COMMENTS AND CORRECTION
Comments submitted for publication must be typed doublespaced, and text length must not exceed 500 words. Complete references must be furnished, as specified in "Information for Authors" (page 1-6). Specific permission to publish should be appended as a postscript. Publication depends on availability of space: we give preference to comment on recent content and to new information. Letters for this section should be concise—the Editor reserves the right to shorten them and make changes that accord with our style. Care for the Homebound Aged TO THE EDITOR: Dr. Brickner and colleagues deserve great credit for the work they have done in providing for the needs of homebound elderly in New York City ( 1 ) . Although the services are provided through a hospital-based program, that program is apparently not part of a home health agency, certified by the Social Security Administration. This would account for the inability of the hospital to bill for some of the services being provided to the aged. This point is of particular interest to us. Certified agencies, following Medicare regulations for reimbursement, cannot meet the total needs of the aged. The home care program at Sinai Hospital of Baltimore is now in its 14th year and is one of only five hospital-based certified home care programs in Maryland. By being certified, the program can bill for certain reimbursable services provided to covered patients. The patients, however, must be selected with great care if the program expenses are to be met. To more clearly illustrate the problem that faces a hospital-based home care program that must make its books balance, we would like to show what would have happened if the three patients who were described in the article had been referred to our agency for care. In each case, because of the patient's age, we assume that the patient has Medicare A and B. Patient 1, with severe chronic obstructive pulmonary disease and cor pulmonale, would have been acceptable to Medicare for home care reimbursement because of the clearly medical nature of acute respiratory failure. Nutritional counseling and management would have been reimbursable only as a supportive measure for the treatment of the acute respiratory problem. Once the patient's condition had become "stabilized," maintenance care would have been considered the responsibility of the patient, and his coverage for home care by Medicare would have ceased. If the patient's condition then deteriorated at home, and he became acutely ill once again, he would have become eligible for home care benefits. After "stabilization" the activities of our agency vis-a-vis the patient would have ceased. Patient 2 would have been acceptable for home care benefits under Medicare because of the massive fluid retention secondary to heart failure. Again, however, once her acute medical problem had improved, she would no longer be able to receive services with Medicare reimbursement. Our agency social worker, who would have been working with the patient in assisting her to return to an independent life, would have had to leave the case once the medical condition had improved.
In describing patient 3, who had severe osteoarthritis, Brickner made the comment "the medical issues in this case are not complex." In order to protect the patient and our agency, we make every effort to insure that the medical problems are complex or serious enough to require skilled nursing care or physical therapy before accepting the patient. For this patient to qualify under Medicare, we would have had to show that the patient needed either physical therapy, which would have contributed to the patient's rehabilitation, or skilled nursing services to monitor the patient for drug side effects while she was being treated for her hypertension. Emphasis on this patient's social needs in the Medicare reimbursement form is a sure way to have the bill rejected. In any case, once the patient had become stable, she would no longer have been eligible for home care benefits under Medicare. At the end of their acute care episodes, all of these patients would have been discharged from our home care program. This has, in fact, happened to many patients for whom we have provided services and has caused enormous problems to these patients, who have continuing needs for supportive services. Recently we received Title III funds from the Baltimore City Commission on Aging, which we are using to pay for services after Medicare eligibility ends. We have no assurance that this funding will continue. Eligibility for home health services should not be limited to only those aged who qualify for skilled care. Dr. Brickner's article once again points out our lack of national policy for long-term care that is comprehensive, coherent, and attentive to the needs of older Americans. JOSEPH I. BERMAN, M.D., M.P.H. MORRIS OSTROFF, M.D., M.P.H.
Department of Community Medicine Sinai Hospital of Baltimore, Inc. Baltimore, Maryland 21215 REFERENCE
1. BRICKNER PW, DUQUE T, KAUFMAN A, et al: The homebound
aged. A medically unreached group. Ann Intern Med 82:1-6, 1975
TO THE EDITOR: In many hospitals, including those affiliated with universities, chronic disabling diseases, advancing years, and patient-compliance problems elicit an automatic reflex—"nursing home placement." For the past 9 months we have been fortunate to be one of several VA hospitals funded for a multidisciplinary home care unit. To date our experiences have paralleled Dr. Brickner's (Reference 1 above); that is, home care appears to save nursing home funds, improve accessibility to health care for the disabled, promote patient emotional health, and often accomplish medical therapeutic goals that hospitals, nursing homes, and clinics have failed to achieve. The next issue to examine is whether these health care gains can be measured in other than financial terms and can show a significant improvement over the outcome of nursing home care. Certainly, there can be little that is more dehumanizing and demoralizing to a patient inflicted with a severe illness than to be exiled from his own home. In answer to the editorial comment by Somers and 717
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Bryant (Ann Intern Med 82:111-112, 1975) that questioned which hospital department should assume home care responsibility, we feel that the logical function for a home care unit is as an activity of a hospital-based model primary care practice in those hospitals with housestaff training programs. With role models and practice examples to emulate in such a setting, perhaps the next generation of primary care physicians will be more inclined to seek care for the elderly and disabled in their own homes. JAMES W. HAINER, M.D. SANDRA KING, R.N.
Medical Comprehensive Care Unit Seattle Veterans Administration Hospital Seattle, Washington 98108 TO THE EDITOR: I read with mixed emotions the lead article by Brickner and associates (Reference 1 above). On the one hand, I was pleased that these authors and their hospital undertook such a meaningful project and, on the other hand, I was chagrined after a few of my simple mathematical calculations placed the study in a more realistic perspective. In 16 months, 620 home visits were made for a rough average of fewer than 1.3 "house calls" per day. My father, a general practitioner (or "family physician") in Ohio, probably doubled or tripled that average over the last 30 years. Too bad he didn't write up his experience for our journal. My emotions remained mixed on reading the editorial by Somers and Bryant in the same issue (Ann Intern Med 82: 111-112, 1975). As a practicing chest specialist, I must admit to a daily house call average far below that of my father and of Brickner and associates. I must agree (with a certain amount of guilt) with the statement that "most physicans are not interested in chronic illness, most are not interested in home care. . . . " Somers and Bryant offer some possible solutions to the present dilemma. I would add another. Why not require that each and every graduating medical student spend 6 to 12 months providing home care for the aged as a part of his or her training experience? Every student of medicine is aware of the requirements for becoming a physician: premedical, medical school, internship, residency; the period of training is being shortened by 3-year medical schools, straight internships, and similar changes. Could anyone subscribing to the Hippocratic oath object to the addition of a period of providing home care medicine to his or her training program? And would not such a period of training provide future hospital-based specialists with a much better understanding and appreciation of the role of the primary care physician in the community? My father and many family physicians like him may have missed an opportunity to write the lead article in the Annals; the internists of today, those of us who read this journal, must not miss the opportunity to provide an answer to the question posed by Somers and Bryant: "For whose benefit are we operating our $100 billion a year healthcare economy"? FREDERICK R. BODE, M.D., LT COL, USAF, MC
Wilford Hall USAF Medical Center (SGHMP) Lackland Air Force Base, Texas 78236 Recertification TO THE EDITOR: I took the Recertification Examination 718
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because, with all the talk of recertification in the air, this seemed to be the only concrete thing to do, better than getting various credits for meetings attended. I also wanted to force myself to review the entire field of internal medicine. This worked, illustrating Jung's principle that "need is a better incentive than desire." I read the American College of Physicians' Self-Assessment Syllabus, bought a new Harrison, and checked out a few difficult questions with subspecialist friends. The syllabus is superb and was enjoyable reading. Because of the preliminary announcement that the Examination would be based on it, and perhaps 70% of the questions were, the procedure was eminently fair and amazingly free from ambiguity. The examination showed much care and thoughtful writing. Was it representative of what internists do in practice? The answer is assuredly, "No." Although several questions did go to the heart of internal medicine (A6, 35, 36, 39, 52-54, 59-62, B18, 19, 40), many showed narrow specialty interests (A55-58, 67-70, 93-95, B17, 42, 117), and quite a few had to do with points a conscientious physician would look up, rather than consult a faulty memory (A28, B12,17, 48, 60-64). I would have preferred more questions on more relatively common situations on the ward or in the office that clinically call for quick decisions where it is awkward to look up information or ask colleagues; for example, about disturbances of electrolytes or blood gases, abnormal biochemical data, or hemograms, rather than problems with rare diseases, about which we undoubtedly would get consultation (B93, 98, 99, 123) or even schedule a case for grand rounds, if one ever turned up (B5, 33, 37, 98, 99, 105). Perhaps a good internist should know more than he can use—after all he is to some degree a scholar—but our chief value to our patient is the ability to make decisions. To store and retain for any length of time the amount of information this examination covers is not compatible with an active life in practice and the committee activities in which most of us are engaged. To know all this material suggests either getting the constant reinforcement that occurs in a medical school setting—where it is highly appropriate—or a preoccupation with literature at the expense of action—and that is not so good. Despite all these second thoughts, I found the entire exercise highly beneficial and more valuable than the Merit Project, which was more representative of what I do but did not make me study and learn. I hope to have the strength to do it again in 7 years. R A L P H O. WALLERSTEIN, M.D.
