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North Carolina
Medical Journal
For Doctors and their Patients
North Carolina Medical Society's Spring Leadership Conference February 25-28, Durham Omni
he Way It Was
Carteret County Physician ecounts the Beginnings of is Practice 40 Years Ago
alter M. Brady, M.D. ntents 2
CONDENSED BRIEF SUMMARY
Zantac 15G Tablets (ranllidine hydrocliloride) Zantac 3Q0 Tablets (ranitidine bydfocblnride) Zantac Syrup (ranitidine hydrochloride)
The tollowing fs a bnel summary only. Belore prescribing, see complete pre- scribing information in Zantac" product latjehng. INDICATIONS AND USAGE: Zantac* is indicated in: 1 Sborl-term treatment of active duodenal ulcer. Most patients heal within 4 weeks Studies available to date have not assesseri the safety of ranllidine in uncomplicated duodenal utcer lor periods of more than 8 v/eeks.
2, Maintenance therapy (or duodenal ulcer patients at reduced tJosage alter healing of acute ulcers.
3. The treatment ot palhological hypersecretory conditions (e.g , Zollmger- Ellison syndrome and systemic mastocytosis)
4 Shorl-lerm treatment ot active, benign gastric ulcer. Most patients heal within 6 weeks and the usetulness ot lurther treatment has not been demon- strated Studies available to date have not assessed the safety of ranitidine in uncomplicated, benign gastric ulcer for periods ot more than 6 weeks
5, Treatment ot gastroesophageal relliri disease (GERD). Symptomatic re- liet commonly occurs within 1 or 2 weeks after starting therapy with Zantac 150 mg bid
6. Treatment of endoscopicaiiy diagnosed erosive esophagitis. Healing ot endoscoplcally diagnosed erosive esophagitis occurs at 4 weeks (47%) 8 weeks (71%), and 12 weeks (84%) ot therapy with Zantac 150 mg q.i d.' Symptomatic relief of heartburn commonly occurs within 24 hours ot therapy Initiation with Zantac.
Concomilant antacids should be given as needed for pain relief to patients with active duodenal ulcer; active, benign gastric ulcer; hypersecretory stales; GERD; and erosive esophagitis.
CONTRAINOICATIONS: Zantac' is contraindicated lor patienis known to have hyppi' ■ ' '' '. ■ ■'■-.'drug.
PRECAUTIONS General: 1 Symptomatic response to Zantac" therapy does not preclude the presence of gastric malignancy 2 Since Zantac is excreted primarily by Ihe kidney, dosage should be adjusted in patients with impaired renal function (see DOSAGE AND ADMINISTRATION) Caution should be ob- served in patients with hepatic dysfunction since Zantac is metabolized in the liver
Laboraloiy Tests: False-posilive tests lor urine protein with Multistix - may occur during Zantac therapy, and therefore testing with sultosalicylic acid is recommended
Drug Interactions: Although recommended doses of Zantac do not inhibil Ihe action of cytochrome P-450 enzymes in the liver, there have been isolated re- ports of drug interactions that suggest that Zantac may affect the bioavail- ability ot certain drugs by some mechanism as yet unidentified (e g a pH- dependent effect on absorption or a change in volume of distribution)
Increased or decreased prothrombin times have been reported during con- current use of ranitidine and warfarin. However, in human pharmacokinetic studies with dosages ot ranitidine up to 400 mg per day, no interaction oc- curred; ranitidine had no effect on warfarin clearance or prothrombin time The possibility ot an interaction with warfarin at dosages of ranitidine higher than 400 mg per day has not been investigated. Pregnancy: Teralogenic Cllecis: Pregnancy Category B: Reproduction stud- ies have been performed in rats and rabbits at doses up to 160 times the hu- man dose and have revealed no evidence of impaired fertility or harm to the fetus due to Zantac. There are, however, no adequate and well-controlled studies in pregnant women Because animal reproduction studies are not al- ways predictive ot human response, this drug should be used during preg- nancy nnly it clearly needed
Nursing Mothers: Zantac is secreted in human milk. Caution should be exer- cised when Zantac is administered to a nursing mother. Pediatric Use: Safety and effectiveness in children have not been established ADVERSE REACTIONS: Headache, sometimes severe, seems to be related lo Zantac" administration Conslipalion, diarrhea, nausea/vomiting abdominal discomlort/pain, and, rarely, pancrealilis have been reported There have been rare reports of malaise, dizziness, somnolence, insomnia, vertigo, lachycar- dla, bradycardia, atrioventricular block, premature ventricular beats, and arthralgias Rare cases ol reversible mental confusion, agitation, depression, and hallucinations have been reported, predominantly in severely ill elderly patients. Rare cases ol reversible blurred vision suggeslive ol a change in ac- commodation have been reported Rare reports of reversible involuntary mo- tor disturbances have been received
