The New England Journal of Medicine

Correspondence

The Health Care Costs of Smoking

To the Editor: The conclusion by Barendregt et al. (Oct. 9 issue)1 that smoking cessation would eventually lead to increased health care costs is questionable because the authors underestimate differences in health care use between smokers and nonsmokers. They attribute to smoking the leading smoking-related diseases, including heart disease, stroke, lung and some other cancers, and chronic obstructive pulmonary disease. According to the Surgeon Generals reports, smokers are also at higher risk for a variety of other diseases, including pneumonia and influenza, abdominal aortic aneurysm, gastric and duodenal ulcers, and cataracts. Adding these conditions increases by more than 30 percent the estimate of short-term hospital days for diseases linked to smoking.2 Smokers also have higher utilization rates and expenditures for coexisting diseases not related to smoking. Coexisting disorders increase the resources required to treat many smoking-related conditions; hospital stays are longer, more tests and procedures may be required, and so forth. The authors report that per capita health care costs are up to 40 percent higher among male smokers and up to 25 percent higher among female smokers, as compared with nonsmokers. However, in the United States, peak differences in costs between smokers and nonsmokers can be more than 100 percent for men and almost 70 percent for women.3 Limiting the calculation of smoking-related costs to the diseases noted in the article omits substantial mor-

bidity and health care utilization and severely underestimates the lifetime medical expenditures associated with smoking. The authors emphasize the results at lower discount rates that support the conclusion that a nonsmoking population would eventually have higher health care costs. But their sensitivity analysis of the discount rate renders this conclusion ambiguous, since they calculate lower costs for nonsmoking at discount rates of 4.5 percent and higher. Barendregt et al. reject discounting, however, citing differences of opinion on discounting lifetime costs. There is controversy about discounting health effects such as years of life gained, but not about discounting monetary sums. Discounting future monetary values is universally accepted by economists. Furthermore, given the underestimates in the authors analysis, it is likely that the costs for the nonsmoking population are also lower at the lower discount rates, including the range of 3 to 5 percent generally accepted as most likely to include the social discount rate. Three studies cited by the authors each calculated higher lifetime costs for smokers in the United States. But the authors offer no explanation for the difference between their results and these findings. THOMAS A. HODGSON, PH.D.
Centers for Disease Control and Prevention Hyattsville, MD 20782
1. Barendregt JJ, Bonneux L, van der Maas PJ. The health care costs of smoking. N Engl J Med 1997;337:1052-7. 2. National Center for Health Statistics, Graves EJ, Gillum BS. Detailed diagnoses and procedures, National Hospital Discharge Survey, 1994. Vital and health statistics. Series 13. No. 127. Washington, D.C.: Government Printing Office, 1997. (DHHS publication no. (PHS) 97-1788.) 3. Hodgson TA. Cigarette smoking and lifetime medical expenditures. Milbank Q 1992;70(1):81-125.

To the Editor: Barendregt et al. estimate that the difference in life expectancy from birth between smokers and

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nonsmokers is 7.3 years for men and 6.0 years for women. These estimates were apparently calculated from rate ratios for five categories of tobacco-related diseases, without consideration of competing risks and with the use of fixed rates for all ages. It is of course common for smokers to have more than one of these diseases, and rate ratios should be expected to decrease at older ages as competing risks increase, as should differences in life expectancy with advanced ages. Although sensitivity ranges are given, no analyses of the effects of assuming the lower bounds are provided. The article cited as reporting similar mortality differences,1 and much of the other literature, compares male continuing cigarette smokers with lifelong nonsmokers, without adjustment for confounding risk factors (smokers have more stress, use more alcohol, exercise less, have higher dietary fat intake, and use seat belts less than nonsmokers). Furthermore, an intention-to-treat analysis in 1951 would have included the 50 percent of smokers who subsequently stopped smoking and who had mortality rates similar to those for lifelong nonsmokers. In addition, these differences in mortality rates should narrow at higher ages because of competing risks and in more recent cohorts because of a generally longer life expectancy from birth. The results reported are extremely sensitive to changes in assumptions about mortality rates. Small reductions in mortality rates can make enormous differences in longterm projections, increasing and perpetuating the initial cost savings. JAMES F. FRIES, M.D.
Stanford University School of Medicine Palo Alto, CA 94304-1808
1. Doll R, Peto R, Wheatley K, Gray R, Sutherland I. Mortality in relation to smoking: 40 years observations on male British doctors. BMJ 1994; 309:901-11.