3838 California Street San Francisco, California 94118
Alcoholism: A Disease? TO THE EDITOR: The dispute about alcoholism being a "disease" may result in severe harm to thousands of patients. Classifications are not necessarily "true"; they should be pragmatic. A block of wood may be equally classified as a piece of fuel, a botanic specimen, a chemical specimen, a weapon, or a work of art. It is all of these, and pragmatic reasons will tell us how to classify it at any time. If alcoholic persons can be treated—and I shall describe how they can—in hospitals, by doctors, nurses, psychologists, social workers, counselors, pharmacies, and clinics,
and if they can be restored, in many cases, to a normal and happy life, then alcoholism must be considered a disease. The program at this hospital is duplicated, with variations, in many others, but our treatment is based on the disease concept and is highly effective. If by "effective" we mean a marked decrease in psychological and physical disabilities and a restoration to fairly normal life circumstances, then our Detoxification Section (for treatment of the alcoholic withdrawal syndrome) is 100% effective. After detoxification all patients are offered an intensive 7 to 10 days of orientation and education. This is also offered to all other newly admitted patients and consists of films, videotapes, discussions, lectures, talks, counseling, medication, exposure to Alcoholics Anonymous, and printed material. At this point some individuals become outpatients, and others remain for weeks of rehabilitation. Our statistics for the longer term rehabilitation are incomplete, but we have many records of patients in whom we can point to excellent work rehabilitation, restoration of broken marriages, economic success, psychological improvements, and restoration to a normal and healthy existence. Judging from the long destructive histories of alcoholism given by most of the patients who have come into our program, we believe that without using this medical model such results would not have been achieved. In the January 1975 issue (Ann Intern Med 82:116119) were several letters which suggested that the alcoholic person often rejects treatment. Nevertheless, with the record of success that I have described above, every physician should do his best to get alcoholic patients motivated. This might be best done by seeing that every hospital has a small team concerned with alcoholism. This team could be composed of four or five people, not necessarily physicians, and could include one or more Alcoholics Anonymous members, who would make known to the patients what facilities are available in the hospital or in the community. The large number of applicants we have suggests there are thousands and thousands of alcoholics who do want treatment sooner or later. Throughout these letters runs the feeling on the part of the doctors that they will be "blamed." Because cancer, emphysema, arteriosclerosis, schizophrenia, and practically all other chronic illnesses are incurable, in most cases, or frequently relapse, should we stop practicing medicine? The physician is not more responsible for his alcoholic patient who drinks than for his diabetic patient who violates his diet or insulin needs. We do not care what name you use for alcoholism (although I do consider it a disease), but every physician is obliged to offer each patient some treatment. E M I L ROTHSTEIN, M.D.
Veterans Administration Hospital Brockton, Massachusetts 02401
Group-Y Meningococcal Disease TO THE EDITOR: The article "Group-Y meningococcal disease" by J. D. Smilack in the December issue (Ann Intern Med 81:740-745, 1974) was read with interest. Two cases of pneumonia occurred among 12 cases of group-Y meningococcemia. I wish to present briefly our experience with pneumonitis among cases of group-C meningococcemia seen at Madigan General Hospital during 1969. These data were presented at the VA Armed Forces Pulmonary Disease
Research Conference in Cincinnati in 1970 and have not been published. Ninety-four cases of meningococcal disease among recruits were documented by either blood culture or cerebrospinal fluid culture. Admission chest roentgenograms from those 94 patients showed 8 (8.5%) to have evident pulmonary infiltrates. Neisseria meningitidis was cultured from the blood in 5 of these cases, and the other 3 cerebrospinal fluid cultures showed positive results, but the blood culture did not grow that organism. In a single patient the blood culture, the cerebrospinal fluid, and the sputum all grew Neisseria meningitidis. There was 1 patient with group-B meningococcal disease. In some of the patients, Diplococcus pneumoniae or Klebsiella organisms were recovered from the sputum. Each of the 8 patients with pneumonia were hypoxic at the time of admission to the hospital. There were also no deaths among the 8 patients with pneumonitis. In the larger group of 94 patients there were five deaths. It seemed reasonable to us to conclude that pneumonitis was surprisingly common among patients with acute meningococcal disease due to group C, and that, in most of these cases, the pneumonitis was likely due to the meningococcal organism. It would seem that the presence of pneumonia in acute meningococcal disease does not worsen the prognosis. It also would seem that the frequency of pneumonia among cases of acute meningococcal disease of group C does not differ substantially from the frequency of pneumonia in group-Y meningococcal disease. MARK E. REINECKE, M.D.
Marshfield Clinic Marshfield, Wisconsin 54449 In comment: Dr. Reinecke's observations are of interest and confirm those of others cited in my paper. I should mention that three cases of primary meningococcal pneumonia were described, two in the main text and one in the addendum. It is not clear whether the meningococcus was the etiologic agent for pneumonitis in the cases cited by Dr. Reinecke; nor is it stated which of the eight patients with pulmonary infiltrates had clinical evidence of central nervous system infection. It seems likely that a high risk of aspiration pneumonia might exist in the patient with meningitis or meningoencephalitis; viral or mycoplasmal pneumonia might accompany meningococcal infection. Young and colleagues (1) have suggested that influenza viral infection might predispose to meningococcal disease. In the series of patients with group-Y meningococcal infection that I reported, the three patients with pneumonia had no obvious extrapulmonary focus. Although small numbers are involved, comparison with other series suggested a disproportionately high prevalence of primary pneumonia in our patients with group-Y disease. It is unfortunate that prospective studies addressed to the question of the incidence of primary meningococcal pneumonia are lacking. Parenthetically, I wish to add that Risko and Hodges (2) have noted an increasing incidence of group-Y meningococcal infection in a naval training center; none of their six patients had pulmonary involvement. JERRY D. SMILACK, M.D.
Infectious Disease Laboratory Comments and Corrections
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The Methodist Hospital Houston, Texas 77025
REFERENCES
1. WEAVER GH: Diphtheria carriers. JAMA 76:831-835, 1921 2. MILLER LW, BICKHAM S, JONES WL, et al: Diphtheria carriers
REFERENCES
1. YOUNG LS, LAFORCE FM, HEAD JJ, et al: A simultaneous out-
break of meningococcal and influenza infections. N Engl J Med 287:5-9, 1972 2. RISKO J A, HODGES GR: Neisseria meningitidis serogroup Y: incidence and description of clinical illness. Am J Med Sci 261: 345-352, 1974
and the effect of erythromycin therapy. Antimicrob Agents Chemother 6:166-169, 1974 3. DOULL J A, LARA H: The epidemiologic importance of diphtheria carriers. Am J Hyg 5:508-529, 1925 4. MILLER LW, OLDER JJ, DRAK J, et al: Diphtheria immunization:
effect upon carriers and the control of outbreaks. Am J Dis Child 123:197-199, 1972 In comment:
Diphtheria Carriers TO THE EDITOR: McCloskey and colleagues reported in the December 1974 issue (Ann Intern Med 81:788-791, 1974) their experience in the treatment of a large number of Cory neb acterium diphtheriae carriers. Although I agree with the need to treat carriers and the recommendation that erythromycin be the preferred antibiotic, I feel it is important to mention several problems related to the C. diphtheriae carrier state and the evaluation of its treatment. McCloskey and associates stated that treatment of diphtheria carriers is superior to no treatment because one Russian report showed that only 12% of carriers become C. diphtheriae-negativQ when followed for 1 month. However, there is evidence from the literature during the preantibiotic era that 50% of carriers became culture-negative within 10 days of their discovery, and 8 1 % were culturenegative by 1 month ( 1 ) . Another problem with rationalizing therapy of carriers on the argument that therapy renders a much larger percentage of carriers culture-negative than no therapy is that success in therapy, as in McCloskey's paper, is usually based only on follow-up cultures 1 and 2 days after therapy. Because this is usually 8 or 9 days after identification of the carrier, little is known about the culture status of treated carriers at 1 month. We observed 72 diphtheria carriers treated with erythromycin and found a 9 9 % "success rate" 1 and 2 days after therapy. However, reculture 2 weeks later showed that 15% had relapsed to the carrier state. Comparison of our observation with information from the preantibiotic era showed no significant difference in the proportion of carriers culture-positive 25 days after their identification ( 2 ) . What then is the value of treating carriers? There are two major reasons: [1] treatment renders diphtheria carriers culture-negative within 48 hours (2) and thus reduces the carrier's risk of becoming a symptomatic case and [2] because carriers are responsible for the transmission of the majority of cases of symptomatic diphtheria in a community ( 3 ) , treatment of carriers reduces the spread of disease and helps to control outbreaks ( 4 ) . Because carrier relapse has been documented as a problem, it is important that we do not delude ourselves by assuming eradication of the carrier state when cultures are negative 1 and 2 days after therapy. Follow-up cultures 2 to 3 weeks after therapy are needed in order to assure eradication of the organism. Evaluation of drug therapy should be based not only on the results of cultures taken immediately after therapy, but also on cultures taken to identify relapses 2 or more weeks after therapy. Louis W. MILLER, M.D.
Department of Social and Preventive Medicine University of Maryland School of Medicine Baltimore, Maryland 21201 720
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The group investigating the outbreak of diphtheria in San Antonio followed Dr. Miller's experiences in the Elgin, Texas, outbreak with interest. We hold that diphtheria carriers should be treated with erythromycin for the same two reasons stated clearly by Dr. Miller. We stated that all treatment regimens are associated with some failures, and we are not surprised that as many as 15% of carriers may have relapsed (or may have been reinfected) when recultured 2 or 3 weeks after treatment was stopped. Because there is some evidence that newer phage types of Cory neb acterium diphtheriae were involved in the Texas outbreak ( 1 ) , comparison of posttreatment results with preantibiotic era studies may not be valid—a criticism that may be applied to our studies, as well as to Dr. Miller's reports. RICHARD V. MCCLOSKEY, M.D.
Albert Einstein Medical Center Daroff Division Philadelphia, Pennsylvania 19147 REFERENCE
1. MCCLOSKEY RV, SARAGEA A, MAXIMESCU P: Phage typing in
diphtheria outbreak in the Southwest 1970-71. J Infect Dis 126: 196-199, 1972
Immune-Complex Disease in Typhoid Fever TO THE EDITOR: During an episode of typhoid fever, a patient developed transient proteinuria, microscopic hematuria, as well as urinary hyaline and granular casts and pericarditis. Concurrent low complement levels suggested that these unusual manifestations were due to immunecomplex disease involving Salmonella antigens. A 23-year-old man became suddenly ill with diarrhea, vomiting, and fever. When admitted 7 days latter he had a temperature of 39 °C, the spleen tip was palpable, and on proctoscopic examination the mucosa was friable and hemorrhagic. Urinalysis showed proteinuria of 3.25 g/litre and the sediment contained erythrocytes as well as hyaline and granular casts. A urine culture showed negative results. Widal agglutination tests gave titers of 1:160 with O antigen and 1:40 with H antigen of Salmonella group A; as well as titers of 1:320 with O antigen and of 1:40 with H antigen of Salmonella group B. Seven days after first seen he developed jugular regurgitation and cyanosis. A pericardial rub appeared. Lupus erythromatosus cells and antinuclear antibodies were negative. Serum C3 was less than 28 mg/100 ml (normal, 80 to 120 mg/100 ml); the 50% hemolytic complement activity was 0.62 units (normal, 30 to 60 units). Salmonella typhi A was cultured from the feces. Blood cultures showed negative results. Despite trimethoprim-sulfamethoxazole treatment he developed severe melena that prompted surgery. The resected 70 cm of small bowel showed characteristic typhoid lesions. He recovered well after surgery. With chloramphenicol, the fever
and the pericardial rub disappeared, and urinalysis became normal and remained so. This patient was seen in 1972 when there was an epidemic of chloramphenicol-resistant salmonellosis in Mexico. However, the urinary and pericardial findings caused much diagnostic confusion. When it became evident that he indeed had typhoid fever, the urinary findings, pericardial involvement, and low complement were all attributed to immune-complex disease secondary to typhoid fever. The report by Sitprija and colleagues (Ann Intern Med 81:210-213, 1974) supports that contention. DONATO ALARCON-SEGOVIA, M.D., F.A.C.P. JORGE C. ALCOCER, M.D.
