Letters
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should: • Include no more than 400 words of text, three authors, and five references • Type with double-spacing • Send with the letter a transfer-ofcopyright form (see Table of Contents for location) signed by all authors • Provide a self-addressed envelope if they want to be notified that the letter was received Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified only if their letter is accepted. Unpublished letters cannot be returned. Hepatitis C after Needlestick Injuries To the Editors: Kiyosawa and colleagues' article (1) on hepatitis C in hospital employees raises the question of why hepatitis C virus (HCV) was not added to the Centers for Disease Control (CDC) guidelines issued in July. These guidelines were intended to prevent transmission of human immunodeficiency virus (HIV) or hepatitis B virus (HBV) from infected health care workers to patients. The guidelines recommend that health care workers determine their HIV and HBV status and, if infected, refrain from doing invasive procedures. Hepatitis C virus should be added to those guidelines for the following reasons: 1) In blood donors and, presumably, in the general population, including health care professionals, seropositivity is greater for HCV than for HBV. 2) Hepatitis C virus more frequently results in persistent infection than does HBV. 3) Seroconversion to hepatitis C may occur after approximately 1 of every 37 needlestick exposures to HCV according to the study by Kiyosawa and colleagues (1), whereas, after similar exposure to HIV, the seroconversion rate is about 1 in 240. 4) Hepatitis C is more generally distributed in the population than is hepatitis B or HIV infection because of some differences in transmission risk behavior (for example, hepatitis C is not as associated with homosexual activity as HIV infection is). 5) Hepatitis C frequently leads to chronic liver disease, which may progress to cirrhosis, and is associated with development of primary liver cancer. An invasive procedure accident appears to be more likely both to transmit HCV—than to transmit either HIV or HBV— and to result in a greater number of chronically infected patients. Omission of HCV from the CDC guidelines therefore seems inappropriate. Norwood O. Hill, MD 3808 Townsend Dallas, TX 75229 Reference 1. Kiyosawa K, Sodeyama T, Tanaka E, et al. Hepatitis C in hospital employees with needlestick injuries. Ann Intern Med. 1991 ;115: 367-9. To the Editors: As a hospital epidemiologist who deals regularly with the transmission of bloodborne infections from patients to health care workers, I was interested by Kiyosawa and colleagues' article (1). The investigators concluded that the risk for hepatitis C virus (HCV) infection after an accidental
needlestick from an anti-HCV-positive donor is "exceedingly low . . . compared with the 67% risk found in needlestick accidents involving hepatitis B e antigen (HBeAg)-positive donors." This comparison between hepatitis B virus (HBV) and HCV deserves further consideration. This comparison does not take into account the possibility that, as is the case with HBV, infectivity may not be homogeneous among anti-HCV-positive donors. A subset of infected individuals may indeed pose a higher than 4% risk for HCV transmission to needlestick recipients. Until an indicator of HCV infectivity (similar to HBeAg in HBV infection) is found, this possibility remains. Nor does this comparison take into account the efficacy of previous vaccination and proper prophylaxis after needlestick exposure to HBV. Indeed, the investigators' own data suggest an overall transmission rate of 1.5% (much lower than 67%) for a HBSAg-positive needlestick when HBV immunoglobulin or HBV vaccine is administered or when previous serologic immunity to HBV is documented (1); this rate is not significantly different from the 4% rate cited for HCV transmission (Fisher exact test, P > 0.1). Finally, the long-term health consequences of HBV and HCV should also be compared. Because at least 50% of individuals with acute HCV infection are expected to develop chronic hepatitis and because, of these, 20% to 50% may eventually develop cirrhosis (2), 0.4% to 1% of health care workers who were exposed to anti-HCV-positive needlesticks in the study can be expected to develop irreversible liver damage with its attendant complications. Conversely, because 3% of those with HBV infection will ultimately develop cirrhosis (3), only 0.045% (3% of the 1.5% infected in the study) of recipients may be expected to develop this complication after an HBSAg-positive needlestick. Therefore, the relative risk for long-term hepatic complications after an anti-HCVpositive needlestick may actually be much higher (9- to 22-fold) than after an HBSAg-positive needlestick when standard postexposure management for the latter is used. These calculations do not take into account the potential efficacy of alpha-interferon for treatment of chronic hepatitis due to HBV or HCV; however, the initial response rate to this drug appears to be quite similar for both conditions (4, 5). In conclusion, until an effective HCV prophylaxis is developed, even though transmission of HCV by needlestick may be infrequent, this virus may pose a greater threat to health care workers than does properly managed HBV infection. Farrin A. Manian, MD, MPH St. John's Mercy Medical Center St. Louis, MO 63141-8277 References 1. Kiyosawa K, Sodeyama T, Tanaka E, et al. Hepatitis C in hospital employees with needlestick injuries. Ann Intern Med. 1991;115: 367-9. 2. Davis GL. Hepatitis C virus. In: Mandell GL, Douglas RG, Bennett JE, eds. Principles and Practice of Infectious Disease. Update 10. New York: Churchill Livingstone; 1991:3-11. 3. Hirschman SZ. Chronic hepatitis. In: Mandell GL, Douglas RG, Bennett JE, eds. Principles and Practice of Infectious Disease. New York: Churchill Livingstone; 1990:1017-24. 4. Perrilo RP, Schiff ER, Davis GL, et al. A randomized, controlled trial of interferon alfa-2b alone and after prednisone withdrawal for the treatment of chronic hepatitis B. N Engl J Med. 1990;323:295-301. 5. Davis GL, Balart LA, Schiff ER, et al. Treatment of chronic hepatitis C with recombinant interferon alpha: A multicenter randomized, controlled trial. N Engl J Med. 1989;321:1501-6.
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To the Editors: Kiyosawa and colleagues (1) determined the risk for hepatitis C virus (HCV) transmission after needlestick injury from an anti-HCV-positive donor to range from 2.7% to 4%. They mention that "the efficacy of prophylactic gamma globulin in this circumstance is unknown." Immune serum globulin (kept at < 96 °F) after blood transfusion significantly reduces the incidence of icteric but not of anicteric non-A, non-B hepatitis (2). More recently, immune serum globulin given shortly before transfusion has been shown to decrease the incidence of non-A, non-B hepatitis significantly (3). Pretransfusion administration also significantly decreases the incidence of biopsy-proved chronic non-A, non-B hepatitis (4). Kiyosawa and colleagues (1) have clearly demonstrated that there is a low but significant risk for developing HCV infection after needlestick injury. Considering the low cost and side effect profile of immune serum globulin, its use should be strongly considered for persons who sustain a needlestick injury with infectious material from anti-HCV-positive patients who have active hepatitis and who are most likely to transmit this virus (5). Leonard A. Mermel, DO, ScM Rhode Island Hospital and Brown University School of Medicine Providence, RI References 1. Kiyosawa K, Sodeyama T, Tanaka E, et al. Hepatitis C in hospital employees with needlestick injuries. Ann Intern Med. 1991 ;115: 367-9. 2. Seef LB, Zimmerman HJ, Wright EC, et al. A randomized, double blind controlled trial of the efficacy of immune serum globulin for the prevention of post-transfusion hepatitis. A Veterans Administration Cooperative Study. Gastroenterology. 1977;72:111-21. 3. Sanchez-Quijano A, Lissen E, Diaz-Torres MA, et al. Prevention of post-transfusion non-A, non-B hepatitis by non-specific immunoglobulin in heart surgery patients. Lancet. 1988;1:1245-9. 4. Knodell RG, Conrad ME, Ishak KG. Development of chronic liver disease after acute non-a, non-B post-transfusion hepatitis. Role of r-globulin prophylaxis in its prevention. Gastroenterology. 1977;72: 902-9. 5. Esteban JI, Gonzalez A, Hernandez JM, et al. Evaluation of antibodies to hepatitis C virus in a study of transfusion-associated hepatitis. N Engl J Med. 1990;323:1107-12.