1. Office of Population Census Surveys. General household survey 1994. London: Her Majestys Stationery Office, 1994. 2. Drummond MF, Stoddart GL, Torrance GW. Methods for the economic evaluation of health care programmes. Oxford, England: Oxford University Press, 1987. 3. Taylor TN, Davis PH, Torner JC, Holmes J, Meyer JW, Jacobson MF. Lifetime cost of stroke in the United States. Stroke 1996;27:1459-66.

To the Editor: . . . The study by Barendregt et al. does not account for the possibility that exsmokers, who are presumably included in the population of nonsmokers, have a greater proportion of morbidity and mortality than those who have never regularly smoked. In the United Kingdom, over half of persons over 60 years old previously smoked regularly.1 Sophisticated incidence-based data sets are necessary to establish the true health care costs incurred by smoking. Health care economists accept that prevalence-based costof-illness studies give little insight into expected lifetime costs and that incidence-based studies are theoretically superior.2 If the data in this study are recalculated with the usual discount rate for time preference of 5 percent and with the incorporation of additional smoking-related costs, such as the lifetime costs of care after a stroke,3 it is unlikely that the break-even year after smoking cessation would ever occur. It is reasonable to assume that growing old gracefully without smoking-related morbidity is likely to result in a lesser burden on health care systems. DOMINIC HEANEY, B.M., B.CH.
National Hospital for Neurology and Neurosurgery London WC1N 3BG, United Kingdom

To the Editor: Contrary to what Barendregt et al. suggest, any smoking-related disease that generates substantial health care costs in excess of health care cost savings from premature death could change their results, though perhaps not their overall conclusions. For example, the results shown in Figure 2 of their article could change if the costs of pediatric disease from parental smoking were included. The $4.6 billion per year in U.S. health care costs for such disease is almost three times as much as the $1.7 billion in undiscounted health care cost savings from the deaths (6200 deaths of children [mostly infants] each year from parental smoking,1 times $3,600 per year in per capita health care costs, times 75 years of life lost [U.S. life expectancy] 2). In addition, the authors results could change if the health care costs among adult nonsmokers for generally nonfatal asthma exacerbations from secondhand smoke and burn and blast injuries from others careless smoking 3 exceeded the health care cost savings from premature death. The authors results could also change if the health care costs for expensive, nonfatal smoking-related injuries (e.g., back strains and orthopedic injuries)3,4 were included. Such injuries may account for a substantial portion of the 12 percent of U.S. health care costs that are due to injuries.2 The total health care costs associated with smoking include the costs of disease in children due to parental smoking, nonfatal smoking-related injuries and cataracts in smokers, and the often nonfatal secondhand effects of others smoking in nonsmoking adults. These factors, especially in combination with the use of a discount rate, reduce the likelihood that excess health care costs due to smoking cessation will be seen in our lifetimes, or ever. BRUCE N. LEISTIKOW, M.D.
University of California Davis, CA 95616

TED R. MILLER, PH.D.

National Public Services Research Institute Landover, MD 20785
1. Aligne CA, Stoddard JJ. Tobacco and children: an economic evaluation of the medical effects of parental smoking. Arch Pediatr Adolesc Med 1997;151:648-53. 2. Fingerhut LA, Warner M. Injury chartbook, health, United States, 19961997. Hyattsville, Md.: National Center for Health Statistics, 1997. 3. Leistikow BN. Injury prevention. N Engl J Med 1998;338:133. 4. Kwiatkowski TC, Hanley EN Jr, Ramp WK. Cigarette smoking and its orthopedic consequences. Am J Orthop 1996;25:590-7.