Department of Immunology and Rheumatology Instituto Nacional de la Nutrition Mexico 22, D.F., Mexico
Ethics in Vasodilator Therapy TO THE EDITOR: The article "Chronic Vasodilator Therapy in the Management of Cardiogenic Shock and Intractable Left Ventricular Failure" (Ann Intern Med 81:777-780, 1974) is an interesting, reasonably convincing demonstration of the effects of ventricular unloading on the management of left ventricular dysfunction. I am concerned, however, about an aspect of the paper somewhat removed from the scientific content and which, I believe, is an example of "ethical unloading." Having found both subjective and objective benefits of the therapy in this severely ill patient, I find it difficult to understand why after 6 months of therapy they elected to discontinue one aspect of the therapy, substituting a placebo drug (which must have been done without the patient's knowledge) while he was an outpatient and having him return 7 days later in "incipient pulmonary edema with diaphoresis, pedal edema, and a weight gain of 5 kg [11 lb]." On 2 December, 13 December, 19 December, 12 January, and 26 March, repeated studies had shown the efficacy of their therapeutic intervention, with evidence of rapid deterioration on discontinuation of this therapy. I would imagine that by this time the investigators had sufficient confidence in what they were doing, so that a 7-day interruption in therapy 6 months after its onset with the patient not under close observation seems hardly justified, especially when this modification in therapy was undertaken without the patient's knowledge and, by their own description, resulted in a life-threatening deterioration in the patient's condition. I can see no justification for this in the case report and would be interested in the authors' explanation. DAVID SHANDER, M.D., F.A.C.P.
General Rose Memorial Hospital 1050 Clermont Street Denver, Colorado 80220 In reply: Dr. Shander raises a moral issue pertinent to all therapeutic studies of new drugs. Investigators who assume the responsibility of testing new treatment regimens must design their experiments to minimize bias on the part of the physician or of the patient, while still protecting the patient from possible harm.
When a new and unapproved therapy is being evaluated, as in the use of nitrates to treat heart failure, the burden is on the investigator to prove that the treatment is beneficial when compared with conventional therapy. Uncontrolled observations are notoriously unreliable and have led in the past to enthusiasm for drugs that have subsequently been shown in carefully designed studies to be nonefficacious. It is most unusual for an investigator to be criticized for stopping an experimental drug and continuing conventional treatment for the disease. Only by this type of experimental design can the efficacy and safety of experimental drugs be proved in a relatively small number of people, so that the population as a whole will be exposed only to agents that are clinically useful. In the case under discussion, the placebo regimen was begun because two of the physicians assisting in follow-up of the patient expressed a reasonable doubt about the clinical efficacy of the nitrates. Therefore, we were not as willing as Dr. Shander to assume from our acute hemodynamic observations that long-term nitrate therapy was playing a vital role in the patient's management. A trial cessation of therapy can be justified not only on the basis of good investigation but of good clinical practice. Too many patients receive unnecessary but potentially toxic drugs because their physicians are loathe to withdraw them. The apparent demonstration of efficacy in our patient should not by itself convince anyone of the practical usefulness of the nitrates in the treatment of heart failure. It is highly unlikely that the Food and Drug Administration and the medical community would be swayed on the basis of our limited observations to approve and prescribe the nitrates for the treatment of all patients with severe heart failure. This therapy, therefore, should still be viewed as experimental, and further controlled studies must be carried out, even at the risk of withholding an effective treatment from some patients. JAY N. COHN, M.D.
Cardiovascular Division University of Minnesota Medical School Minneapolis, Minnesota, 55455
"Munchausen" Case TO THE EDITOR: Fialk and Murray (Ann Intern Med 8 1 : 562, 1974) and Sparandero (Ann Intern Med 82:123, 1975) have reported experiences with a patient having the prolapsing mitral valve syndrome and "Munchausen" syndrome. We have seen a patient, who is probably the same person, at our hospital and have uncovered records of at least 10 admissions to this and other hospitals in the Philadelphia-southern New Jersey area. The patient, a 28-year-old white man, was transferred to Thomas Jefferson University Hospital because of persistent chest pain. He stated that he was hospitalized in October 1973 because of an acute myocardial infarction. At that time cardiac catheterization in a United States Army hospital in Munich, Germany, showed "blockage of a coronary artery" and prolapse of the mitral valve. He was also told that he had Marfan's syndrome. He reported recurrent episodes of palpitations associated with syncope since the age of 16. Although his chest pain over the past 7 years had generally been precipitated by exertion and relieved by nitroglycerine, for the past 10 days he had had continuing chest discomfort at rest. It was described as substernal and pressurelike with radiation to the neck. Present medications included propranolol, digoxin, warfarin, and Comments and Corrections
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quinidine. The patient stated that he was a graduate student at Princeton University. Physical examination showed a white man with marfanoid measurements of the extremities. There was a high-arched palate, but no ectopia of the optic lens. The heart had a midto-late systolic murmur at the apex and along the left sternal border after a midsystolic click. Laboratory tests showed creatinine phosphokinase of 900 U/ml, although there was no elevation of lactic dehydrogenase or serum glutamic oxalacetic transaminase. The hemoglobin was 10.6 gm/100 ml and the hematocrit was 33%. Myocardial metabolic studies showed normal results, indicating that his chest pain was not due to coronary disease. Before further evaluation could be done, the patient signed out of the hospital, stating that he had to participate in rowing competition with the Princeton crew team in Switzerland. Subsequently obtained records from other hospitals showed admissions for multiple reasons, including decompression sickness and gastrointestinal hemorrhage secondary to aspirin or Coumadin ingestion, or both. This patient has become a medical economic factor in the Philadelphia, New York, and New Jersey area in his own right. The association of prolapsed mitral valve syndrome and neuropsychiatric disorders has been reported in the past ( 1 ) . This patient may be an example of a severe personality disorder with this cardiac disease. His case suggests again the potential hazards of multiple drug therapy, particularly with anticoagulants, in patients with apparent psychiatric disease. JUDITH M. DEGLIN, PHARM.D.
Department of Pharmacy STUART M. DEGLIN, M.D.
Department of Medicine Thomas Jefferson University Hospital Philadelphia, Pennsylvania 19107 REFERENCE
are in error, as 50 mg of calcium gluconate contains 4.5 mg of calcium, or 0.225 meq of calcium. Perhaps the metric system is not the panacea we are led to believe it is, and we must all double check to make sure we have our micrograms, milligrams, millilitres, and milliequivalents in the right place. ALAN W. H O P E F L , PHARM.D.
University of Michigan Medical Center Pharmacy Department Ann Arbor, Michigan 48104 In reply: Dr. Hopefl makes two points in his letter that warrant our comments. First, he states that mithramycin should not be considered the drug of choice in treating all hypercalcemias, as it has serious side effects other than the transient nausea and vomiting we mentioned. It would have been better if we had inserted the word "refractory" before hypercalcemia to exclude cases when the underlying cause can be treated (hyperparathyroidism, vitamin D intoxication, and so forth), or when a response can be obtained with more conservative measures, such as hydration, diuresis, corticosteroids, and oral phosphate preparations. Other side effects, which might have been mentioned, occurring with longer term mithramycin therapy include hemorrhage, at least in part due to depressed platelet counts, hepatotoxicity, nephrotoxicity, drug fever, dermatitis, and hyperuricemia. Dr. Hopefl has correctly observed that an error was made in the calculation of the milliequivalents of calcium in the calcium gluconate solution. The quantities of calcium gluconate in milligrams and grams were reported correctly, but the milliequivalents are erroneous. ROBERT D. LINDEMAN, M.D., F.A.C.P. SOLOMON PAPPER, M.D., F.A.C.P.