In normal volunteers, SGPT values were increased to at least twice the pretrealment levels in 6 of 12 subjects receiving 100 mg q i d intravenously for 7 days, and m 4 of 24 subjects receiving 50 mg q i d intravenously lor 5 days There have been occasional reports ol hepalilis, hepaiocellular or hepa- tocanalicular or mixed, with or without laundice, in such circumstances rani- tidine should be immedialely discontinued These events are usually re- versible, bul in exceedingly rare circumstances death has occurred
Blood count changes (leukopenia, granulocytopenia, and thrombocytope- nia) have occurred in a lew palienls. These were usually reversible. Rare cases of agranulocytosis, pancytopenia, sometimes with marrow hypoplasia and aplastic anemia and exceedingly rare cases ol acquired immune hemolytic anemia have been reported
Although controlled sludies have shown no anliandrogenic aclivity occa- sional cases of gynecomastia, impotence, and loss of libido have beeii re- ported in male palienls receiving Zantac, but Ihe incidence did not difler from that in the general populalion
Incidents of rash, including rare cases suggeslive ol mild erylhema multi- forme, and, rarely, alopecia, have been reported, as well as rare cases ol hy- persensilivily reactions (eg, bronchospasm, (ever, rash, eosinophilia) ana- phylaxis, angioneufolic edema, and small increases in serum crealinine, OVERDOSAGE: There has been limited experience with overdosage Reported acute ingestions ol up to 1 8 g orally have been associaled with transienl adverse effecls similar lo those encountered in normal clinical ex- perience (see ADVERSE REACTIONS) In addilion, abnormalities of gait and hypotension have been reported
When overdosage occurs, the usual measures lo remove unabsorbed ma- terial Irom the gastrointestinal tract, clinical monitoring, and supportive ther- apy should be employed
Studies in dogs receiving dosages ot Zantac' in excess ol 225 mg/kg per day have shown muscular tremors, vomiting, and rapid respiration Single oral doses ol 1 ,000 mg/kg in mice and rats were not lethal. Intravenous LDsn values in mice and rals were 77 and S3 mg/kg, respectively DOSAGE AND ADMINISTRATION: (See complele prescribing inlormalion in Zantac" produc! labeling.)
Dosage Adiuslment lor Patienis Wllh Impaired Renal Function: On the ba- sis of experience wllh a group ol subjecis with severely impaired renal lunc- tion treated with Zantac, the recommended dosage in palienls with a creati- nine clearance less than 50 mL per minute is 150 mg or 1 0 mL 2 leaspoon- luls equivalent lo 1 50 mg ot ranitidine) every 24 hours. Should the patient's condition require, the Irequency ol dosing may he increased lo every 1 2 hours or even further with caution. Hemodialysis reduces the level of circu- lating ranitidine. Ideally, the dosing schedule should be adjusted so that the liming of a scheduled dose coincides with Ihe end ol hemodialysis
May 1992
^ G/axo Pharmaceuticals
DMSIOH Of GLAXO IHd
Zanlac" 150 Tablels/Zanlac" 300 Tablets:
Glaxo Pharmaceuticals, Research Triangle Park, NC 27709
Zanlac" Syrup
Manufactured for Glaxo Pharmaceuticals, Research Triangle Park
NC 27709 by Roxane Laboralories, Inc., Columbus, OH 43216
i9 Copyright 1992, Glaxo Inc. All righls resen/ed.
ZA261 7 Printed in USA October 1992
#:
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Glaxo/^^
NORTH CAROLINA MEDICAL JOURNAL
For Doctors and their Patients
Published Monthly as the Official Organ of the North Carolina Medical Society
January 1993, Volume 54, Number 1 (ISSN 0029-2559)
/EorroR
Francis A. Neelon, M.D.
DEPUTY EDrrOR
Edward C. Halperin, M.D.
CONSULTING EDFTOR
Eugene A. Stead, Jr., MJ).
ASSOCIATE EDITORS
Eben Alexander, Jr., MX).
Winston-Salem William B. Blythe, MX).
Chapel Hill F. Maxton Mauney, Jr., M.D.
Asheville Walter J. Pories, M.D.
Greenville
MANAGING EDITOR
Jeanne C. Yohn
EDITORIAL ASSISTANT
Jane Whalen
SECTION EDITORS
Eugene W. Linfors, M.D. Daniel J. Sexton, M.D.
BUSINESS MANAGER
George E. Moore Raleigh
EDPTORIAL BOARD
CHAIR
Margaret N. Harker, M.D., Morehead City
MEMBERS
Jay Arena. M.D.
Durham William B. Blythe, M.D.
Chapel Hill Jack Hughes, M.D.
Durham Timothy W. Lane, M.D.
Greensboro Walter J. Pories, M.D.
Greenville Robert W. Prichard, M.D.
Winston-Salem Mary J. Raab, M.D.
Greenville Lx)uis deS. Shaffrier, MX).
Winston-Salem
The Society is not to be considered as endorsing the views and opinions advanced by authors of papers delivered at the Annual Meeting or published in the official pubhcation of the Society. — Constitution and Bylaws of the North Carolina Medical Society. Chap. IV, Section 3, pg. 4.