To the Editor: The calculations of the health care costs of smoking reported by Barendregt et al. may be interesting, but their conclusion that eventually, smoking cessation would lead to increased health care costs is mislead-

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ing and dangerous. The authors infer that continued smoking would reduce the health care costs in the long run and nonsmokers are therefore, in the long run, health carecost producers. The authors, however, do not take into consideration the years lost through smoking-related morbidity and mortality. The productivity to stay strictly within the context of the authors economic terms of a human being during these lost years certainly outweighs by far the health care costs associated with later years in life. . . . CHRISTIAN SAUTER, M.D.
University Hospital CH-8091 Zurich, Switzerland

The authors reply: To the Editor: Hodgson correctly points out that there are more smoking-related diseases than the major ones we included, but additional diseases would change our conclusions only if they posed a clear excess risk for smokers, accounted for large costs, and had a low associated risk of mortality. We can think of no such diseases. Four of the five diseases Hodgson mentions have high mortality rates, and we discussed cataracts. Hodgson finds much higher differences in per capita costs. The cited 100 percent and 70 percent higher costs for male and female smokers, respectively, however, are in just one age group. The differences in the other age groups are more in line with our results, and the differences are even much smaller for the elderly.1 We do not reject discounting. Discounting involves the evaluation of future resources as part of a decision about which of two or more alternative choices is preferred. Hodgson ignores the distinction we make between the estimation of population costs for smokers and nonsmokers and the evaluation of an intervention. In the former case, we reject discounting because when estimating costs, we are not evaluating which of the alternatives we prefer. Moreover, in the stationary-population interpretation of the life table, there is no time hence, no future. The application of discounting to the life-table results lowers costs incurred at higher ages, not at a future moment in time, and may very well explain the different results of other studies, because nonsmokers are older on average. When evaluating an intervention, we do discount and show that the intervention can be economically attractive because savings precede the eventually higher costs. We can assure Fries that in our analysis competing risks are taken into account and that the differences in mortality between smokers and nonsmokers do narrow at a higher age: the age-independent rate ratios are based on disease incidence, not on mortality. Because of the nonlinear relation between incidence and mortality, the rate ratios for disease-specific mortality decline with age, and so do the rate ratios for total mortality: for men, from 2.5 at 65 years to 1.6 at 90 years, and for women, from 2.2 to 1.6; with the lower bounds, the rate ratios are 1.9 to 1.4 for men and 1.7 to 1.4 for women, with a difference in life expectancy of 5.2 and 4.1 years, respectively. Heaney is correct that a large proportion of current nonsmokers are in fact former smokers. The problem plagues epidemiologic studies; rate ratios will be biased

when not measured for smokers as compared with persons who have never smoked. We ignored this problem on the grounds that the bias will be well within the sensitivity range of the rate ratios. Whether incidence-based studies are superior depends on the purpose of the study. When estimating population costs for smokers and nonsmokers, population-based prevalence data are perfectly adequate. Leistikow and Miller rightly mention the costs due to smoking among nonsmokers in particular, children. However, including these costs would not change our conclusions. The total costs for lung diseases among persons from infancy to 19 years of age, for example, account for less than 1 percent of all costs among men and just over 0.5 percent of costs among women. Sauter points to the costs of lost productivity. Like some other financial differences between smokers and nonsmokers, such as pensions and tobacco taxes, these are not health care costs and are therefore outside the scope of our article. JAN J. BARENDREGT, M.A. LUC BONNEUX, M.D. PAUL J. VAN DER MAAS, PH.D.
Erasmus University 3000 DR Rotterdam, the Netherlands
1. Hodgson TA. Cigarette smoking and lifetime medical expenditures. Milbank Q 1992;70(1):81-125.

Smoking in the Young

To the Editor: In the October 9 issue, Rigotti et al.1 report on an evaluation of the effectiveness of enforcing laws that ban tobacco sales to minors as a strategy to reduce tobacco use by adolescents. The authors conclude, We found no meaningful difference in smoking behavior between communities that implemented enforcement programs and those that did not. This conclusion is intriguing, given the results: the prevalence of 30-day current tobacco use increased significantly over time in the intervention communities (P 0.01) but not in the control communities (P 0.93). Contrary to the authors hypothesis, current tobacco use increased by 2.8 percentage points in the intervention communities as compared with only 0.2 percentage point in the control communities (P 0.05). Thus, the intervention appears to have had a negative effect. The authors considered this effect to be of borderline significance and dismissed it. A negative effect cannot be disregarded on substantive grounds, since other researchers might have predicted such an effect on the basis of a forbidden fruit rationale.2 Had the authors found an effect of similar magnitude but in the hypothesized direction, we suspect they would have featured it. We believe the negative intervention effect should be dismissed because the study used a weak, quasi-experimental design that is subject to numerous threats to internal validity.3 Three intervention communities, in which health departments adopted tobacco-sales regulations, were contrasted with three nearby control communities of