In response: We agree with Dr. Hill's proposition. As Dr. Manian mentioned, the first-generation assay for antibody to HCV (anti-C100-3) is not a satisfactory indicator of HCV infectivity. Most, but not all, anti-C100-3-positive sera contain HCV-RNA. In contrast, some anti-C100-3-negative sera contain HCV-RNA (1). Our preliminary results with the anti-HCV-2 assay indicate that the prevalence of HCV infection is almost 50% among high-risk persons, such as drug abusers and patients receiving hemodialysis, or almost twofold the prevalence of anti-C100-3. However, the prevalence of HCV infection in hospital employees is almost the same (2%) according to the first- and the second-generation assays. Infection with HCV therefore is not common in health care workers. The long-term sequelae of acute transfusion-transmitted hepatitis C are very serious (2). The long-term sequelae of patients with HCV infection after a needlestick accident are unknown. Omata and colleagues (3) recently reported that interferon therapy during the acute phase of post-transfusion hepatitis C is very effective in preventing progression to chronic hepatitis C. Interferon therapy therefore should be considered for patients with needlestick-transmitted hepatitis C. Kendo Kiyosawa, MD Shinshu University School of Medicine 3-1-1, Asahi, Matsumoto 390 Japan References 1. Okamoto H, Okada S, Sugiyama Y, et al. Detection of hepatitis C virus RNA by a two-stage polymerase chain reaction with two pairs of primers deduced from the 5'-noncoding region. Jap J Exp Med. 1990;60:213-22.
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2. Kiyosawa K, Sodeyama T, Tanaka E, et al. Inter-relationship between blood transfusion, non-A, non-B hepatitis and hepatocellular carcinoma: Analysis by detection of antibody to hepatitis C virus. Hepatology. 1991;12:671-5. 3. Omata M, Yokosuka O, Takano S, et al. Resolution of acute hepatitis C after therapy with natural beta interferon. Lancet. 1991;338:914-5.
Hilar Adenopathy in Aspergillosis To the Editors: In their case report, Hantsch and Tanus (1) describe hilar adenopathy in association with allergic bronchopulmonary aspergillosis. As a radiologist, I am concerned about their analysis of the radiographs presented. I believe the perihilar opacities shown in Figure 1 (1) are typical of dilated, mucus-filled central bronchi. The investigators state that "subtle findings consistent with central bronchiectasis were detected on retrospective evaluation of a computed tomographic scan of the chest." The opacities shown would be evident on a computed tomographic examination, which would also permit the distinction between dilated bronchi and lymph node enlargement. Unfortunately, appropriate images were not published. Hilar lymph nodes are peribronchial and perivascular nodes, located within the confines of the visceral pleura. As such, they are not accessible to mediastinoscopic evaluation. I do not believe the opacities shown in Figure 1 (1) were biopsied at the time of mediastinoscopy. Despite the investigators' disclaimer that "pseudohilar adenopathy cannot be ruled out," their assertion that the opacities represent enlarged hilar lymph nodes is unconvincing. Howard Mann, MD LDS Hospital Salt Lake City, UT 84143 Reference 1. Hantsch CE, Tanus T. Allergic bronchopulmonary aspergillosis with adenopathy. Ann Intern Med. 1991;115:546-7.
To the Editors: Hantsch and Tanus (1) reported a case of allergic bronchopulmonary aspergillosis with adenopathy. Histopathologic examination of mediastinal lymph node biopsy specimens showed infiltration of eosinophils and plasma cells. The adenopathy resolved after treatment with corticosteroids. This case shows that allergic bronchopulmonary aspergillosis might be accompanied by true adenopathy. We report a similar case with both hilar and mediastinal lymphadenopathy. A 19-year old man presented in 1986 with wheezing, coughing of yellow sputum, and weight loss. He had never smoked tobacco or marijuana. The symptoms appeared to have started in 1972 and were slowly progressive. The chest roentgenogram showed infiltration of the right lower lobe and bronchopathy of the lingula but no signs of adenopathy. Laboratory tests confirmed the diagnosis of allergic bronchopulmonary aspergillosis. In 1990, the patient returned with the same complaints and a total IgE of 16.993 IE/L and a blood eosinophil count of 0.645 x 109/L. His specific IgE antibodies against Aspergillus fumigatus were RAST class 4 (Phadebas), and specific IgG antibodies were 113.0 E/mL by enzyme-linked immunosorbent assay. The Ouchterlony precipitation test showed one line and one band. The chest roentgenogram showed bronchopathy of the lingula, infiltration in the right upper lobe and hilar and superior mediastinal lymphadenopathy. Pulmonary function tests showed obstruction without restriction and a normal diffusion capacity. The levels of angiotensin-converting enzyme and lactate dehydrogenase were normal. A bronchoscopy with bronchoalveolar lavage revealed the classical picture of allergic bronchopulmonary aspergillosis, with brownish-yellow plugs in segmental bronchi. Because of severe hyperemia of the mucosa, we decided not to take transbronchial biopsy specimens. Cultures of the plugs showed A. fumigatus. The bronchoalveolar lavage fluid had normal cell counts and the following differential: lymphocytes, 6%; macrophages, 51%; eosinophils, 13%; and neutrophils, 30%. The patient was treated with prednisone, 1 mg/kg body weight per day for 4 months, after which the lymphadenopathy and infiltrates disappeared. Pulmonary function returned to
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normal. His total IgE decreased to 3340 IE/L, and the specific IgE count returned to class 0. We conclude that, although it happens rarely, allergic bronchopulmonary aspergillosis can be associated with hilar as well as with mediastinal lymphadenopathy. Paul M. van den Berg, MD Henk C. Hoogsteden, MD University Hospital Rotterdam 3015 GD Rotterdam The Netherlands
ation of interferon therapy (4). Whether the nephrotic syndrome in that case was secondary to the myeloma and would have improved with further treatment is by no means clear (5). This case emphasizes the potential nephrotoxicity of interferons and suggests that close monitoring for the development of proteinuria is essential, regardless of the dose. Kenneth S. Weiss, MD Kaiser Permanente Medical Center Cleveland, OH 44130
Reference 1. Hantsch CE, Tanus T. Allergic bronchopulmonary aspergillosis with adenopathy. Ann Intern Med. 1991;115:546-7.