1. JERESATY RM: Mitral valve prolapse—Click Syndrome. Prog Cardiovasc Dis 40:623-652, 1973
Hypercalcemia and Hypocalcemia: Treatment TO THE EDITOR: The recent paper by Drs. Lindeman and Papper (Ann Intern Med 82:64-70, 1975) deserves correction on several points. A major error in the paper was in dosage of mithramycin, which was incorrectly given as 25 mg/kg body weight, when in reality it is 25 /xg/kg body weight (a thousandfold difference). The same error was again made a few lines later when the weekly dosage was given. I would hope that this was a printer's error, but, further, I also do not think that mithramycin should be considered the drug of choice for all hypercalcemia, as hinted at in the article, because of its serious side effects, which certainly lie beyond the transient nausea and vomiting stated in the article. The drug has its place in therapy, but it should only be used by those with experience in chemotherapy and when other more benign therapy has failed or is contraindicated. They also state in the section on hypocalcemia that a 10 ml ampule of 10% calcium gluconate contains 50 meq of calcium, when in reality it contains 4.8 meq of calcium (93 mg of calcium). Fifty milliequivalents of calcium would be equal to 1 g of elemental calcium, which would be contained in 10.7 g of calcium gluconate. The rate of intravenous infusion is later given correctly as 50 mg of calcium gluconate (0.5 m l / m i n ) , but the milliequivalents 722
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Veterans Administration Hospital 921 Northeast 13th Street Oklahoma City, Oklahoma 73104 The error in mithramycin dosage was pointed out in the March issue (p. 421).—The Editor
Dextran 40 TO THE EDITOR: We believe that the review article on dextran 40 by Data and Nies (Ann Intern Med 81:500504, 1974) deserves comments on the "paradoxes" reported by the authors from their selective review of the dextran 40 literature. Dextran 40 is neither an anticoagulant nor an antiplatelet agent. Because increased platelet aggregation, blood viscosity, and elevated plasma fibrinogen concentration may lead to disseminated intravascular coagulation or shock lung, or both, in severely traumatized patients ( 1 ) , many clinicians would regard decreased concentration of factors V, VIII, and IX (due largely to hemodilution) and decreased platelet adhesiveness (but not count) after dextran 40 infusion at the recommended dosage (1.5 g/kg body weight) to be most desirable in treatment of shock. At the above recommended dosage, bleeding time is not affected ( 2 ) , and postoperative bleeding is not increased
(3). Systemic bleeding complications, for example, gastrointestinal bleeding, are more evident (4), and dosage control is far more complex with warfarin compared with dextran 40. However, wound oozing after infusion with dextran 40, used experimentally for prophylaxis of postoperative thromboembolism, has been shown to be dosedependent and of minor clinical significance at the suggested investigational dosage—1000 ml on the day of surgery, starting intraoperatively, followed by 500 ml/day for the following 3 days, and 500 ml every other day thereafter until the patient is ambulatory*. No anaphylactoid reactions were reported when dextran was used in treatment of shock during the period 19551968. Review of our worldwide records on dextran 40 during the period 1962-1972 shows more than 15 million units of dextran 40 used with 49 reported cases of hypotension reactions in postoperative patients, which gives an incidence of one reaction per 300 000 bottles used. Most anuria secondary to shock is due to fall in arterial blood pressure and decreased plasma volume. Infusion with dextran 40 and adequate crystalloid solutions results in a spontaneous increase in urine output due to increased cardiac output, plasma volume, and renal perfusion ( 5 ) , unless there is preexistant renal damage. Dextran 40 does not interfere with blood typing and cross-matching unless the outdated enzyme method is used. As a general rule, however, it is recommended that blood samples for all laboratory studies (including blood bank) be drawn from the Emergency Room patient before any drug is given. The published reports on dextran 40 show that the benefits to the shock patient overwhelmingly exceed the risk of any adverse reaction. F o r investigational use in other indications, however, the attending physician must weigh the documented clinical benefit against the risk of using the drug for each clinical situation. ERICH F . SCHINAGL, M.D. RIDA A L I , PH.D.
Pharmacia Laboratories, Inc. 800 Centennial Ave. Piscataway, New Jersey 08854 REFERENCES
1. BLAISDELL RJ: Intravascular coagulation and pulmonary changes following shock and trauma, in Acute Fluid Replacement in the Therapy of Shock, edited by MALINEN TI, New York, Stratton Intercontinental Medical Book Corp., 1974 2. CRONBERG F, ROBERTSON B, NILLSON IM, et al:
Suppressive
We wish to comment on several points raised by Drs. Schinagl and Ali. First, the reference cited (3 above), stating that the bleeding time was unaffected at recommended dosage, deals with normal volunteers given a single dose and is not pertinent to what would happen on prolonged administration to the diseased patient. With continued administration, the larger molecular weight fragments would accumulate and probably would mimic the effect of higher molecular weight that dextrans did increase bleeding time. Second, the paper by Salzman and colleagues (Reference 4 above) does not indicate an increased bleeding with warfarin and states that "the four groups (warfarin, aspirin, dipyridamole, dextran) did not differ significantly in frequency of bleeding complications, estimated blood loss at operation, volume of blood transfused during operation, or wound drainage from suction catheters in the first 24 hours after operation." It does state that warfarin was withdrawn in four patients because of bleeding. In addition Salzman's article points to several problems with dextran. Some patients did not like the continuous intravenous infusions, and in six patients mild allergic reactions developed. Sixteen percent of the patients needed to have the infusion discontinued, a significant rejection rate. Third, in addition to the hypotensive allergic reactions mentioned by Drs. Schinagl and Ali, it would be of interest to have data on the incidence of other allergic manifestations to dextran that would limit its extended use. Fourth, with regard to renal function, dextran may well increase urine output provided there is no preexisting renal damage, but ischemic damage secondary to shock has a different time course in different persons. Also one cannot pick the ideal patient to develop shock, and many of the individuals in shock may well have underlying a t h e r o sclerotic, hypertensive or diabetic vascular changes, or both, in the kidney and elsewhere, responsible for unrecognized preexisting renal damage that may well limit the usefulness of dextran. Cautious use of this colloid is recommended in all patients to prevent further impairment of renal function. We agree with the conclusion of the letter from Schinagl and Ali that clinical benefit should be weighed against risk for any drug in any clinical situation. The efficacy of dextran, compared with alternative therapies, needs to be carefully evaluated in controlled clinical studies in the diseased patient who is apt to be given dextran for various approved and unapproved indications.
effect of dextran on platelet adhesiveness. Thromb Diath Haemorrh 16:384-394, 1966 3. EVARTS CM, FEIL EI: Prevention of thromboembolic
A L A N S. N I E S , M.D.
disease
after elective surgery of the hip. / Bone Joint Surg [Am] 53: 1271-1280, 1971 4. SALZMAN EW, HARRIS WH, D E SANCTIS RW:
JOANN L. DATA, M.D.
Reduction
in
venous thromboembolism by agents affecting platelet function. N Engl J Med 284:1287-1292, 1971 5. MATHESON NA: Renal effects of low molecular weight dextran. Monogr Surg Sci 3:303-364, 1966
In comment: The section on paradoxes in the dextran 40 paper was included to emphasize to physicians using the colloid the inconsistencies between proposed uses and reported adverse reactions. The likelihood of an adverse reaction in a given patient is unknown. * EVARTS CM: Personal communication.
School of Medicine Vanderbilt University Nashville, Tennessee 37232
Raw Diet and Diabetes Meilitus TO THE EDITOR: Dr. Douglass {Ann Intern Med 82:61-62, 1975) suggests that the salutary effect of a raw diet on diabetic control may be due to "non-inactivated enzymes that are present in raw items or with the fast transit time that is inherent in a raw diet." It is unlikely that enzymes not absorbed in active form have any notable effect during their brief enteric lives, particularly in view of their being active during a relatively long shelf life, shared with foods that are ultimately cooked. The implication of a rapid Comments and Corrections
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transit time seems to be that caloric absorption is decreased. But, as "a patient on insulin may have his insulin requirement reduced without significant reduction in weight," it would seem to follow that neither is there a significant reduction in ultimate caloric absorption. Contemporary Western diet has been accused in the aetiology of a glut of afflictions, with its presumably dietary postprandial hyperglycemic peaks, as well as of being "stressful to the human system in general," being particularly implicated in coronary artery disease and adult onset diabetes mellitus (1-3). The diet of our preculinary ancestry protected the homeostasis of the milieu interieur from rapid flux in three ways. First, cooking and other refinements generally "digest" food stuffs to the extent that a highly refined meal—for example, a peanut butter and jam sandwich, a piece of cake, and a cup of coffee (yet another refinement)—becomes (overstated) a rapidly absorbed bolus of glucose. A raw diet leaves to the gastrointestinal tract its function of "separating the wheat from the chaff." Second, the chaff (or bulk), by being bulky, dampens but does not necessarily decrease both consumption and rate of absorption. Finally, the value of numerous small feedings has been recognized by the ancestors of the omnivorous nibbler in the management of diabetics who may feed five or six times daily, rather than three. Common sense diet might be of more value in the prevention than the treatment of diabetes. Dietary education may prove the cornerstone of preventive medicine, assuming, of course, the public to be educable. However, random observation of the smoking habits and gastronomical indiscretions of an optimally educated sample—physicians—suggests this assumption to be as yet unfounded. GARFIELD C. PICKELL, M.D.
Department of Medicine Dalhousie University Halifax, Nova Scotia, Canada REFERENCES
1. EPSTEIN F H : Hyperglycemia. A risk factor in coronary heart disease. Circulation 36:609-619, 1967 2. HURST JW, LOGUE RB: The Heart. New York, McGraw-Hill
Book Company, 1974, pp. 124, 991 3. Companion to Medical Studies, edited by PASSMORE R, ROBSON JS. Philadelphia, F. A. Davis Co., 1974, pp. 23, 83-85
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Ethylene Oxide: Allergic Response TO THE EDITOR: In their paper on anaphylaxis from a product or products of ethylene oxide in January issue {Ann Intern Med 82:58-60, 1975), Dr. Poothullil and associates have observed that "previously documented complications of ethylene oxide have not generally been attributed to allergy." I draw attention to a paper by Drs. Sexton and Henson ( 1 ) . During this experiment three of the subjects became sensitized and developed itching and urticaria after exposure to ethylene oxide. The authors pointed out the ability of ethylene oxide to act as antigen by combining with body protein and elicit an allergic skin reaction. B. H. AVASHIA, M.D.
Union Carbide Corporation Charleston, West Virginia 25330 REFERENCE
1. SEXTON RJ, HENSON EV: Experimental ethylene oxide human skin injuries. Arch Ind Hyg Occup Med 2:549-564, 1950
Sexual Qualities in Case Reports TO THE EDITOR: A recent Letter to the Editor (1) raised an interesting editorial point. Should a female be reported as "attractive" on physical examination? Because the article was not concerned with reconstructive plastic surgery, I found the adjective immaterial to diagnosis. I perused several back issues and found no case reports in which adjectives describing sexual attractiveness of men were used. Perhaps the letter on page 858 of the same issue (2) should be appended to read "a 52-year-old handsome, white, male school bus driver." CHERILL M. PARMENTIER-PERERA, B.A.