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similar size and household income.1 Reasonable estimates of the intervention effect can be obtained only if one can rule out plausible alternative hypotheses associated with the assignment to the intervention.3 The intervention and control communities did not have equivalent rates of tobacco use before the intervention. As compared with control subjects, intervention subjects were much less likely to use tobacco at base line (30-day prevalence, 22.5 percent vs. 29.8 percent).1 Furthermore, both groups had lower prevalence rates than those in a 1993 statewide survey of Massachusetts youth (30.2 percent for cigarette use and 9.4 percent for use of smokeless tobacco).4 In the present study, what appeared to be an intervention effect may have been an artifact of statistical regression extreme observations tend to regress toward the mean when remeasured.3 Fitting alternative statistical models to the data in an attempt to bracket the estimated effect could provide a more valid test of the intervention.3,5 Future research would benefit from stronger study designs, including the use of longitudinal response data and communities that are matched according to base-line tobacco use. JOEL M. MOSKOWITZ, PH.D. JANET MALVIN, PH.D.
University of California, Berkeley Berkeley, CA 94720
1. Rigotti NA, DiFranza JR, Chang Y, Tisdale T, Kemp B, Singer DE. The effect of enforcing tobacco-sales laws on adolescents access to tobacco and smoking behavior. N Engl J Med 1997;337:1044-51. 2. Glantz SA. Preventing tobacco use the youth access trap. Am J Public Health 1996;86:156-8. 3. Cook TD, Campbell DT. Quasi-experimentation: design and analysis issues for field settings. Chicago: Rand McNally, 1979. 4. Kann L, Warren CW, Harris WA, et al. Youth risk behavior surveillance United States, 1993. MMWR CDC Surveill Summ 1995;44(SS-1): 1-56. 5. Reichardt C, Gollub H. Taking uncertainty into account when estimating effects. In: Mark R, Shotland R, eds. Multiple methods in program evaluation. No. 35 of New directions for program evaluation. San Francisco: JosseyBass, 1987:7-22.

munity-level data do not exist. Instead, we matched the communities according to median household income, the best available proxy, since income is correlated with tobacco use. More similar base-line smoking rates would have reduced the concern about regression to the mean. We did not select study communities on the basis of high or low smoking rates, making regression to the mean a less likely alternative explanation of our findings. What does explain our observations? Enforcement more than doubled compliance rates among merchants, but this change did not have a strong effect, in either direction, on smoking among youth. Tobacco use by adolescents clearly did not fall. Drs. Moskowitz and Malvin raise the possibility that enforcement may actually induce tobacco use among youth, but there was at best a weak effect in this direction. We favor the simpler explanation that the marked improvement in compliance in the intervention communities was not good enough. Stores continued to sell enough tobacco to minors to provide a sufficient supply for them. Illegal tobacco sales to minors is a stubborn problem. Our results serve as a warning to communities pursuing law enforcement that stronger efforts, such as increasing the frequency of compliance tests or raising penalties for violations, are likely to be needed to stop sales. As our intervention communities learned, there are many political obstacles to such an aggressive approach. Nonetheless, we remain optimistic that vigorous enforcement of the law is possible and can stop the illegal sale of tobacco to children. NANCY A. RIGOTTI, M.D. DANIEL E. SINGER, M.D.
Massachusetts General Hospital Boston, MA 02114

JOSEPH R. DIFRANZA, M.D.