In response: We appreciate both letters about our case report (1). Computed tomographic (CT) scan images were not published because of space limitations. The CT scan of the chest obtained at that time exhibited extensive hilar masses consistent with adenopathy. Visualization of the central bronchi revealed no intraluminal mucus collection; therefore, no evidence of pseudohilar adenopathy was seen. Although the adjacent mediastinum was partly obscured by the hilar densities, the mediastinum also appeared to have significant adenopathy. This observation was later confirmed by mediastinoscopy and node biopsies. As Dr. Mann noted, the hila themselves are inaccessible via this surgical procedure. However, radiologic and surgical mediastinal findings combine to provide convincing evidence of extensive adenopathy extending from the mediastinum to the hila. We agree with the assessment of Drs. van den Berg and Hoogsteden that, although it happens rarely, adenopathy can accompany allergic bronchopulmonary aspergillosis. Tonny Tanus, MD Christina E. Hantsch Evanston Hospital and Northwestern University Evanston, IL 60201 Reference 1. Hantsch CE, Tanus T. Allergic bronchopulmonary aspergillosis with adenopathy. Ann Intern Med. 1991;115:546-7.
Nephrotic Range of Proteinuria and Interferon Therapy To the Editors: Nephrotic range proteinuria is a well-documented side effect of recombinant gamma interferon and all other interferons (1-3). The doses reported to cause this effect have been in the range of 0.25 mg/m2 to 1 mg/m2 body surface area (activity, 1 x 107 units per milligram of protein). I report a case of nephrotic-range proteinuria in a patient receiving therapy at a much lower dose. A 64-year-old man had wide excision and skin grafting for a Clark level-IV (11.2 mm-thick) malignant melanoma on his midback. He soon thereafter developed axillary adenopathy, consistent with metastatic melanoma. He agreed to participate in the Eastern Cooperative Oncology Group Protocol EST 4687, a phase-II trial of recombinant gamma interferon in malignant melanoma. He was randomly assigned to the first arm of the protocol and received gamma interferon, 0.01 mg/m2, as an intravenous infusion three times per week. Although the patient tolerated treatment quite well, urinalysis revealed 4+ proteinuria after 4 weeks of treatment and treatment was stopped. A 24-hour urine collection showed normal creatinine clearance but nephrotic-range proteinuria of 8.45 g. Ultrasound of the kidney, computed tomographic scan of the abdomen, complement studies, and antinuclear antibodies (ANA) all had negative results. A repeat 24-hour urine collection snowed a nephrotic-range proteinuria of 8 g. One week later, the proteinuria had resolved. Proteinuria has been reported to develop with doses of gamma interferon as low as 0.25 mg/m2 (activity not indicated) but with no indication of a nephrotic-range proteinuria. We have encountered only one case of the nephrotic syndrome during treatment with lymphoblastoid interferon A, in a patient with multiple myeloma whose proteinuria worsened with initi-
References 1. Bennett C, Vogelzang N, Ratain M, et al. Severe toxicity (r-Ifn gamma) phase I trial of vinblastine (VLB) and recombinant gammainterferon. Proc ASCO. 1986;5:223. 2. Sriskandian K, Garner D, Watkinson J, et al. A toxicity study of recombinant interferon gamma given by intravenous infusion to patients with advanced cancer. Cancer Chemother Pharmacol. 1986; 18: 63-8. 3. Garnick MB, Reich SD, Richie JP. Phase I/I I study of interferon gamma (Immuneron) in advanced renal cell carcinoma (RCC) [Abstract]. J Urol. 1986;135:166A. 4. Selby P, Kohn J, Raymond J, et al. Nephrotic syndrome during treatment with interferon [Letter]. Br J Med. 1985;290:1180. 5. Sriskandian K, Tee DE, Pettingale KW. Nephrotic syndrome during treatment with interferon. Br Med J. 1985;290:1590-1.
Crimson Crescents—A Possible Association with the Chronic Fatigue Syndrome To the Editors: Approximately 80% of patients with the chronic fatigue syndrome, as defined by the Centers for Disease Control (1-3), seen in the Winthrop-University Hospital Chronic Fatigue Syndrome Center, have a peculiar purplish discoloration of both anterior pharyngeal pillars. The crescents are an intense crimson color and are well demarcated along the margins of both anterior pharyngeal pillars. They are not associated with pharyngitis or discoloration of the posterior pharyngeal pillars or uvula or accompanied by either anterior or posterior cervical adenopathy. In patients without tonsils, the crimson crescents assume a posterior position in the oropharynx. This appearance is most closely associated with high IL-2 receptor levels in our patients. The patients do not complain of a sore throat, but, occasionally, they complain of a sore neck anteriorly above the thyroid gland. The "crimson crescents" gradually fade over a period of 3 to 6 months, as the patient's condition improves, and eventually become indistinguishable in color from the normal oropharyngeal mucosa. We suggest that studies of the chronic fatigue syndrome systematically evaluate the possible association between these crimson crescents and the syndrome. Burke A. Cunha, MD Winthrop-University Hospital Mineola, NY 11501 References 1. Komaroff AL, Buchwald D. Symptoms and signs of chronic fatigue syndrome. Rev Infect Dis. 1991;13(Suppl 1):8-11. 2. Holmes GP. Defining the chronic fatigue syndrome. Rev Infect Dis. 1991;13(suppl l):53-5. 3. Klein NC, Cunha BA. Chronic fatigue syndrome. Infect Dis Practice. 1991;15:1-7.
Improving Cardiac Resuscitation in the Community To the Editors: I read with interest and emotion Dr. Cleaveland's description (1) of his failed attempt at out-of-hospital cardiopulmonary resuscitation (CPR). In the past 5 years, I have twice provided CPR to pedestrians who revived and returned to full neurologic function. Both incidents occurred near a health care facility, decreasing the delay in the arrival of equipment for definitive care (defibrillation, intubation, and intravenous access). In Dr. Cleaveland's case, supplemental oxygenation was delayed for 20 minutes and definitive care technology arrived even later. Despite adherence to American Heart Association resuscitation protocol, the patient died.
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The greatest predictor of survival in patients with cardiac arrest (from ventricular fibrillation or pulseless ventricular tachycardia) is the length of time to the onset of CPR and to the onset of definitive care (2). If the delay in definitive care is much longer than 8 minutes, the chance for meaningful survival is small. The use of CPR can " b u y " minutes by providing a modicum of cardiac output. One response to this problem is to deploy automatic external defibrillators at sites of large public gatherings. These devices are designed to read cardiac rhythms and to deliver defibrillations, when appropriate, without the assistance of trained personnel. The leads are easily placed by laypersons, and the machines are able to read cardiac rhythms with a sensitivity of more than 90% and a specificity of more than 95% (3). Moreover, safeguards prevent inadvertent or malicious shocking of persons who are not suffering ventricular fibrillation or ventricular tachycardia. At the 1986 Vancouver World's Exposition, Weaver and colleagues (4) trained security personnel to use these tools, and two lives were saved. Had such a device been available to Dr. Cleaveland, his patient might have had a reasonable chance of surviving. These defibrillators could be placed in easily identifiable locations behind alarmed glass windows, as fire extinguishers are. People could be trained in their use during standard CPR courses. The question of who is to pay for such equipment remains problematic. When a patient asks a physician for suggestions on how to advance medicine, he or she should be told that donating an automatic external defibrillator would make an excellent contribution to any community. Neil A. Solomon, MD Hospital of the University of Pennsylvania Philadelphia, PA 19104 References 1. Cleaveland CR. CPR. Ann Intern Med. 1991;115:570-1. 2. Weaver WD, Cobb LA, Hallstrom AP, et al. Factors influencing survival after out-of-hospital cardiac arrest. J Am Coll Cardiol. 1986; 7:752-7. 3. Atkins JM, Streiger HM, Burstein TL, et al. Improved survival rates with automatic defibrillators. Prehospital Disaster Medicine 1989;4: 69. 4. Weaver WD, Sutherland K, Wirkus MJ, Bachman R. Emergency medical care requirements for large public assemblies and a new strategy for managing cardiac arrest in this setting. Ann Emerg Med. 1989;18:155-60.