School of Public Health and Community Medicine University of Washington Seattle, Washington, 98195 REFERENCES 1. ARONSON MD, KAMINSKY D, PHILLIPS CA: Parainfluenza virus
type 3 isolated in a case of bloody diarrhea. Ann Intern Med 81:856-857, 1974 2. PRCHKOV VK, MOOKHERJEE S, SCHIESS W, et al: Variant anginal
syndrome, coronary artery spasm, and ventricular fibrillation in the absence of chest pain. Ann Intern Med 81:858-859, 1974
Comments submitted for publication must be typed doublespaced, and text length must not exceed 500 words. Complete references must be furnished, as specified in "Information for Authors" (page 1-6). Specific permission to publish should be appended as a postscript. Publication depends on availability of space: we give preference to comment on recent content and to new information. Letters for this section should be concise—the Editor reserves the right to shorten them and make changes that accord with our style. Care for the Homebound Aged TO THE EDITOR: Dr. Brickner and colleagues deserve great credit for the work they have done in providing for the needs of homebound elderly in New York City ( 1 ) . Although the services are provided through a hospital-based program, that program is apparently not part of a home health agency, certified by the Social Security Administration. This would account for the inability of the hospital to bill for some of the services being provided to the aged. This point is of particular interest to us. Certified agencies, following Medicare regulations for reimbursement, cannot meet the total needs of the aged. The home care program at Sinai Hospital of Baltimore is now in its 14th year and is one of only five hospital-based certified home care programs in Maryland. By being certified, the program can bill for certain reimbursable services provided to covered patients. The patients, however, must be selected with great care if the program expenses are to be met. To more clearly illustrate the problem that faces a hospital-based home care program that must make its books balance, we would like to show what would have happened if the three patients who were described in the article had been referred to our agency for care. In each case, because of the patient's age, we assume that the patient has Medicare A and B. Patient 1, with severe chronic obstructive pulmonary disease and cor pulmonale, would have been acceptable to Medicare for home care reimbursement because of the clearly medical nature of acute respiratory failure. Nutritional counseling and management would have been reimbursable only as a supportive measure for the treatment of the acute respiratory problem. Once the patient's condition had become "stabilized," maintenance care would have been considered the responsibility of the patient, and his coverage for home care by Medicare would have ceased. If the patient's condition then deteriorated at home, and he became acutely ill once again, he would have become eligible for home care benefits. After "stabilization" the activities of our agency vis-a-vis the patient would have ceased. Patient 2 would have been acceptable for home care benefits under Medicare because of the massive fluid retention secondary to heart failure. Again, however, once her acute medical problem had improved, she would no longer be able to receive services with Medicare reimbursement. Our agency social worker, who would have been working with the patient in assisting her to return to an independent life, would have had to leave the case once the medical condition had improved.
In describing patient 3, who had severe osteoarthritis, Brickner made the comment "the medical issues in this case are not complex." In order to protect the patient and our agency, we make every effort to insure that the medical problems are complex or serious enough to require skilled nursing care or physical therapy before accepting the patient. For this patient to qualify under Medicare, we would have had to show that the patient needed either physical therapy, which would have contributed to the patient's rehabilitation, or skilled nursing services to monitor the patient for drug side effects while she was being treated for her hypertension. Emphasis on this patient's social needs in the Medicare reimbursement form is a sure way to have the bill rejected. In any case, once the patient had become stable, she would no longer have been eligible for home care benefits under Medicare. At the end of their acute care episodes, all of these patients would have been discharged from our home care program. This has, in fact, happened to many patients for whom we have provided services and has caused enormous problems to these patients, who have continuing needs for supportive services. Recently we received Title III funds from the Baltimore City Commission on Aging, which we are using to pay for services after Medicare eligibility ends. We have no assurance that this funding will continue. Eligibility for home health services should not be limited to only those aged who qualify for skilled care. Dr. Brickner's article once again points out our lack of national policy for long-term care that is comprehensive, coherent, and attentive to the needs of older Americans. JOSEPH I. BERMAN, M.D., M.P.H. MORRIS OSTROFF, M.D., M.P.H.
Department of Community Medicine Sinai Hospital of Baltimore, Inc. Baltimore, Maryland 21215 REFERENCE
1. BRICKNER PW, DUQUE T, KAUFMAN A, et al: The homebound
aged. A medically unreached group. Ann Intern Med 82:1-6, 1975
TO THE EDITOR: In many hospitals, including those affiliated with universities, chronic disabling diseases, advancing years, and patient-compliance problems elicit an automatic reflex—"nursing home placement." For the past 9 months we have been fortunate to be one of several VA hospitals funded for a multidisciplinary home care unit. To date our experiences have paralleled Dr. Brickner's (Reference 1 above); that is, home care appears to save nursing home funds, improve accessibility to health care for the disabled, promote patient emotional health, and often accomplish medical therapeutic goals that hospitals, nursing homes, and clinics have failed to achieve. The next issue to examine is whether these health care gains can be measured in other than financial terms and can show a significant improvement over the outcome of nursing home care. Certainly, there can be little that is more dehumanizing and demoralizing to a patient inflicted with a severe illness than to be exiled from his own home. In answer to the editorial comment by Somers and 717
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Bryant (Ann Intern Med 82:111-112, 1975) that questioned which hospital department should assume home care responsibility, we feel that the logical function for a home care unit is as an activity of a hospital-based model primary care practice in those hospitals with housestaff training programs. With role models and practice examples to emulate in such a setting, perhaps the next generation of primary care physicians will be more inclined to seek care for the elderly and disabled in their own homes. JAMES W. HAINER, M.D. SANDRA KING, R.N.
Medical Comprehensive Care Unit Seattle Veterans Administration Hospital Seattle, Washington 98108 TO THE EDITOR: I read with mixed emotions the lead article by Brickner and associates (Reference 1 above). On the one hand, I was pleased that these authors and their hospital undertook such a meaningful project and, on the other hand, I was chagrined after a few of my simple mathematical calculations placed the study in a more realistic perspective. In 16 months, 620 home visits were made for a rough average of fewer than 1.3 "house calls" per day. My father, a general practitioner (or "family physician") in Ohio, probably doubled or tripled that average over the last 30 years. Too bad he didn't write up his experience for our journal. My emotions remained mixed on reading the editorial by Somers and Bryant in the same issue (Ann Intern Med 82: 111-112, 1975). As a practicing chest specialist, I must admit to a daily house call average far below that of my father and of Brickner and associates. I must agree (with a certain amount of guilt) with the statement that "most physicans are not interested in chronic illness, most are not interested in home care. . . . " Somers and Bryant offer some possible solutions to the present dilemma. I would add another. Why not require that each and every graduating medical student spend 6 to 12 months providing home care for the aged as a part of his or her training experience? Every student of medicine is aware of the requirements for becoming a physician: premedical, medical school, internship, residency; the period of training is being shortened by 3-year medical schools, straight internships, and similar changes. Could anyone subscribing to the Hippocratic oath object to the addition of a period of providing home care medicine to his or her training program? And would not such a period of training provide future hospital-based specialists with a much better understanding and appreciation of the role of the primary care physician in the community? My father and many family physicians like him may have missed an opportunity to write the lead article in the Annals; the internists of today, those of us who read this journal, must not miss the opportunity to provide an answer to the question posed by Somers and Bryant: "For whose benefit are we operating our $100 billion a year healthcare economy"? FREDERICK R. BODE, M.D., LT COL, USAF, MC
Wilford Hall USAF Medical Center (SGHMP) Lackland Air Force Base, Texas 78236 Recertification TO THE EDITOR: I took the Recertification Examination 718
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because, with all the talk of recertification in the air, this seemed to be the only concrete thing to do, better than getting various credits for meetings attended. I also wanted to force myself to review the entire field of internal medicine. This worked, illustrating Jung's principle that "need is a better incentive than desire." I read the American College of Physicians' Self-Assessment Syllabus, bought a new Harrison, and checked out a few difficult questions with subspecialist friends. The syllabus is superb and was enjoyable reading. Because of the preliminary announcement that the Examination would be based on it, and perhaps 70% of the questions were, the procedure was eminently fair and amazingly free from ambiguity. The examination showed much care and thoughtful writing. Was it representative of what internists do in practice? The answer is assuredly, "No." Although several questions did go to the heart of internal medicine (A6, 35, 36, 39, 52-54, 59-62, B18, 19, 40), many showed narrow specialty interests (A55-58, 67-70, 93-95, B17, 42, 117), and quite a few had to do with points a conscientious physician would look up, rather than consult a faulty memory (A28, B12,17, 48, 60-64). I would have preferred more questions on more relatively common situations on the ward or in the office that clinically call for quick decisions where it is awkward to look up information or ask colleagues; for example, about disturbances of electrolytes or blood gases, abnormal biochemical data, or hemograms, rather than problems with rare diseases, about which we undoubtedly would get consultation (B93, 98, 99, 123) or even schedule a case for grand rounds, if one ever turned up (B5, 33, 37, 98, 99, 105). Perhaps a good internist should know more than he can use—after all he is to some degree a scholar—but our chief value to our patient is the ability to make decisions. To store and retain for any length of time the amount of information this examination covers is not compatible with an active life in practice and the committee activities in which most of us are engaged. To know all this material suggests either getting the constant reinforcement that occurs in a medical school setting—where it is highly appropriate—or a preoccupation with literature at the expense of action—and that is not so good. Despite all these second thoughts, I found the entire exercise highly beneficial and more valuable than the Merit Project, which was more representative of what I do but did not make me study and learn. I hope to have the strength to do it again in 7 years. R A L P H O. WALLERSTEIN, M.D.