University of Massachusetts Medical Center Worcester, MA 01655

The authors reply: To the Editor: We agree with Drs. Moskowitz and Malvin that it would have been preferable to use a stronger study design ideally, a randomized controlled trial to address our research question. However, we were evaluating the effect of public policy in the real world, and we used the strongest design available. We could not have recruited Massachusetts communities for a study in which the investigators, not public health officials, decided whether to enforce laws governing tobacco sales. Our compromise, a quasi-experimental design with longitudinal data collection, permitted us to address, in a controlled study, an important and previously unanswered question about the effects of enforcing a tobacco-sales law. The use of this controversial tobacco-control strategy is becoming widespread in the absence of firm data about its effects. Closer matching of intervention and control communities according to the base-line prevalence of smoking among youth might have been possible, but precise com-

Pulmonary Lymphangiomyomatosis in a Preadolescent Girl

To the Editor: A 12-year-old girl presented in 1996 with cough and dyspnea on exertion. A chest roentgenogram taken when she was three years old showed reticulonodular infiltrations that were interpreted as evidence of recurrent pneumonia. At the age of 10 years the chest roentgenogram showed bilateral patchy interstitial infiltrates with a reticular and vesicular pattern. The results of openlung biopsy were initially interpreted as showing interstitial fibrosis and emphysema. Corticosteroid treatment resulted in symptomatic improvement, but the roentgenographic picture remained unchanged. Eight months later bilateral reticulonodular infiltrates and chylous effusion developed. A reappraisal of the open-lungbiopsy specimen and detailed immunohistochemical study established the diagnosis of lymphangiomyomatosis. The proliferating smooth-muscle cells positive for alphasmooth-muscle actin in the lung showed a strong progesterone-receptor positivity (Fig. 1) and estrogen-receptor negativity. No signs

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2. Dishner W, Cordasco EM, Blackburn J, Demeter S, Levin H, Carey WD. Pulmonary lymphangiomyomatosis. Chest 1984;85:796-9.

Management of Traumatic Lacerations

To the Editor: In their review of the evaluation and management of traumatic lacerations, Singer et al. (Oct. 16 issue)1 provide much helpful information, but the technique recommended for suture closure includes a dangerous surgical practice. In the diagrams of the placement of both a simple suture (Fig. 1) and a deep suture (Fig. 2), the surgeon everts the wound by retracting the edge of the skin to receive the suture with a finger. This puts the surgeons finger in the path of the oncoming suture needle. The most common injury during surgery is a needle stick to the surgeons nondominant index finger during suturing by doing exactly what is shown in these figures.2 In a survey of injuries to medical personnel during operating-room surgery, such a needle stick occurred in 4.9 percent of operations.3 Given the prevalence of bloodborne pathogens such as hepatitis viruses and the human immunodeficiency virus (HIV), this practice poses an unnecessary risk. The edge of the skin to be pierced by the oncoming needle can easily be everted by gentle downward pressure with a forceps. Once the needle is through the skin, the needle can easily be grasped with this same forceps. There is no advantage to the use of ones finger, and contaminated suture needles should be handled with instruments whenever possible. JAMES M. SPENCER, M.D.
University of Miami Miami, FL 33136
1. Singer AJ, Hollander JE, Quinn JV. Evaluation and management of traumatic lacerations. N Engl J Med 1997;337:1142-8. 2. Spencer J, Katz BE. The potential role of simple dermatologic surgery techniques in transmitting HIV infection. Semin Dermatol 1995;14:21927. 3. Panlilio AL, Foy DR, Edwards JR, et al. Blood contacts during surgical procedures. JAMA 1991;265:1533-7.

Figure 1. Lymphangiomyomatosis Characterized by the Subpleural Proliferation of Smooth-Muscle Cells with Progesterone-Receptor Positivity (Right) (ABC Immunoperoxidase Staining for Progesterone Receptor, 400).