In response: Dr. Solomon presents several important points. The chief deterrents to the placement of automatic external defibrillators are the cost of the equipment and unsettled issues of liability. A semi-automatic external defibrillator costs $7000. In Pennsylvania, under existing law, who would be empowered to apply and to use the devices is uncertain. Perhaps the most useful and cost-effective interim strategy would be to establish centralized first-aid stations, with personnel who are fully trained in cardiopulmonary resuscitation, in shopping malls. Clifton R. Cleaveland, MD American College of Physicians Philadelphia, PA 19106-1572
To the Editors: I would like to report three kinds of unexpected problems that patients have encountered in trying to complete advance directives. Some elderly patients lead very isolated lives and are unable to identify a trusted confidante whom they are willing to designate with a durable power of attorney. The second is a bit more puzzling. Several patients have been unwilling, apparently due to embarrassment, to ask their neighbors simply to witness either a living will or a durable power of attorney. They seem to feel that discussing plans for their dying with neighbors and friends would be an
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Thomas E. Finucane, MD The Johns Hopkins University Baltimore, MA 21205 Reference 1. Greco PJ, Schulman KA, Lavizzo-Mourey R, Hansel-Flaschen J. The Patient Self-Determination Act and the future of advance directives. Ann Intern Med. 1991;115:639-43.
To the Editors: Advance planning for health care in case the patient becomes unable to make decisions is a complex and sensitive process, the core of which should occur between the patient and the primary physician. Greco and colleagues' suggestion (1) that health insurance agencies become involved in the process of providing for advance directives was shocking. Expecting insurance agencies to resist the temptation of providing cheaper policies to those who have advance directives to forgo life-sustaining care is naive. Subscribers would be correctly offended and suspicious of finding information or questions about advance directives from insurance agents. Access to affordable health policies is already inequitable without adding this to the risk assessment factors used by insurance agencies. There are also enough barriers to making advance directives without adding legitimate reasons to existing suspicions among potential users. Greco and colleagues' endorsement (1) of discussions about advance directives with lawyers was also distressing. Although most patients acquire their documents through lawyers, advance directives are fundamentally a clinical issue. Lawyers have a limited role, which is to advise the client of constitutional and common law rights and of statutory limitations that apply. They should then refer the client back to the physician. Advance directives have risks as well as benefits. We believe that among the most important safeguards against the risks is a good process of advance planning. The cornerstone of this process must be a physician-patient dialogue within a trusting relationship. Involvement of insurance companies and undue involvement of lawyers is all too likely to undermine that cornerstone and, by promoting misunderstandings and misuse, to lead to undesirable outcomes. Linda L. Emanuel, MD, PhD Massachusetts General Hospital Boston, MA 02114
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impropriety. Finally, spouses or adult children may decline to be designated as agent because, " I can't be the one who pulls the plug." Specific contingency planning for all of the many ways in which a person may be ill and for all of the treatments that might conceivably prolong life is difficult or, in many cases, impossible. The Maryland attorney general has indicated that he will consider a note that is signed by the physician, that is placed in the patient's medical record, and that documents advance directives to be "dispositive." This is a useful and important vehicle for establishing advance directives. For patients who lack advance directives, I agree with Greco (1) that policy "should be designed to promote the patient's best interest," and that it should not be dictated by fear of a morally dogmatic minority.
Ezekiel Emanuel, MD, PhD Dana Farber Cancer Institute Boston, MA 02115 Reference 1. Greco PJ, Schulman KA, Lavizzo-Mourey R, Hansen-Flaschen J. The Patient Self-Determination Act and the future of advance directives. Ann Intern Med. 1991;115:639-43.
In response: Dr. Finucane describes three of the many obstacles that may be encountered in the preparation of advance directives. We might add statutes and institutional policies that
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prohibit the attending physician, hospital employees, or family members from serving as witnesses for these documents (1). We hope that the educational efforts prompted by the Patient Self-Determination Act will reduce the resistance of neighbors, friends, and (when legally permissible) family to participating in this process (2). For some people, involving an attorney or a notary public may be a solution. The idea of health insurers inquiring into and offering information about advance directives is not ours; the Patient SelfDetermination Act mandates that health maintenance organizations do precisely that. Our proposal—that all insurers be subject to this requirement—is designed to increase public knowledge about advance directives before hospitalization. Many advance directive statutes prohibit insurers from requiring an advance directive as a condition of health insurance (1); pending legislation in Pennsylvania would also prohibit insurance discounts for those with advance directives. Where such safeguards do not exist, we reiterate that it would be inappropriate for insurers to require advance directives as a condition of insurance. We agree that advance planning for health care should ideally take place in the context of a trusting relationship between doctor and patient. However, many people do not have a primary care physician, and many physicians are not yet comfortable discussing these issues. We also agree that advance directives are primarily clinical documents. They are designed to be read, interpreted, and implemented by physicians. However, this does not mean that attorneys have no role in the preparation of these documents. Our attorney colleagues tell us that clients who prepare standard wills or durable powers of attorney are extremely receptive to discussing and preparing
medical advance directives at the same time. Only sometimes will this necessitate a conversation with the physician. Peter J. Greco, MD, for all of the authors (2). References 1. Society for the Right to Die. Handbook of Living Will Laws. New York: Society for the Right to Die; 1987:31-134. 2. Greco PJ, Schulman KA, Lavizzo-Mourey R, Hansen-Flaschen J. The Patient Self-Determination Act and the future of advance directives. Ann Intern Med. 1991;115:639-43.
Is Subspecialty Training Financially Worthwhile? To the Editors: I would like to comment on the article on subspecialty training (1). As a practicing internist for approximately 35 years with a multisubspecialty group, I can testify that your estimates are quite correct. Invasive cardiologists, followed by hematologist-oncologists, gastroenterologists, pulmonologists, and nephrologists, are the largest beneficiaries of the additional 2 years of training. General internists, followed by rheumatologists, infectious disease specialists, and endocrinologists, benefit least. Training general internists at least in such procedures as colonoscopy would not only help financially but also would aid in routine screening for colonic polyps. Alexander B. White, MD Olympia Fields Internal Medicine Associates, S.C. Olympia Fields, IL 60461 Reference 1. Prashker MJ, Meenan RF. Subspecialty training: is it financially worthwhile? Ann Intern Med. 1991;115:715-9.