3838 California Street San Francisco, California 94118
Alcoholism: A Disease? TO THE EDITOR: The dispute about alcoholism being a "disease" may result in severe harm to thousands of patients. Classifications are not necessarily "true"; they should be pragmatic. A block of wood may be equally classified as a piece of fuel, a botanic specimen, a chemical specimen, a weapon, or a work of art. It is all of these, and pragmatic reasons will tell us how to classify it at any time. If alcoholic persons can be treated—and I shall describe how they can—in hospitals, by doctors, nurses, psychologists, social workers, counselors, pharmacies, and clinics,
and if they can be restored, in many cases, to a normal and happy life, then alcoholism must be considered a disease. The program at this hospital is duplicated, with variations, in many others, but our treatment is based on the disease concept and is highly effective. If by "effective" we mean a marked decrease in psychological and physical disabilities and a restoration to fairly normal life circumstances, then our Detoxification Section (for treatment of the alcoholic withdrawal syndrome) is 100% effective. After detoxification all patients are offered an intensive 7 to 10 days of orientation and education. This is also offered to all other newly admitted patients and consists of films, videotapes, discussions, lectures, talks, counseling, medication, exposure to Alcoholics Anonymous, and printed material. At this point some individuals become outpatients, and others remain for weeks of rehabilitation. Our statistics for the longer term rehabilitation are incomplete, but we have many records of patients in whom we can point to excellent work rehabilitation, restoration of broken marriages, economic success, psychological improvements, and restoration to a normal and healthy existence. Judging from the long destructive histories of alcoholism given by most of the patients who have come into our program, we believe that without using this medical model such results would not have been achieved. In the January 1975 issue (Ann Intern Med 82:116119) were several letters which suggested that the alcoholic person often rejects treatment. Nevertheless, with the record of success that I have described above, every physician should do his best to get alcoholic patients motivated. This might be best done by seeing that every hospital has a small team concerned with alcoholism. This team could be composed of four or five people, not necessarily physicians, and could include one or more Alcoholics Anonymous members, who would make known to the patients what facilities are available in the hospital or in the community. The large number of applicants we have suggests there are thousands and thousands of alcoholics who do want treatment sooner or later. Throughout these letters runs the feeling on the part of the doctors that they will be "blamed." Because cancer, emphysema, arteriosclerosis, schizophrenia, and practically all other chronic illnesses are incurable, in most cases, or frequently relapse, should we stop practicing medicine? The physician is not more responsible for his alcoholic patient who drinks than for his diabetic patient who violates his diet or insulin needs. We do not care what name you use for alcoholism (although I do consider it a disease), but every physician is obliged to offer each patient some treatment. E M I L ROTHSTEIN, M.D.
Veterans Administration Hospital Brockton, Massachusetts 02401
Group-Y Meningococcal Disease TO THE EDITOR: The article "Group-Y meningococcal disease" by J. D. Smilack in the December issue (Ann Intern Med 81:740-745, 1974) was read with interest. Two cases of pneumonia occurred among 12 cases of group-Y meningococcemia. I wish to present briefly our experience with pneumonitis among cases of group-C meningococcemia seen at Madigan General Hospital during 1969. These data were presented at the VA Armed Forces Pulmonary Disease
Research Conference in Cincinnati in 1970 and have not been published. Ninety-four cases of meningococcal disease among recruits were documented by either blood culture or cerebrospinal fluid culture. Admission chest roentgenograms from those 94 patients showed 8 (8.5%) to have evident pulmonary infiltrates. Neisseria meningitidis was cultured from the blood in 5 of these cases, and the other 3 cerebrospinal fluid cultures showed positive results, but the blood culture did not grow that organism. In a single patient the blood culture, the cerebrospinal fluid, and the sputum all grew Neisseria meningitidis. There was 1 patient with group-B meningococcal disease. In some of the patients, Diplococcus pneumoniae or Klebsiella organisms were recovered from the sputum. Each of the 8 patients with pneumonia were hypoxic at the time of admission to the hospital. There were also no deaths among the 8 patients with pneumonitis. In the larger group of 94 patients there were five deaths. It seemed reasonable to us to conclude that pneumonitis was surprisingly common among patients with acute meningococcal disease due to group C, and that, in most of these cases, the pneumonitis was likely due to the meningococcal organism. It would seem that the presence of pneumonia in acute meningococcal disease does not worsen the prognosis. It also would seem that the frequency of pneumonia among cases of acute meningococcal disease of group C does not differ substantially from the frequency of pneumonia in group-Y meningococcal disease. MARK E. REINECKE, M.D.
Marshfield Clinic Marshfield, Wisconsin 54449 In comment: Dr. Reinecke's observations are of interest and confirm those of others cited in my paper. I should mention that three cases of primary meningococcal pneumonia were described, two in the main text and one in the addendum. It is not clear whether the meningococcus was the etiologic agent for pneumonitis in the cases cited by Dr. Reinecke; nor is it stated which of the eight patients with pulmonary infiltrates had clinical evidence of central nervous system infection. It seems likely that a high risk of aspiration pneumonia might exist in the patient with meningitis or meningoencephalitis; viral or mycoplasmal pneumonia might accompany meningococcal infection. Young and colleagues (1) have suggested that influenza viral infection might predispose to meningococcal disease. In the series of patients with group-Y meningococcal infection that I reported, the three patients with pneumonia had no obvious extrapulmonary focus. Although small numbers are involved, comparison with other series suggested a disproportionately high prevalence of primary pneumonia in our patients with group-Y disease. It is unfortunate that prospective studies addressed to the question of the incidence of primary meningococcal pneumonia are lacking. Parenthetically, I wish to add that Risko and Hodges (2) have noted an increasing incidence of group-Y meningococcal infection in a naval training center; none of their six patients had pulmonary involvement. JERRY D. SMILACK, M.D.
Infectious Disease Laboratory Comments and Corrections
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The Methodist Hospital Houston, Texas 77025
REFERENCES
1. WEAVER GH: Diphtheria carriers. JAMA 76:831-835, 1921 2. MILLER LW, BICKHAM S, JONES WL, et al: Diphtheria carriers
REFERENCES
1. YOUNG LS, LAFORCE FM, HEAD JJ, et al: A simultaneous out-
break of meningococcal and influenza infections. N Engl J Med 287:5-9, 1972 2. RISKO J A, HODGES GR: Neisseria meningitidis serogroup Y: incidence and description of clinical illness. Am J Med Sci 261: 345-352, 1974
and the effect of erythromycin therapy. Antimicrob Agents Chemother 6:166-169, 1974 3. DOULL J A, LARA H: The epidemiologic importance of diphtheria carriers. Am J Hyg 5:508-529, 1925 4. MILLER LW, OLDER JJ, DRAK J, et al: Diphtheria immunization:
effect upon carriers and the control of outbreaks. Am J Dis Child 123:197-199, 1972 In comment:
Diphtheria Carriers TO THE EDITOR: McCloskey and colleagues reported in the December 1974 issue (Ann Intern Med 81:788-791, 1974) their experience in the treatment of a large number of Cory neb acterium diphtheriae carriers. Although I agree with the need to treat carriers and the recommendation that erythromycin be the preferred antibiotic, I feel it is important to mention several problems related to the C. diphtheriae carrier state and the evaluation of its treatment. McCloskey and associates stated that treatment of diphtheria carriers is superior to no treatment because one Russian report showed that only 12% of carriers become C. diphtheriae-negativQ when followed for 1 month. However, there is evidence from the literature during the preantibiotic era that 50% of carriers became culture-negative within 10 days of their discovery, and 8 1 % were culturenegative by 1 month ( 1 ) . Another problem with rationalizing therapy of carriers on the argument that therapy renders a much larger percentage of carriers culture-negative than no therapy is that success in therapy, as in McCloskey's paper, is usually based only on follow-up cultures 1 and 2 days after therapy. Because this is usually 8 or 9 days after identification of the carrier, little is known about the culture status of treated carriers at 1 month. We observed 72 diphtheria carriers treated with erythromycin and found a 9 9 % "success rate" 1 and 2 days after therapy. However, reculture 2 weeks later showed that 15% had relapsed to the carrier state. Comparison of our observation with information from the preantibiotic era showed no significant difference in the proportion of carriers culture-positive 25 days after their identification ( 2 ) . What then is the value of treating carriers? There are two major reasons: [1] treatment renders diphtheria carriers culture-negative within 48 hours (2) and thus reduces the carrier's risk of becoming a symptomatic case and [2] because carriers are responsible for the transmission of the majority of cases of symptomatic diphtheria in a community ( 3 ) , treatment of carriers reduces the spread of disease and helps to control outbreaks ( 4 ) . Because carrier relapse has been documented as a problem, it is important that we do not delude ourselves by assuming eradication of the carrier state when cultures are negative 1 and 2 days after therapy. Follow-up cultures 2 to 3 weeks after therapy are needed in order to assure eradication of the organism. Evaluation of drug therapy should be based not only on the results of cultures taken immediately after therapy, but also on cultures taken to identify relapses 2 or more weeks after therapy. Louis W. MILLER, M.D.
Department of Social and Preventive Medicine University of Maryland School of Medicine Baltimore, Maryland 21201 720
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The group investigating the outbreak of diphtheria in San Antonio followed Dr. Miller's experiences in the Elgin, Texas, outbreak with interest. We hold that diphtheria carriers should be treated with erythromycin for the same two reasons stated clearly by Dr. Miller. We stated that all treatment regimens are associated with some failures, and we are not surprised that as many as 15% of carriers may have relapsed (or may have been reinfected) when recultured 2 or 3 weeks after treatment was stopped. Because there is some evidence that newer phage types of Cory neb acterium diphtheriae were involved in the Texas outbreak ( 1 ) , comparison of posttreatment results with preantibiotic era studies may not be valid—a criticism that may be applied to our studies, as well as to Dr. Miller's reports. RICHARD V. MCCLOSKEY, M.D.
Albert Einstein Medical Center Daroff Division Philadelphia, Pennsylvania 19147 REFERENCE
1. MCCLOSKEY RV, SARAGEA A, MAXIMESCU P: Phage typing in
diphtheria outbreak in the Southwest 1970-71. J Infect Dis 126: 196-199, 1972
Immune-Complex Disease in Typhoid Fever TO THE EDITOR: During an episode of typhoid fever, a patient developed transient proteinuria, microscopic hematuria, as well as urinary hyaline and granular casts and pericarditis. Concurrent low complement levels suggested that these unusual manifestations were due to immunecomplex disease involving Salmonella antigens. A 23-year-old man became suddenly ill with diarrhea, vomiting, and fever. When admitted 7 days latter he had a temperature of 39 °C, the spleen tip was palpable, and on proctoscopic examination the mucosa was friable and hemorrhagic. Urinalysis showed proteinuria of 3.25 g/litre and the sediment contained erythrocytes as well as hyaline and granular casts. A urine culture showed negative results. Widal agglutination tests gave titers of 1:160 with O antigen and 1:40 with H antigen of Salmonella group A; as well as titers of 1:320 with O antigen and of 1:40 with H antigen of Salmonella group B. Seven days after first seen he developed jugular regurgitation and cyanosis. A pericardial rub appeared. Lupus erythromatosus cells and antinuclear antibodies were negative. Serum C3 was less than 28 mg/100 ml (normal, 80 to 120 mg/100 ml); the 50% hemolytic complement activity was 0.62 units (normal, 30 to 60 units). Salmonella typhi A was cultured from the feces. Blood cultures showed negative results. Despite trimethoprim-sulfamethoxazole treatment he developed severe melena that prompted surgery. The resected 70 cm of small bowel showed characteristic typhoid lesions. He recovered well after surgery. With chloramphenicol, the fever
and the pericardial rub disappeared, and urinalysis became normal and remained so. This patient was seen in 1972 when there was an epidemic of chloramphenicol-resistant salmonellosis in Mexico. However, the urinary and pericardial findings caused much diagnostic confusion. When it became evident that he indeed had typhoid fever, the urinary findings, pericardial involvement, and low complement were all attributed to immune-complex disease secondary to typhoid fever. The report by Sitprija and colleagues (Ann Intern Med 81:210-213, 1974) supports that contention. DONATO ALARCON-SEGOVIA, M.D., F.A.C.P. JORGE C. ALCOCER, M.D.