of menarche or secondary sex characteristics were noted at the time of the diagnosis. Serum levels of sex hormones were barely detectable: estradiol, 10 pg per milliliter; follicle-stimulating hormone, 0.6 mIU per milliliter; luteinizing hormone, 0.1 mIU per milliliter; and progesterone, 0.15 ng per milliliter. The manifestation of lymphangiomyomatosis was thought to have been triggered by a surge of sex hormones. Treatment was begun with an analogue of luteinizing hormonereleasing hormone, triptorelin (3.75 mg per month intramuscularly). After 10 months of therapy, the childs lung function had not improved (less than 30 percent of the predicted value) and the roentgenographic findings were unchanged. Several authors have suggested that assays and immunohistochemical tests for estrogen and progesterone receptors in lung-biopsy specimens might be used to determine the most appropriate hormonal treatment for lymphangiomyomatosis.1 Our experience, however, does not seem to support the idea that high-affinity estrogen and progesterone receptors in smooth-muscle cells are the underlying pathogenetic mechanism of lymphangiomyomatosis.2 Drastic hormonal manipulations by means of medroxyprogesterone therapy or oophorectomy are not acceptable in a preadolescent girl, who may be the youngest patient reported to have severe pulmonary manifestations of lymphangiomyomatosis. We are of the opinion that our patients present hormonal silence cannot be maintained for long, because it is associated with psychological problems. Lung transplantation may be an acceptable form of therapy in this girl. BLA NAGY, M.D., PH.D. ZOLTN NBRDY, M.D. ZOLTN NEMES, M.D., D.SC.
University Medical School H-4012 Debrecen, Hungary
1. Taylor JR, Ryu J, Colby TV, Raffin TA. Lymphangioleiomyomatosis: clinical course in 32 patients. N Engl J Med 1990;323:1254-60.

To the Editor: The figures in the article by Singer et al. depict practices that place the physician at increased risk for exposure to and infection with blood-borne pathogens such as HIV, hepatitis B, and hepatitis C. In the figures showing the placement of simple and deep sutures, a finger is being used to retract the edge of the skin. The finger lies directly in the path of the sharp needle and is likely to be punctured. In an observational study of skin contacts with blood during surgery, 80 of 620 hand contacts occurred during suturing.1 One of us maintains an ongoing surveillance data base on percutaneous injuries among health care personnel (the Exposure Prevention Information Network, or EPINet). From 1993 to 1996, in 77 hospitals nationwide, a total of 992 injuries entered in the data base occurred in emergency departments, 105 (10.6 percent) of which were caused by suture needles. Most of the needle-stick injuries (74 percent) occurred during suturing; a minority (26 percent) occurred after suturing or during disposal of the needle. Suturing is a source of avoidable injuries to health care

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personnel. Skin can be retracted by techniques such as the use of instruments, thereby keeping the physicians fingers out of harms way.2 This simple change in practice allows physicians to provide care without themselves becoming patients. SCOTT DEITCHMAN, M.D., M.P.H.
Centers for Disease Control and Prevention Atlanta, GA 30333

en fragments may be imaged with ultrasonography or computed tomography.2 C. WILLIAM KAISER, M.D.
Veterans Affairs Medical Center Manchester, NH 03104
1. Risk management for emergency room physicians: complications of wound management. American College of Emergency Physicians Foresight. Issue 16. September 1990:3. 2. Kaiser CW, Slowick T, Spurling KP Friedman S. Retained foreign bod, ies. J Trauma 1997;43:107-11.

JANINE JAGGER, PH.D.

University of Virginia Charlottesville, VA 22908
1. Tokars JI, Culver DH, Mendelson MH, et al. Skin and mucous membrane contacts with blood during surgical procedures: risk and prevention. Control Hosp Epidemiol 1995;16:703-11. 2. Lewis FR Jr, Short LJ, Howard RJ, Jacobs AJ, Roche NE. Epidemiology of injuries by needles and other sharp instruments: minimizing sharp injuries in gynecologic and obstetric operations. Surg Clin North Am 1995; 75:1105-21.

To the Editor: . . . During wound assessment one must watch for persistent bleeding, even if the injury is not proximate to a major artery. Any wound that requires pressure for control of hemorrhage in order to close the skin must involve the laceration of an artery. At least once a year, my associates and I see a radial-artery false aneurysm resulting from forcible closure of a briskly bleeding puncture wound in the forearm. Singer et al. should also have emphasized that the presence of weak pulses distal to an injury or the absence of a pulse should never be attributed to spasm or adjacent swelling. This situation implies an arterial laceration, which should be assessed by a vascular surgeon. Singer et al. state that deep sutures should be placed so that the knot is buried. This time-honored dictum is not supported by any study. Burying knots can be hard to do properly and is, in my opinion, generally useless with modern synthetic absorbable sutures. JEFFREY L. KAUFMAN, M.D.
Baystate Medical Center Springfield, MA 01199