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The Editors welcome submissions for possible publication in the Letters section. Authors of letters should: • Include no more than 400 words of text, three authors, and five references • Type with double-spacing • Send with the letter a transfer-ofcopyright form (see Table of Contents for location) signed by all authors • Provide a self-addressed envelope if they want to be notified that the letter was received Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified only if their letter is accepted. Unpublished letters cannot be returned. Hepatitis C after Needlestick Injuries To the Editors: Kiyosawa and colleagues' article (1) on hepatitis C in hospital employees raises the question of why hepatitis C virus (HCV) was not added to the Centers for Disease Control (CDC) guidelines issued in July. These guidelines were intended to prevent transmission of human immunodeficiency virus (HIV) or hepatitis B virus (HBV) from infected health care workers to patients. The guidelines recommend that health care workers determine their HIV and HBV status and, if infected, refrain from doing invasive procedures. Hepatitis C virus should be added to those guidelines for the following reasons: 1) In blood donors and, presumably, in the general population, including health care professionals, seropositivity is greater for HCV than for HBV. 2) Hepatitis C virus more frequently results in persistent infection than does HBV. 3) Seroconversion to hepatitis C may occur after approximately 1 of every 37 needlestick exposures to HCV according to the study by Kiyosawa and colleagues (1), whereas, after similar exposure to HIV, the seroconversion rate is about 1 in 240. 4) Hepatitis C is more generally distributed in the population than is hepatitis B or HIV infection because of some differences in transmission risk behavior (for example, hepatitis C is not as associated with homosexual activity as HIV infection is). 5) Hepatitis C frequently leads to chronic liver disease, which may progress to cirrhosis, and is associated with development of primary liver cancer. An invasive procedure accident appears to be more likely both to transmit HCV—than to transmit either HIV or HBV— and to result in a greater number of chronically infected patients. Omission of HCV from the CDC guidelines therefore seems inappropriate. Norwood O. Hill, MD 3808 Townsend Dallas, TX 75229 Reference 1. Kiyosawa K, Sodeyama T, Tanaka E, et al. Hepatitis C in hospital employees with needlestick injuries. Ann Intern Med. 1991 ;115: 367-9. To the Editors: As a hospital epidemiologist who deals regularly with the transmission of bloodborne infections from patients to health care workers, I was interested by Kiyosawa and colleagues' article (1). The investigators concluded that the risk for hepatitis C virus (HCV) infection after an accidental
needlestick from an anti-HCV-positive donor is "exceedingly low . . . compared with the 67% risk found in needlestick accidents involving hepatitis B e antigen (HBeAg)-positive donors." This comparison between hepatitis B virus (HBV) and HCV deserves further consideration. This comparison does not take into account the possibility that, as is the case with HBV, infectivity may not be homogeneous among anti-HCV-positive donors. A subset of infected individuals may indeed pose a higher than 4% risk for HCV transmission to needlestick recipients. Until an indicator of HCV infectivity (similar to HBeAg in HBV infection) is found, this possibility remains. Nor does this comparison take into account the efficacy of previous vaccination and proper prophylaxis after needlestick exposure to HBV. Indeed, the investigators' own data suggest an overall transmission rate of 1.5% (much lower than 67%) for a HBSAg-positive needlestick when HBV immunoglobulin or HBV vaccine is administered or when previous serologic immunity to HBV is documented (1); this rate is not significantly different from the 4% rate cited for HCV transmission (Fisher exact test, P > 0.1). Finally, the long-term health consequences of HBV and HCV should also be compared. Because at least 50% of individuals with acute HCV infection are expected to develop chronic hepatitis and because, of these, 20% to 50% may eventually develop cirrhosis (2), 0.4% to 1% of health care workers who were exposed to anti-HCV-positive needlesticks in the study can be expected to develop irreversible liver damage with its attendant complications. Conversely, because 3% of those with HBV infection will ultimately develop cirrhosis (3), only 0.045% (3% of the 1.5% infected in the study) of recipients may be expected to develop this complication after an HBSAg-positive needlestick. Therefore, the relative risk for long-term hepatic complications after an anti-HCVpositive needlestick may actually be much higher (9- to 22-fold) than after an HBSAg-positive needlestick when standard postexposure management for the latter is used. These calculations do not take into account the potential efficacy of alpha-interferon for treatment of chronic hepatitis due to HBV or HCV; however, the initial response rate to this drug appears to be quite similar for both conditions (4, 5). In conclusion, until an effective HCV prophylaxis is developed, even though transmission of HCV by needlestick may be infrequent, this virus may pose a greater threat to health care workers than does properly managed HBV infection. Farrin A. Manian, MD, MPH St. John's Mercy Medical Center St. Louis, MO 63141-8277 References 1. Kiyosawa K, Sodeyama T, Tanaka E, et al. Hepatitis C in hospital employees with needlestick injuries. Ann Intern Med. 1991;115: 367-9. 2. Davis GL. Hepatitis C virus. In: Mandell GL, Douglas RG, Bennett JE, eds. Principles and Practice of Infectious Disease. Update 10. New York: Churchill Livingstone; 1991:3-11. 3. Hirschman SZ. Chronic hepatitis. In: Mandell GL, Douglas RG, Bennett JE, eds. Principles and Practice of Infectious Disease. New York: Churchill Livingstone; 1990:1017-24. 4. Perrilo RP, Schiff ER, Davis GL, et al. A randomized, controlled trial of interferon alfa-2b alone and after prednisone withdrawal for the treatment of chronic hepatitis B. N Engl J Med. 1990;323:295-301. 5. Davis GL, Balart LA, Schiff ER, et al. Treatment of chronic hepatitis C with recombinant interferon alpha: A multicenter randomized, controlled trial. N Engl J Med. 1989;321:1501-6.
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To the Editors: Kiyosawa and colleagues (1) determined the risk for hepatitis C virus (HCV) transmission after needlestick injury from an anti-HCV-positive donor to range from 2.7% to 4%. They mention that "the efficacy of prophylactic gamma globulin in this circumstance is unknown." Immune serum globulin (kept at < 96 °F) after blood transfusion significantly reduces the incidence of icteric but not of anicteric non-A, non-B hepatitis (2). More recently, immune serum globulin given shortly before transfusion has been shown to decrease the incidence of non-A, non-B hepatitis significantly (3). Pretransfusion administration also significantly decreases the incidence of biopsy-proved chronic non-A, non-B hepatitis (4). Kiyosawa and colleagues (1) have clearly demonstrated that there is a low but significant risk for developing HCV infection after needlestick injury. Considering the low cost and side effect profile of immune serum globulin, its use should be strongly considered for persons who sustain a needlestick injury with infectious material from anti-HCV-positive patients who have active hepatitis and who are most likely to transmit this virus (5). Leonard A. Mermel, DO, ScM Rhode Island Hospital and Brown University School of Medicine Providence, RI References 1. Kiyosawa K, Sodeyama T, Tanaka E, et al. Hepatitis C in hospital employees with needlestick injuries. Ann Intern Med. 1991 ;115: 367-9. 2. Seef LB, Zimmerman HJ, Wright EC, et al. A randomized, double blind controlled trial of the efficacy of immune serum globulin for the prevention of post-transfusion hepatitis. A Veterans Administration Cooperative Study. Gastroenterology. 1977;72:111-21. 3. Sanchez-Quijano A, Lissen E, Diaz-Torres MA, et al. Prevention of post-transfusion non-A, non-B hepatitis by non-specific immunoglobulin in heart surgery patients. Lancet. 1988;1:1245-9. 4. Knodell RG, Conrad ME, Ishak KG. Development of chronic liver disease after acute non-a, non-B post-transfusion hepatitis. Role of r-globulin prophylaxis in its prevention. Gastroenterology. 1977;72: 902-9. 5. Esteban JI, Gonzalez A, Hernandez JM, et al. Evaluation of antibodies to hepatitis C virus in a study of transfusion-associated hepatitis. N Engl J Med. 1990;323:1107-12.