Department of Immunology and Rheumatology Instituto Nacional de la Nutrition Mexico 22, D.F., Mexico
Ethics in Vasodilator Therapy TO THE EDITOR: The article "Chronic Vasodilator Therapy in the Management of Cardiogenic Shock and Intractable Left Ventricular Failure" (Ann Intern Med 81:777-780, 1974) is an interesting, reasonably convincing demonstration of the effects of ventricular unloading on the management of left ventricular dysfunction. I am concerned, however, about an aspect of the paper somewhat removed from the scientific content and which, I believe, is an example of "ethical unloading." Having found both subjective and objective benefits of the therapy in this severely ill patient, I find it difficult to understand why after 6 months of therapy they elected to discontinue one aspect of the therapy, substituting a placebo drug (which must have been done without the patient's knowledge) while he was an outpatient and having him return 7 days later in "incipient pulmonary edema with diaphoresis, pedal edema, and a weight gain of 5 kg [11 lb]." On 2 December, 13 December, 19 December, 12 January, and 26 March, repeated studies had shown the efficacy of their therapeutic intervention, with evidence of rapid deterioration on discontinuation of this therapy. I would imagine that by this time the investigators had sufficient confidence in what they were doing, so that a 7-day interruption in therapy 6 months after its onset with the patient not under close observation seems hardly justified, especially when this modification in therapy was undertaken without the patient's knowledge and, by their own description, resulted in a life-threatening deterioration in the patient's condition. I can see no justification for this in the case report and would be interested in the authors' explanation. DAVID SHANDER, M.D., F.A.C.P.
General Rose Memorial Hospital 1050 Clermont Street Denver, Colorado 80220 In reply: Dr. Shander raises a moral issue pertinent to all therapeutic studies of new drugs. Investigators who assume the responsibility of testing new treatment regimens must design their experiments to minimize bias on the part of the physician or of the patient, while still protecting the patient from possible harm.
When a new and unapproved therapy is being evaluated, as in the use of nitrates to treat heart failure, the burden is on the investigator to prove that the treatment is beneficial when compared with conventional therapy. Uncontrolled observations are notoriously unreliable and have led in the past to enthusiasm for drugs that have subsequently been shown in carefully designed studies to be nonefficacious. It is most unusual for an investigator to be criticized for stopping an experimental drug and continuing conventional treatment for the disease. Only by this type of experimental design can the efficacy and safety of experimental drugs be proved in a relatively small number of people, so that the population as a whole will be exposed only to agents that are clinically useful. In the case under discussion, the placebo regimen was begun because two of the physicians assisting in follow-up of the patient expressed a reasonable doubt about the clinical efficacy of the nitrates. Therefore, we were not as willing as Dr. Shander to assume from our acute hemodynamic observations that long-term nitrate therapy was playing a vital role in the patient's management. A trial cessation of therapy can be justified not only on the basis of good investigation but of good clinical practice. Too many patients receive unnecessary but potentially toxic drugs because their physicians are loathe to withdraw them. The apparent demonstration of efficacy in our patient should not by itself convince anyone of the practical usefulness of the nitrates in the treatment of heart failure. It is highly unlikely that the Food and Drug Administration and the medical community would be swayed on the basis of our limited observations to approve and prescribe the nitrates for the treatment of all patients with severe heart failure. This therapy, therefore, should still be viewed as experimental, and further controlled studies must be carried out, even at the risk of withholding an effective treatment from some patients. JAY N. COHN, M.D.
Cardiovascular Division University of Minnesota Medical School Minneapolis, Minnesota, 55455
"Munchausen" Case TO THE EDITOR: Fialk and Murray (Ann Intern Med 8 1 : 562, 1974) and Sparandero (Ann Intern Med 82:123, 1975) have reported experiences with a patient having the prolapsing mitral valve syndrome and "Munchausen" syndrome. We have seen a patient, who is probably the same person, at our hospital and have uncovered records of at least 10 admissions to this and other hospitals in the Philadelphia-southern New Jersey area. The patient, a 28-year-old white man, was transferred to Thomas Jefferson University Hospital because of persistent chest pain. He stated that he was hospitalized in October 1973 because of an acute myocardial infarction. At that time cardiac catheterization in a United States Army hospital in Munich, Germany, showed "blockage of a coronary artery" and prolapse of the mitral valve. He was also told that he had Marfan's syndrome. He reported recurrent episodes of palpitations associated with syncope since the age of 16. Although his chest pain over the past 7 years had generally been precipitated by exertion and relieved by nitroglycerine, for the past 10 days he had had continuing chest discomfort at rest. It was described as substernal and pressurelike with radiation to the neck. Present medications included propranolol, digoxin, warfarin, and Comments and Corrections
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quinidine. The patient stated that he was a graduate student at Princeton University. Physical examination showed a white man with marfanoid measurements of the extremities. There was a high-arched palate, but no ectopia of the optic lens. The heart had a midto-late systolic murmur at the apex and along the left sternal border after a midsystolic click. Laboratory tests showed creatinine phosphokinase of 900 U/ml, although there was no elevation of lactic dehydrogenase or serum glutamic oxalacetic transaminase. The hemoglobin was 10.6 gm/100 ml and the hematocrit was 33%. Myocardial metabolic studies showed normal results, indicating that his chest pain was not due to coronary disease. Before further evaluation could be done, the patient signed out of the hospital, stating that he had to participate in rowing competition with the Princeton crew team in Switzerland. Subsequently obtained records from other hospitals showed admissions for multiple reasons, including decompression sickness and gastrointestinal hemorrhage secondary to aspirin or Coumadin ingestion, or both. This patient has become a medical economic factor in the Philadelphia, New York, and New Jersey area in his own right. The association of prolapsed mitral valve syndrome and neuropsychiatric disorders has been reported in the past ( 1 ) . This patient may be an example of a severe personality disorder with this cardiac disease. His case suggests again the potential hazards of multiple drug therapy, particularly with anticoagulants, in patients with apparent psychiatric disease. JUDITH M. DEGLIN, PHARM.D.
Department of Pharmacy STUART M. DEGLIN, M.D.
Department of Medicine Thomas Jefferson University Hospital Philadelphia, Pennsylvania 19107 REFERENCE
are in error, as 50 mg of calcium gluconate contains 4.5 mg of calcium, or 0.225 meq of calcium. Perhaps the metric system is not the panacea we are led to believe it is, and we must all double check to make sure we have our micrograms, milligrams, millilitres, and milliequivalents in the right place. ALAN W. H O P E F L , PHARM.D.
University of Michigan Medical Center Pharmacy Department Ann Arbor, Michigan 48104 In reply: Dr. Hopefl makes two points in his letter that warrant our comments. First, he states that mithramycin should not be considered the drug of choice in treating all hypercalcemias, as it has serious side effects other than the transient nausea and vomiting we mentioned. It would have been better if we had inserted the word "refractory" before hypercalcemia to exclude cases when the underlying cause can be treated (hyperparathyroidism, vitamin D intoxication, and so forth), or when a response can be obtained with more conservative measures, such as hydration, diuresis, corticosteroids, and oral phosphate preparations. Other side effects, which might have been mentioned, occurring with longer term mithramycin therapy include hemorrhage, at least in part due to depressed platelet counts, hepatotoxicity, nephrotoxicity, drug fever, dermatitis, and hyperuricemia. Dr. Hopefl has correctly observed that an error was made in the calculation of the milliequivalents of calcium in the calcium gluconate solution. The quantities of calcium gluconate in milligrams and grams were reported correctly, but the milliequivalents are erroneous. ROBERT D. LINDEMAN, M.D., F.A.C.P. SOLOMON PAPPER, M.D., F.A.C.P.