To the Editor: Singer et al. assert wrongly that the use of vasoconstrictors should be avoided in areas with end arterioles, such as the fingers, toes, penis, and tip of the nose. This advice enshrines the old medical school mnemonic device fingers, toes, penis, and nose all extremities of a sort but not all containing end arteries. Ears and noses have a network pattern of vascularity without any end arteries. Rhinoplasties and otoplasties are carried out every day, and these procedures would be blood baths without the use of epinephrine-containing local anesthetics. Unless tissue is severely devitalized, vasoconstrictors should be recommended for the repair of nasal and ear wounds. As far as the penis is concerned, the skin circulation is essentially a random arterial network; only the deep vessels in the corpora are end arteries. Therefore, lacerations that do not penetrate deeply should be treated with the patient under local anesthesia with epinephrine. RICHARD H.S. KARPINSKI, M.D.
200 Central Park South New York, NY 10019

The authors reply: To the Editor: Dr. Spencer and Drs. Deitchman and Jagger correctly point out the risk of accidental puncture of the wound-retracting finger with the suture needle. If a finger is used to retract tissues, it should never be put in the potential pathway of the needle. Alternatively, tissues may be gently lifted with a fine forceps while care is taken not to cause any additional trauma to the tissues from crushing. The purpose of the figures was to illustrate the angle of needle entry during placement of sutures and not to mislead readers. As we mentioned in our review, the possibility of any injury to underlying structures (such as arteries) must be ruled out before wound closure is attempted. We agree with Dr. Kaufman that if hemorrhage cannot be adequately controlled in the emergency room, operative exploration may be necessary to rule out arterial injury. Failure to recognize the presence of foreign bodies in wounds may indeed have grave consequences, as Dr. Kaiser points out. Physicians can avoid this possibility by obtaining a detailed history of the mechanism of injury and, as we indicated, by thoroughly examining the wound. Appropriate imaging studies may be indicated in suspiciousappearing wounds. We agree with Dr. Karpinski that under certain circumstances the use of a local vasoconstrictor in lacerations involving the nose and ears may be necessary. However, in

To the Editor: In their excellent article, Singer et al. should have mentioned the importance of seeking a foreign body and the need to perform x-ray imaging studies to detect such foreign bodies, which usually manifest themselves later with complications such as poor wound healing, infection, and neurovascular or tendon damage. The failure to identify a retained foreign body is one of the most common misdiagnoses attributed to emergency room physicians, and imaging studies are infrequently performed in such settings. In one series, imaging studies were performed in only 31 percent of urgent care patients later found to have a retained foreign body.1,2 Virtually all retained glass foreign bodies that are larger than 2 mm and are not overlying bone can be detected on a standard anteroposterior roentgenogram. Similarly, wood-

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our experience, most such wounds will have stopped bleeding by the time of wound closure. At that point, the use of vasoconstrictors would be unnecessary and could lead to further tissue devitalization. ADAM J. SINGER, M.D.
State University of New York Stony Brook, NY 11794

JUDD E. HOLLANDER, M.D.

University of Pennsylvania Philadelphia, PA 19104

premiums from individual members and small businesses), deny coverage for expensive treatments, and encourage young, healthy people to enroll while shunning potential subscribers who are old or sick. They refuse to cover preexisting conditions and increase their economic clout through mergers and acquisitions. For-profit hospital chains are buying up nonprofit hospitals, laying off staff, increasing their economic clout through mergers and acquisitions, and refusing to provide uncompensated care, even when they have the resources to do so. Since the private sector is the cause of these problems, it is unlikely that the private sector will provide the solution. ROBERT J. YAES, M.D.
15 Quantum Pl. Gaithersburg, MD 20877

JAMES V. QUINN, M.D.

University of Michigan Ann Arbor, MI 48109

The Health Care Market

To the Editor: In the article entitled Trends in Health Care Coverage and Financing and Their Implications for Policy, Smith (Oct. 2 issue)1 analyzes the health care market and concludes that the market has failed to provide adequate amounts of uncompensated care. Actually, the market has not failed at all. It is the belief that everyone can have all the health care they want at the expense of everybody else that has failed. Markets are mechanisms for creating wealth through voluntary exchange. Insurance companies, as market entities, are not tax-supported welfare agencies. If they do not make a profit, by providing a service at a price customers are able and willing to pay, they run out of money with which to continue providing the service, and shareholders invest their hard-earned money somewhere else. The insurance companies that do not make a profit go out of business. Even nonprofit companies must provide goods or services that others will voluntarily pay for and raise at least as much money as it costs to do so to continue to exist. SANDY SHAW
Spectrum Technology Service Tonopah, NV 89049
1. Smith BM. Trends in health care coverage and financing and their implications for policy. N Engl J Med 1997;337:1000-3.