In response: We agree with Dr. Hill's proposition. As Dr. Manian mentioned, the first-generation assay for antibody to HCV (anti-C100-3) is not a satisfactory indicator of HCV infectivity. Most, but not all, anti-C100-3-positive sera contain HCV-RNA. In contrast, some anti-C100-3-negative sera contain HCV-RNA (1). Our preliminary results with the anti-HCV-2 assay indicate that the prevalence of HCV infection is almost 50% among high-risk persons, such as drug abusers and patients receiving hemodialysis, or almost twofold the prevalence of anti-C100-3. However, the prevalence of HCV infection in hospital employees is almost the same (2%) according to the first- and the second-generation assays. Infection with HCV therefore is not common in health care workers. The long-term sequelae of acute transfusion-transmitted hepatitis C are very serious (2). The long-term sequelae of patients with HCV infection after a needlestick accident are unknown. Omata and colleagues (3) recently reported that interferon therapy during the acute phase of post-transfusion hepatitis C is very effective in preventing progression to chronic hepatitis C. Interferon therapy therefore should be considered for patients with needlestick-transmitted hepatitis C. Kendo Kiyosawa, MD Shinshu University School of Medicine 3-1-1, Asahi, Matsumoto 390 Japan References 1. Okamoto H, Okada S, Sugiyama Y, et al. Detection of hepatitis C virus RNA by a two-stage polymerase chain reaction with two pairs of primers deduced from the 5'-noncoding region. Jap J Exp Med. 1990;60:213-22.
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2. Kiyosawa K, Sodeyama T, Tanaka E, et al. Inter-relationship between blood transfusion, non-A, non-B hepatitis and hepatocellular carcinoma: Analysis by detection of antibody to hepatitis C virus. Hepatology. 1991;12:671-5. 3. Omata M, Yokosuka O, Takano S, et al. Resolution of acute hepatitis C after therapy with natural beta interferon. Lancet. 1991;338:914-5.
Hilar Adenopathy in Aspergillosis To the Editors: In their case report, Hantsch and Tanus (1) describe hilar adenopathy in association with allergic bronchopulmonary aspergillosis. As a radiologist, I am concerned about their analysis of the radiographs presented. I believe the perihilar opacities shown in Figure 1 (1) are typical of dilated, mucus-filled central bronchi. The investigators state that "subtle findings consistent with central bronchiectasis were detected on retrospective evaluation of a computed tomographic scan of the chest." The opacities shown would be evident on a computed tomographic examination, which would also permit the distinction between dilated bronchi and lymph node enlargement. Unfortunately, appropriate images were not published. Hilar lymph nodes are peribronchial and perivascular nodes, located within the confines of the visceral pleura. As such, they are not accessible to mediastinoscopic evaluation. I do not believe the opacities shown in Figure 1 (1) were biopsied at the time of mediastinoscopy. Despite the investigators' disclaimer that "pseudohilar adenopathy cannot be ruled out," their assertion that the opacities represent enlarged hilar lymph nodes is unconvincing. Howard Mann, MD LDS Hospital Salt Lake City, UT 84143 Reference 1. Hantsch CE, Tanus T. Allergic bronchopulmonary aspergillosis with adenopathy. Ann Intern Med. 1991;115:546-7.
To the Editors: Hantsch and Tanus (1) reported a case of allergic bronchopulmonary aspergillosis with adenopathy. Histopathologic examination of mediastinal lymph node biopsy specimens showed infiltration of eosinophils and plasma cells. The adenopathy resolved after treatment with corticosteroids. This case shows that allergic bronchopulmonary aspergillosis might be accompanied by true adenopathy. We report a similar case with both hilar and mediastinal lymphadenopathy. A 19-year old man presented in 1986 with wheezing, coughing of yellow sputum, and weight loss. He had never smoked tobacco or marijuana. The symptoms appeared to have started in 1972 and were slowly progressive. The chest roentgenogram showed infiltration of the right lower lobe and bronchopathy of the lingula but no signs of adenopathy. Laboratory tests confirmed the diagnosis of allergic bronchopulmonary aspergillosis. In 1990, the patient returned with the same complaints and a total IgE of 16.993 IE/L and a blood eosinophil count of 0.645 x 109/L. His specific IgE antibodies against Aspergillus fumigatus were RAST class 4 (Phadebas), and specific IgG antibodies were 113.0 E/mL by enzyme-linked immunosorbent assay. The Ouchterlony precipitation test showed one line and one band. The chest roentgenogram showed bronchopathy of the lingula, infiltration in the right upper lobe and hilar and superior mediastinal lymphadenopathy. Pulmonary function tests showed obstruction without restriction and a normal diffusion capacity. The levels of angiotensin-converting enzyme and lactate dehydrogenase were normal. A bronchoscopy with bronchoalveolar lavage revealed the classical picture of allergic bronchopulmonary aspergillosis, with brownish-yellow plugs in segmental bronchi. Because of severe hyperemia of the mucosa, we decided not to take transbronchial biopsy specimens. Cultures of the plugs showed A. fumigatus. The bronchoalveolar lavage fluid had normal cell counts and the following differential: lymphocytes, 6%; macrophages, 51%; eosinophils, 13%; and neutrophils, 30%. The patient was treated with prednisone, 1 mg/kg body weight per day for 4 months, after which the lymphadenopathy and infiltrates disappeared. Pulmonary function returned to
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normal. His total IgE decreased to 3340 IE/L, and the specific IgE count returned to class 0. We conclude that, although it happens rarely, allergic bronchopulmonary aspergillosis can be associated with hilar as well as with mediastinal lymphadenopathy. Paul M. van den Berg, MD Henk C. Hoogsteden, MD University Hospital Rotterdam 3015 GD Rotterdam The Netherlands
ation of interferon therapy (4). Whether the nephrotic syndrome in that case was secondary to the myeloma and would have improved with further treatment is by no means clear (5). This case emphasizes the potential nephrotoxicity of interferons and suggests that close monitoring for the development of proteinuria is essential, regardless of the dose. Kenneth S. Weiss, MD Kaiser Permanente Medical Center Cleveland, OH 44130
Reference 1. Hantsch CE, Tanus T. Allergic bronchopulmonary aspergillosis with adenopathy. Ann Intern Med. 1991;115:546-7.