1. JERESATY RM: Mitral valve prolapse—Click Syndrome. Prog Cardiovasc Dis 40:623-652, 1973
Hypercalcemia and Hypocalcemia: Treatment TO THE EDITOR: The recent paper by Drs. Lindeman and Papper (Ann Intern Med 82:64-70, 1975) deserves correction on several points. A major error in the paper was in dosage of mithramycin, which was incorrectly given as 25 mg/kg body weight, when in reality it is 25 /xg/kg body weight (a thousandfold difference). The same error was again made a few lines later when the weekly dosage was given. I would hope that this was a printer's error, but, further, I also do not think that mithramycin should be considered the drug of choice for all hypercalcemia, as hinted at in the article, because of its serious side effects, which certainly lie beyond the transient nausea and vomiting stated in the article. The drug has its place in therapy, but it should only be used by those with experience in chemotherapy and when other more benign therapy has failed or is contraindicated. They also state in the section on hypocalcemia that a 10 ml ampule of 10% calcium gluconate contains 50 meq of calcium, when in reality it contains 4.8 meq of calcium (93 mg of calcium). Fifty milliequivalents of calcium would be equal to 1 g of elemental calcium, which would be contained in 10.7 g of calcium gluconate. The rate of intravenous infusion is later given correctly as 50 mg of calcium gluconate (0.5 m l / m i n ) , but the milliequivalents 722
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Veterans Administration Hospital 921 Northeast 13th Street Oklahoma City, Oklahoma 73104 The error in mithramycin dosage was pointed out in the March issue (p. 421).—The Editor
Dextran 40 TO THE EDITOR: We believe that the review article on dextran 40 by Data and Nies (Ann Intern Med 81:500504, 1974) deserves comments on the "paradoxes" reported by the authors from their selective review of the dextran 40 literature. Dextran 40 is neither an anticoagulant nor an antiplatelet agent. Because increased platelet aggregation, blood viscosity, and elevated plasma fibrinogen concentration may lead to disseminated intravascular coagulation or shock lung, or both, in severely traumatized patients ( 1 ) , many clinicians would regard decreased concentration of factors V, VIII, and IX (due largely to hemodilution) and decreased platelet adhesiveness (but not count) after dextran 40 infusion at the recommended dosage (1.5 g/kg body weight) to be most desirable in treatment of shock. At the above recommended dosage, bleeding time is not affected ( 2 ) , and postoperative bleeding is not increased
(3). Systemic bleeding complications, for example, gastrointestinal bleeding, are more evident (4), and dosage control is far more complex with warfarin compared with dextran 40. However, wound oozing after infusion with dextran 40, used experimentally for prophylaxis of postoperative thromboembolism, has been shown to be dosedependent and of minor clinical significance at the suggested investigational dosage—1000 ml on the day of surgery, starting intraoperatively, followed by 500 ml/day for the following 3 days, and 500 ml every other day thereafter until the patient is ambulatory*. No anaphylactoid reactions were reported when dextran was used in treatment of shock during the period 19551968. Review of our worldwide records on dextran 40 during the period 1962-1972 shows more than 15 million units of dextran 40 used with 49 reported cases of hypotension reactions in postoperative patients, which gives an incidence of one reaction per 300 000 bottles used. Most anuria secondary to shock is due to fall in arterial blood pressure and decreased plasma volume. Infusion with dextran 40 and adequate crystalloid solutions results in a spontaneous increase in urine output due to increased cardiac output, plasma volume, and renal perfusion ( 5 ) , unless there is preexistant renal damage. Dextran 40 does not interfere with blood typing and cross-matching unless the outdated enzyme method is used. As a general rule, however, it is recommended that blood samples for all laboratory studies (including blood bank) be drawn from the Emergency Room patient before any drug is given. The published reports on dextran 40 show that the benefits to the shock patient overwhelmingly exceed the risk of any adverse reaction. F o r investigational use in other indications, however, the attending physician must weigh the documented clinical benefit against the risk of using the drug for each clinical situation. ERICH F . SCHINAGL, M.D. RIDA A L I , PH.D.
Pharmacia Laboratories, Inc. 800 Centennial Ave. Piscataway, New Jersey 08854 REFERENCES
1. BLAISDELL RJ: Intravascular coagulation and pulmonary changes following shock and trauma, in Acute Fluid Replacement in the Therapy of Shock, edited by MALINEN TI, New York, Stratton Intercontinental Medical Book Corp., 1974 2. CRONBERG F, ROBERTSON B, NILLSON IM, et al:
Suppressive
We wish to comment on several points raised by Drs. Schinagl and Ali. First, the reference cited (3 above), stating that the bleeding time was unaffected at recommended dosage, deals with normal volunteers given a single dose and is not pertinent to what would happen on prolonged administration to the diseased patient. With continued administration, the larger molecular weight fragments would accumulate and probably would mimic the effect of higher molecular weight that dextrans did increase bleeding time. Second, the paper by Salzman and colleagues (Reference 4 above) does not indicate an increased bleeding with warfarin and states that "the four groups (warfarin, aspirin, dipyridamole, dextran) did not differ significantly in frequency of bleeding complications, estimated blood loss at operation, volume of blood transfused during operation, or wound drainage from suction catheters in the first 24 hours after operation." It does state that warfarin was withdrawn in four patients because of bleeding. In addition Salzman's article points to several problems with dextran. Some patients did not like the continuous intravenous infusions, and in six patients mild allergic reactions developed. Sixteen percent of the patients needed to have the infusion discontinued, a significant rejection rate. Third, in addition to the hypotensive allergic reactions mentioned by Drs. Schinagl and Ali, it would be of interest to have data on the incidence of other allergic manifestations to dextran that would limit its extended use. Fourth, with regard to renal function, dextran may well increase urine output provided there is no preexisting renal damage, but ischemic damage secondary to shock has a different time course in different persons. Also one cannot pick the ideal patient to develop shock, and many of the individuals in shock may well have underlying a t h e r o sclerotic, hypertensive or diabetic vascular changes, or both, in the kidney and elsewhere, responsible for unrecognized preexisting renal damage that may well limit the usefulness of dextran. Cautious use of this colloid is recommended in all patients to prevent further impairment of renal function. We agree with the conclusion of the letter from Schinagl and Ali that clinical benefit should be weighed against risk for any drug in any clinical situation. The efficacy of dextran, compared with alternative therapies, needs to be carefully evaluated in controlled clinical studies in the diseased patient who is apt to be given dextran for various approved and unapproved indications.
effect of dextran on platelet adhesiveness. Thromb Diath Haemorrh 16:384-394, 1966 3. EVARTS CM, FEIL EI: Prevention of thromboembolic
A L A N S. N I E S , M.D.
disease
after elective surgery of the hip. / Bone Joint Surg [Am] 53: 1271-1280, 1971 4. SALZMAN EW, HARRIS WH, D E SANCTIS RW:
JOANN L. DATA, M.D.
Reduction
in
venous thromboembolism by agents affecting platelet function. N Engl J Med 284:1287-1292, 1971 5. MATHESON NA: Renal effects of low molecular weight dextran. Monogr Surg Sci 3:303-364, 1966
In comment: The section on paradoxes in the dextran 40 paper was included to emphasize to physicians using the colloid the inconsistencies between proposed uses and reported adverse reactions. The likelihood of an adverse reaction in a given patient is unknown. * EVARTS CM: Personal communication.
School of Medicine Vanderbilt University Nashville, Tennessee 37232
Raw Diet and Diabetes Meilitus TO THE EDITOR: Dr. Douglass {Ann Intern Med 82:61-62, 1975) suggests that the salutary effect of a raw diet on diabetic control may be due to "non-inactivated enzymes that are present in raw items or with the fast transit time that is inherent in a raw diet." It is unlikely that enzymes not absorbed in active form have any notable effect during their brief enteric lives, particularly in view of their being active during a relatively long shelf life, shared with foods that are ultimately cooked. The implication of a rapid Comments and Corrections
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transit time seems to be that caloric absorption is decreased. But, as "a patient on insulin may have his insulin requirement reduced without significant reduction in weight," it would seem to follow that neither is there a significant reduction in ultimate caloric absorption. Contemporary Western diet has been accused in the aetiology of a glut of afflictions, with its presumably dietary postprandial hyperglycemic peaks, as well as of being "stressful to the human system in general," being particularly implicated in coronary artery disease and adult onset diabetes mellitus (1-3). The diet of our preculinary ancestry protected the homeostasis of the milieu interieur from rapid flux in three ways. First, cooking and other refinements generally "digest" food stuffs to the extent that a highly refined meal—for example, a peanut butter and jam sandwich, a piece of cake, and a cup of coffee (yet another refinement)—becomes (overstated) a rapidly absorbed bolus of glucose. A raw diet leaves to the gastrointestinal tract its function of "separating the wheat from the chaff." Second, the chaff (or bulk), by being bulky, dampens but does not necessarily decrease both consumption and rate of absorption. Finally, the value of numerous small feedings has been recognized by the ancestors of the omnivorous nibbler in the management of diabetics who may feed five or six times daily, rather than three. Common sense diet might be of more value in the prevention than the treatment of diabetes. Dietary education may prove the cornerstone of preventive medicine, assuming, of course, the public to be educable. However, random observation of the smoking habits and gastronomical indiscretions of an optimally educated sample—physicians—suggests this assumption to be as yet unfounded. GARFIELD C. PICKELL, M.D.
Department of Medicine Dalhousie University Halifax, Nova Scotia, Canada REFERENCES
1. EPSTEIN F H : Hyperglycemia. A risk factor in coronary heart disease. Circulation 36:609-619, 1967 2. HURST JW, LOGUE RB: The Heart. New York, McGraw-Hill
Book Company, 1974, pp. 124, 991 3. Companion to Medical Studies, edited by PASSMORE R, ROBSON JS. Philadelphia, F. A. Davis Co., 1974, pp. 23, 83-85
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Ethylene Oxide: Allergic Response TO THE EDITOR: In their paper on anaphylaxis from a product or products of ethylene oxide in January issue {Ann Intern Med 82:58-60, 1975), Dr. Poothullil and associates have observed that "previously documented complications of ethylene oxide have not generally been attributed to allergy." I draw attention to a paper by Drs. Sexton and Henson ( 1 ) . During this experiment three of the subjects became sensitized and developed itching and urticaria after exposure to ethylene oxide. The authors pointed out the ability of ethylene oxide to act as antigen by combining with body protein and elicit an allergic skin reaction. B. H. AVASHIA, M.D.
Union Carbide Corporation Charleston, West Virginia 25330 REFERENCE
1. SEXTON RJ, HENSON EV: Experimental ethylene oxide human skin injuries. Arch Ind Hyg Occup Med 2:549-564, 1950
Sexual Qualities in Case Reports TO THE EDITOR: A recent Letter to the Editor (1) raised an interesting editorial point. Should a female be reported as "attractive" on physical examination? Because the article was not concerned with reconstructive plastic surgery, I found the adjective immaterial to diagnosis. I perused several back issues and found no case reports in which adjectives describing sexual attractiveness of men were used. Perhaps the letter on page 858 of the same issue (2) should be appended to read "a 52-year-old handsome, white, male school bus driver." CHERILL M. PARMENTIER-PERERA, B.A.
School of Public Health and Community Medicine University of Washington Seattle, Washington, 98195 REFERENCES 1. ARONSON MD, KAMINSKY D, PHILLIPS CA: Parainfluenza virus
type 3 isolated in a case of bloody diarrhea. Ann Intern Med 81:856-857, 1974 2. PRCHKOV VK, MOOKHERJEE S, SCHIESS W, et al: Variant anginal
syndrome, coronary artery spasm, and ventricular fibrillation in the absence of chest pain. Ann Intern Med 81:858-859, 1974
