over 95 percent for identifying DVT of the proximal leg vein. For DVT of the calf, however, the test is less reliable. The use of contrast venography or, in centers with experienced staff, magnetic resonance imaging (MRI) is appropriate when clinical suspicion of DVT remains high but the ultrasound is negative or nondiagnostic.

At the present time, the standard approach to patients with suspected acute PE should include a history, physical examination, arterial blood gas analysis, chest radiography and electrocardiography. The chest radiography and electrocardiography may be useful in proving alternative diagnoses but rarely are diagnostic of PE. Unexplained hypoxemia may suggest PE but is neither sensitive nor specific for the diagnosis.

The ventilation perfusion (V/Q) scan has long been the diagnostic cornerstone. However, this technique is usually not definitively negative or positive and, generally, additional testing is indicated. Even when PE is ultimately proved by pulmonary angiography (the gold standard), the V/Q scan is commonly nondiagnostic.⁴ The V/Q scan is useful, however, when results are normal (proving the absence of PE) or high probability (proving PE except under unusual circumstances).

Contrast-enhanced spiral computed tomography (CT) with a contrast bolus is becoming increasingly used for the diagnosis of suspected PE.^5,6 This technique appears useful for PE that occurs in the main, interlobar and segmental pulmonary arterial branches but is less sensitive and specific for clots occurring in subsegmental branches. Reader expertise is crucial, but the technology is improving and further clinical trials appear to be forthcoming.⁷

Caution is recommended with interpretation of CT studies, and the threshold for pulmonary arteriography should be low. The quality of the CT images must be optimal. Some experts, however, are still reluctant to rely on CT in the absence of additional clinical research trials.⁸ When the diagnosis is uncertain after chest CT or a V/Q scan, or both, evaluation of the lower extremities appears to be a useful option.⁹ If DVT is present, the treatment is generally the same as if PE is diagnosed.

Finally, the D-dimer, a product of cross-linked fibrin degradation, has been evaluated increasingly in diagnosis of suspected DVT and PE and appears promising.¹⁰ Although the enzyme-linked immunosorbent assay (ELISA) D-dimer test has appeared to be sensitive for venous thromboembolism in several clinical trials, none of the available assays are specific for the diagnosis. Positive tests are common and therefore not helpful, particularly in persons with cancer, infections or inflammatory disease states. The development of more rapid bedside D-dimer assays, especially used in combination with other diagnostic tests, may prove useful, but the wide variability among the assays continues to limit their diagnostic utility.

Venous thromboembolism results in a substantial number of what appear to be potentially unnecessary deaths. Our increasingly sophisticated diagnostic repertoire, together with carefully designed clinical trials and interpretation of the available data in the form of clinical guidelines, should enhance our diagnostic yield of DVT and PE. Nonetheless, clinical suspicion remains an absolutely essential component of the diagnostic approach.

REFERENCES

Goldhaber SZ, Hennekens CH, Evans DA, Newton EC, Godleski JJ. Factors associated with correct antemortem diagnosis of major pulmonary embolism. Am J Med 1982 Dec;73(6):822-6.

Evidence-based medicine. A new approach to teaching the practice of medicine. Evidence-Based Medicine Working Group. JAMA 1992;268(17): 2420-5.

Tapson VF, Carroll BA, Davidson BL, Elliott CG, Fedullo PF, Hales CA, et al. The diagnostic approach to acute venous thromboembolism. Clinical practice guideline. American Thoracic Society. Am J Respir Crit Care Med 1999;160(3):1043-66.

Value of the ventilation/perfusion scan in acute pulmonary embolism. Results of the prospective investigation of pulmonary embolism diagnosis (PIOPED). The PIOPED Investigators. JAMA 1990; 263(20):2753-9.

Mayo JR, Remy-Jardin M, Muller NL, Remy J, Worsley DF, Hossein-Foucher C, et al. Pulmonary embolism: prospective comparison of spiral CT with ventilation-perfusion scintigraphy. Radiology 1997;205(2):447-52.

Tapson VF. Pulmonary embolism--new diagnostic approaches. N Engl J Med 1997;336(20):1449-51.

Remy-Jardin M, Remy J, Artaud D, Deschildre F, Duhamel A. Peripheral pulmonary arteries: optimization of the spiral CT acquisition protocol. Radiology 1997;204(1):157-63.

Drucker EA, Rivitz SM, Shepard JA, Boiselle PM, Trotman-Dickenson B, Welch TJ, et al. Acute pulmonary embolism: assessment of helical CT for diagnosis. Radiology 1998;209(1):235-41.

Hull RD, Raskob GE, Ginsberg JS, Panju AA, Brill-Edwards P, Coates G, et al. A noninvasive strategy for the treatment of patients with suspected pulmonary embolism. Arch Intern Med 1994;154(3): 289-97.

Perrier A, Bounameaux H, Morabia A, de Moerloose P, Slosman D, Didier D, et al. Diagnosis of pulmonary embolism by a decision analysis-based strategy including clinical probability, D-dimer levels, and ultrasonography: a management study. Arch Intern Med 1996;156(5):531-6.

Dr. Tapson is the director of the Duke Pulmonary Outpatient Clinic and medical director of the Duke University Medical Center Lung Transplant Program at Duke University Medical Center, Durham, N.C.

Address correspondence to Victor Tapson, M.D., Division of Pulmonary and Critical Care, Box 31175, Duke University Medical Center, Durham NC 27710.

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