In response: We appreciate both letters about our case report (1). Computed tomographic (CT) scan images were not published because of space limitations. The CT scan of the chest obtained at that time exhibited extensive hilar masses consistent with adenopathy. Visualization of the central bronchi revealed no intraluminal mucus collection; therefore, no evidence of pseudohilar adenopathy was seen. Although the adjacent mediastinum was partly obscured by the hilar densities, the mediastinum also appeared to have significant adenopathy. This observation was later confirmed by mediastinoscopy and node biopsies. As Dr. Mann noted, the hila themselves are inaccessible via this surgical procedure. However, radiologic and surgical mediastinal findings combine to provide convincing evidence of extensive adenopathy extending from the mediastinum to the hila. We agree with the assessment of Drs. van den Berg and Hoogsteden that, although it happens rarely, adenopathy can accompany allergic bronchopulmonary aspergillosis. Tonny Tanus, MD Christina E. Hantsch Evanston Hospital and Northwestern University Evanston, IL 60201 Reference 1. Hantsch CE, Tanus T. Allergic bronchopulmonary aspergillosis with adenopathy. Ann Intern Med. 1991;115:546-7.
Nephrotic Range of Proteinuria and Interferon Therapy To the Editors: Nephrotic range proteinuria is a well-documented side effect of recombinant gamma interferon and all other interferons (1-3). The doses reported to cause this effect have been in the range of 0.25 mg/m2 to 1 mg/m2 body surface area (activity, 1 x 107 units per milligram of protein). I report a case of nephrotic-range proteinuria in a patient receiving therapy at a much lower dose. A 64-year-old man had wide excision and skin grafting for a Clark level-IV (11.2 mm-thick) malignant melanoma on his midback. He soon thereafter developed axillary adenopathy, consistent with metastatic melanoma. He agreed to participate in the Eastern Cooperative Oncology Group Protocol EST 4687, a phase-II trial of recombinant gamma interferon in malignant melanoma. He was randomly assigned to the first arm of the protocol and received gamma interferon, 0.01 mg/m2, as an intravenous infusion three times per week. Although the patient tolerated treatment quite well, urinalysis revealed 4+ proteinuria after 4 weeks of treatment and treatment was stopped. A 24-hour urine collection showed normal creatinine clearance but nephrotic-range proteinuria of 8.45 g. Ultrasound of the kidney, computed tomographic scan of the abdomen, complement studies, and antinuclear antibodies (ANA) all had negative results. A repeat 24-hour urine collection snowed a nephrotic-range proteinuria of 8 g. One week later, the proteinuria had resolved. Proteinuria has been reported to develop with doses of gamma interferon as low as 0.25 mg/m2 (activity not indicated) but with no indication of a nephrotic-range proteinuria. We have encountered only one case of the nephrotic syndrome during treatment with lymphoblastoid interferon A, in a patient with multiple myeloma whose proteinuria worsened with initi-
References 1. Bennett C, Vogelzang N, Ratain M, et al. Severe toxicity (r-Ifn gamma) phase I trial of vinblastine (VLB) and recombinant gammainterferon. Proc ASCO. 1986;5:223. 2. Sriskandian K, Garner D, Watkinson J, et al. A toxicity study of recombinant interferon gamma given by intravenous infusion to patients with advanced cancer. Cancer Chemother Pharmacol. 1986; 18: 63-8. 3. Garnick MB, Reich SD, Richie JP. Phase I/I I study of interferon gamma (Immuneron) in advanced renal cell carcinoma (RCC) [Abstract]. J Urol. 1986;135:166A. 4. Selby P, Kohn J, Raymond J, et al. Nephrotic syndrome during treatment with interferon [Letter]. Br J Med. 1985;290:1180. 5. Sriskandian K, Tee DE, Pettingale KW. Nephrotic syndrome during treatment with interferon. Br Med J. 1985;290:1590-1.
Crimson Crescents—A Possible Association with the Chronic Fatigue Syndrome To the Editors: Approximately 80% of patients with the chronic fatigue syndrome, as defined by the Centers for Disease Control (1-3), seen in the Winthrop-University Hospital Chronic Fatigue Syndrome Center, have a peculiar purplish discoloration of both anterior pharyngeal pillars. The crescents are an intense crimson color and are well demarcated along the margins of both anterior pharyngeal pillars. They are not associated with pharyngitis or discoloration of the posterior pharyngeal pillars or uvula or accompanied by either anterior or posterior cervical adenopathy. In patients without tonsils, the crimson crescents assume a posterior position in the oropharynx. This appearance is most closely associated with high IL-2 receptor levels in our patients. The patients do not complain of a sore throat, but, occasionally, they complain of a sore neck anteriorly above the thyroid gland. The "crimson crescents" gradually fade over a period of 3 to 6 months, as the patient's condition improves, and eventually become indistinguishable in color from the normal oropharyngeal mucosa. We suggest that studies of the chronic fatigue syndrome systematically evaluate the possible association between these crimson crescents and the syndrome. Burke A. Cunha, MD Winthrop-University Hospital Mineola, NY 11501 References 1. Komaroff AL, Buchwald D. Symptoms and signs of chronic fatigue syndrome. Rev Infect Dis. 1991;13(Suppl 1):8-11. 2. Holmes GP. Defining the chronic fatigue syndrome. Rev Infect Dis. 1991;13(suppl l):53-5. 3. Klein NC, Cunha BA. Chronic fatigue syndrome. Infect Dis Practice. 1991;15:1-7.
Improving Cardiac Resuscitation in the Community To the Editors: I read with interest and emotion Dr. Cleaveland's description (1) of his failed attempt at out-of-hospital cardiopulmonary resuscitation (CPR). In the past 5 years, I have twice provided CPR to pedestrians who revived and returned to full neurologic function. Both incidents occurred near a health care facility, decreasing the delay in the arrival of equipment for definitive care (defibrillation, intubation, and intravenous access). In Dr. Cleaveland's case, supplemental oxygenation was delayed for 20 minutes and definitive care technology arrived even later. Despite adherence to American Heart Association resuscitation protocol, the patient died.
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The greatest predictor of survival in patients with cardiac arrest (from ventricular fibrillation or pulseless ventricular tachycardia) is the length of time to the onset of CPR and to the onset of definitive care (2). If the delay in definitive care is much longer than 8 minutes, the chance for meaningful survival is small. The use of CPR can " b u y " minutes by providing a modicum of cardiac output. One response to this problem is to deploy automatic external defibrillators at sites of large public gatherings. These devices are designed to read cardiac rhythms and to deliver defibrillations, when appropriate, without the assistance of trained personnel. The leads are easily placed by laypersons, and the machines are able to read cardiac rhythms with a sensitivity of more than 90% and a specificity of more than 95% (3). Moreover, safeguards prevent inadvertent or malicious shocking of persons who are not suffering ventricular fibrillation or ventricular tachycardia. At the 1986 Vancouver World's Exposition, Weaver and colleagues (4) trained security personnel to use these tools, and two lives were saved. Had such a device been available to Dr. Cleaveland, his patient might have had a reasonable chance of surviving. These defibrillators could be placed in easily identifiable locations behind alarmed glass windows, as fire extinguishers are. People could be trained in their use during standard CPR courses. The question of who is to pay for such equipment remains problematic. When a patient asks a physician for suggestions on how to advance medicine, he or she should be told that donating an automatic external defibrillator would make an excellent contribution to any community. Neil A. Solomon, MD Hospital of the University of Pennsylvania Philadelphia, PA 19104 References 1. Cleaveland CR. CPR. Ann Intern Med. 1991;115:570-1. 2. Weaver WD, Cobb LA, Hallstrom AP, et al. Factors influencing survival after out-of-hospital cardiac arrest. J Am Coll Cardiol. 1986; 7:752-7. 3. Atkins JM, Streiger HM, Burstein TL, et al. Improved survival rates with automatic defibrillators. Prehospital Disaster Medicine 1989;4: 69. 4. Weaver WD, Sutherland K, Wirkus MJ, Bachman R. Emergency medical care requirements for large public assemblies and a new strategy for managing cardiac arrest in this setting. Ann Emerg Med. 1989;18:155-60.