Ms. Smith replies: To the Editor: Although Shaw and Yaes appear to approach the issue of declining insurance coverage and the increasing need for uncompensated care from opposite perspectives, their letters reflect agreement that the operation of the private insurance market in and of itself will not lead to expansions of coverage. This indeed is the main thesis of my article: that the growth of managed care and the market consolidation that followed has resulted in cost containment but at the expense of decreased insurance coverage, which will lead to substantial financial instability of the health care delivery system as well as to broader social instability. The measure of the private health care markets success must be whether it operates both to contain costs and to expand coverage; otherwise, the issue of health-system stability and the issues of quality of care and access that are affected by financial instability will go unaddressed. Both correspondents agree that the market will not operate to expand coverage and that such expansion will not occur in the absence of government intervention. Where they differ is in whether or not they view the expansion of coverage, stability of the health care delivery system, and access to care as values worthy of government intervention. That disagreement frames the political debate that will almost certainly accompany any effort to expand insurance coverage in this country. BARBARA MARKHAM SMITH, J.D.
George Washington University Medical Center Washington, DC 20006

To the Editor: If there is a single thread connecting the problems of health care coverage and financing that Smith considers, it is that corporations are under intense pressure from Wall Street to produce ever-increasing quarterly earnings. Consequently, they are reducing employee health costs. They do this directly by dropping health coverage entirely, or subtly by forcing employees into health maintenance organizations (HMOs), which then decrease access to and the quality of care. The recent stock-market boom may have been financed in part by this decrease in employee health benefits. For-profit HMOs and corporate health care providers are under the same pressure. HMOs use their economic clout to negotiate lower prices from providers (and higher

Emergency Postcoital Contraception

To the Editor: We were very pleased to see Glasiers timely and thorough discussion of emergency postcoital contraception (Oct. 9 issue).1 However, two points dealing with missed oral-contraceptive pills are troublesome. First, the instructions for taking missed pills that are shown in Figure 1 are those used in the United Kingdom, not in the United States, and therefore may be confusing to readers accustomed to the instructions approved by the Food and Drug Administration now included in all U.S. pill packets. Physicians have no way of knowing why the

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instructions differ from those used in the United States or whether to apply them when making decisions about prescribing emergency contraception or when counseling their patients about handling missed pills in general. Specifically, the U.K. instructions for missed pills advise using back-up contraception for the next seven days if a single pill is taken 12 hours late. This would suggest the need for emergency contraception if back-up contraception was not used during the seven-day period after any one pill is taken more than 12 hours late. In contrast, the instructions approved by the Food and Drug Administration do not advise the use of back-up contraception unless pills are missed on two or more consecutive 24-hour days. Second, Dr. Glasiers statement that emergency contraception is not usually indicated when one or more oral-contraceptive pills have been forgotten, because there are established and effective rules for the use of a barrier method as secondary prevention under these circumstances could be misinterpreted. The reason most women need emergency contraception is that they have not followed established and effective rules for regular or back-up contraception. For example, in a recent study of 103 women taking oral-contraceptive pills, back-

up contraception was used in only 3 percent of the acts of intercourse in which it was indicated. In addition, that statement diverts attention from a situation in which emergency contraception may prevent a pregnancy that would otherwise result from an act of intercourse before the pills were missed (e.g., an active pill is taken on schedule on Saturday night, intercourse occurs on Sunday evening, and active pills are missed on Sunday, Monday, and Tuesday nights). LINDA S. POTTER, DR.P.H. JAMES TRUSSELL, PH.D.
Princeton University Princeton, NJ 08544

LISA RARICK, M.D.

Food and Drug Administration Rockville, MD 20857
1. Glasier A. Emergency postcoital contraception. N Engl J Med 1997; 337:1058-64. 1998, Massachusetts Medical Society.

HOSSEIN JADVAR, M.D.

Vol ume 338

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