In response: Dr. Solomon presents several important points. The chief deterrents to the placement of automatic external defibrillators are the cost of the equipment and unsettled issues of liability. A semi-automatic external defibrillator costs $7000. In Pennsylvania, under existing law, who would be empowered to apply and to use the devices is uncertain. Perhaps the most useful and cost-effective interim strategy would be to establish centralized first-aid stations, with personnel who are fully trained in cardiopulmonary resuscitation, in shopping malls. Clifton R. Cleaveland, MD American College of Physicians Philadelphia, PA 19106-1572
To the Editors: I would like to report three kinds of unexpected problems that patients have encountered in trying to complete advance directives. Some elderly patients lead very isolated lives and are unable to identify a trusted confidante whom they are willing to designate with a durable power of attorney. The second is a bit more puzzling. Several patients have been unwilling, apparently due to embarrassment, to ask their neighbors simply to witness either a living will or a durable power of attorney. They seem to feel that discussing plans for their dying with neighbors and friends would be an
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Thomas E. Finucane, MD The Johns Hopkins University Baltimore, MA 21205 Reference 1. Greco PJ, Schulman KA, Lavizzo-Mourey R, Hansel-Flaschen J. The Patient Self-Determination Act and the future of advance directives. Ann Intern Med. 1991;115:639-43.
To the Editors: Advance planning for health care in case the patient becomes unable to make decisions is a complex and sensitive process, the core of which should occur between the patient and the primary physician. Greco and colleagues' suggestion (1) that health insurance agencies become involved in the process of providing for advance directives was shocking. Expecting insurance agencies to resist the temptation of providing cheaper policies to those who have advance directives to forgo life-sustaining care is naive. Subscribers would be correctly offended and suspicious of finding information or questions about advance directives from insurance agents. Access to affordable health policies is already inequitable without adding this to the risk assessment factors used by insurance agencies. There are also enough barriers to making advance directives without adding legitimate reasons to existing suspicions among potential users. Greco and colleagues' endorsement (1) of discussions about advance directives with lawyers was also distressing. Although most patients acquire their documents through lawyers, advance directives are fundamentally a clinical issue. Lawyers have a limited role, which is to advise the client of constitutional and common law rights and of statutory limitations that apply. They should then refer the client back to the physician. Advance directives have risks as well as benefits. We believe that among the most important safeguards against the risks is a good process of advance planning. The cornerstone of this process must be a physician-patient dialogue within a trusting relationship. Involvement of insurance companies and undue involvement of lawyers is all too likely to undermine that cornerstone and, by promoting misunderstandings and misuse, to lead to undesirable outcomes. Linda L. Emanuel, MD, PhD Massachusetts General Hospital Boston, MA 02114
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impropriety. Finally, spouses or adult children may decline to be designated as agent because, " I can't be the one who pulls the plug." Specific contingency planning for all of the many ways in which a person may be ill and for all of the treatments that might conceivably prolong life is difficult or, in many cases, impossible. The Maryland attorney general has indicated that he will consider a note that is signed by the physician, that is placed in the patient's medical record, and that documents advance directives to be "dispositive." This is a useful and important vehicle for establishing advance directives. For patients who lack advance directives, I agree with Greco (1) that policy "should be designed to promote the patient's best interest," and that it should not be dictated by fear of a morally dogmatic minority.
Ezekiel Emanuel, MD, PhD Dana Farber Cancer Institute Boston, MA 02115 Reference 1. Greco PJ, Schulman KA, Lavizzo-Mourey R, Hansen-Flaschen J. The Patient Self-Determination Act and the future of advance directives. Ann Intern Med. 1991;115:639-43.
In response: Dr. Finucane describes three of the many obstacles that may be encountered in the preparation of advance directives. We might add statutes and institutional policies that
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prohibit the attending physician, hospital employees, or family members from serving as witnesses for these documents (1). We hope that the educational efforts prompted by the Patient Self-Determination Act will reduce the resistance of neighbors, friends, and (when legally permissible) family to participating in this process (2). For some people, involving an attorney or a notary public may be a solution. The idea of health insurers inquiring into and offering information about advance directives is not ours; the Patient SelfDetermination Act mandates that health maintenance organizations do precisely that. Our proposal—that all insurers be subject to this requirement—is designed to increase public knowledge about advance directives before hospitalization. Many advance directive statutes prohibit insurers from requiring an advance directive as a condition of health insurance (1); pending legislation in Pennsylvania would also prohibit insurance discounts for those with advance directives. Where such safeguards do not exist, we reiterate that it would be inappropriate for insurers to require advance directives as a condition of insurance. We agree that advance planning for health care should ideally take place in the context of a trusting relationship between doctor and patient. However, many people do not have a primary care physician, and many physicians are not yet comfortable discussing these issues. We also agree that advance directives are primarily clinical documents. They are designed to be read, interpreted, and implemented by physicians. However, this does not mean that attorneys have no role in the preparation of these documents. Our attorney colleagues tell us that clients who prepare standard wills or durable powers of attorney are extremely receptive to discussing and preparing
medical advance directives at the same time. Only sometimes will this necessitate a conversation with the physician. Peter J. Greco, MD, for all of the authors (2). References 1. Society for the Right to Die. Handbook of Living Will Laws. New York: Society for the Right to Die; 1987:31-134. 2. Greco PJ, Schulman KA, Lavizzo-Mourey R, Hansen-Flaschen J. The Patient Self-Determination Act and the future of advance directives. Ann Intern Med. 1991;115:639-43.
Is Subspecialty Training Financially Worthwhile? To the Editors: I would like to comment on the article on subspecialty training (1). As a practicing internist for approximately 35 years with a multisubspecialty group, I can testify that your estimates are quite correct. Invasive cardiologists, followed by hematologist-oncologists, gastroenterologists, pulmonologists, and nephrologists, are the largest beneficiaries of the additional 2 years of training. General internists, followed by rheumatologists, infectious disease specialists, and endocrinologists, benefit least. Training general internists at least in such procedures as colonoscopy would not only help financially but also would aid in routine screening for colonic polyps. Alexander B. White, MD Olympia Fields Internal Medicine Associates, S.C. Olympia Fields, IL 60461 Reference 1. Prashker MJ, Meenan RF. Subspecialty training: is it financially worthwhile? Ann Intern Med. 1991;115:715-9.
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