NORTH CAROLINA MEDICAL JOURNAL
Box 3910, Duke University Medical Center, Durham NC 2T710, (919-28«- «41(Vrax: 919-28<i-9219), is owned and published by The North Carolina Medi cal Society under the direction of its Edi tonal Board. Copyright© 1993 The North Carolina Medical Society. Address manuscripts and communications regarding editorial matters, subscription rales . etc. , to the Managing Editor at the Durham address listed above. All advertisements are accepted subject to the approval of the Editorial Board of the North Carolina Medical Journal. The appearance of an advertisement in this publication does not constitute any endoisement of the subject or claims of the advertisement.
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Annual subscription: $17 (plus 6% tax in NC). Single copies: $2 Second-class postage paid at Raleigh NC 27601 , and at additional mailing offices. Postmaster Send address changes to the North Carolina Medical Society. 222 N. Person St., Raleigh NC 27601.
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NCMJ / January 1993, Volume 54 Number 1 1
North Carolina Medical Journal
FOR DOCTORS AND THEIR PATIENTS
Contents / January 1993, Volume 54, Number 1
On the cover: "Portsmouth Island Remembered," (walercolor, 1963) by Charles R. McNeill of Morehead Cily, depicts part of rural Carteret County, which Dr. Walter M. Brady describes in his article on page 38. Island resident EUzabeth Pigott, who died in 1960 and whose headstone is in the foreground, was one of Dr. Brady 's first patients when he established his practice 40 years ago. Painting property of the author, used with the artist's permission.
A PIECE OF A NORTH CAROUNA DOCTORS MIND
6 The Road to Hell: New Rules to "Protect" Patients from Being Infected with HIV by Their Doctors
Charles Ellenbogen, M.D.
MEDICINE IN THE TIME OF AIDS
9 Tuberculosis in the AIDS Era
Charles Ellenbogen, M.D.
16 AIDS Cholangiopathy as the First Sign of HIV Infection John G. Lee, M.D., Paul Grech, MRCP. FRCR, Paul Edwards, M.B., M.S.. FRACP, and Joanne A. P. Wilson, M.D., FACP
18 Psychosocial Issues in Pediatric AIDS
Chris Weedy, MS.W.
HEALTH WATCH
25 Breast Cancer: Early Detection May Mean Cure Margaret L. Bertrand, MD., and Annie L. Hayes, R.N., M.P.H.
MODERN MEDICINE
30 Chronic Temporomandibular Joint Disease and Head Pain William S. Kirk, Jr., DDS.
TOXIC ENCOUNTERS
35 The Night the Light Went Off in Sestos: Roundup® (Glyphosphate) Poisoning
Ronald B. Mack, M.D.
NORTH CAROLINA HISTORY
38 The Way It Was: A Carteret County Physician Recounts the Beginnings of His Practice 40 Years Ago
Waller M. Brady, M.D.
COMPASSIONATE CAREGIVING
41 The Ministry of Caring, Part 2
Mar got Hover, D. Min.
LETTERS TO THE EDITOR
5 Medicare Cost Shifting In Tribute 45 Prescription for Prose
34 EDITORIAL Francis A. Neelon, MD.
43 CAROLINA PHYSICIAN'S BOOKSHELF
BULLETIN BOARD
23 Instructions for Authors
24 Subscription Form
46 New Members
47 Continuing Medical Education
50 Classified Advertisements
51 Aphorisms of the Month 51 Index to Advertisers
NCMJ / January 1993, Volume 54 Number I
WHAT HAVE OVER 2000
NORTH CAROLINA PHYSICIANS
DISCOVERED ABOUT THEIR PRACTICE?
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REMEMBER
1 975?
JANUARY 1H.R. HALDEMANN, JOHN C. MITCHELL AND JOHN D. EHRLICHMAN, FORMER TOP AIDES OF PRESIDENT RICHARD NIXON, ARE CONVICTED OF CONSPIRACY TO OBSTRUCT JUSTICE IN THE WATERGATE CASE.FEBRUARY 1 1 MARGARET THATCHER IS ELECTED LEADER OF THE CONSERVATIVE PARTY, BECOMING THE FIRST WOMAN TO HEAD A BRITISH POLITICAL PARTY.APRIL 30THE SOUTH VIETNAMESE GOVERNMENT SURRENDERS TO THE COMMUNISTS, ENDING THE WAR IN VIETNAM>SEP- TEMBER 29 THE MALPRACTICE SITUATION IN NORTH CAROLINA REACHES A CRISIS AFTER THE LAST COMMERCIAL INSURANCE COMPANY ANNOUNCES IT WILL NO LONGER PROVIDE MALPRACTICE COVERAGE IN THE STATE> OCTOBER UN MANILA, MUHAMMED ALI DEFEATS JOE FRA- ZIER IN THE FIFTEENTH ROUND TO RETAIN THE WORLD HEAVY- ^ WEIGHT BOXING TITLE> OCTOBER 23 NORTH CAR- OLINA PHYSICIANS CREATE A MUTUAL INSUR- ANCE COMPANY TO ASSURE A STABLE, FAIR PROFESSIONAL LIABILITY MARKET.^ THE YEAR S TOP FILMS INCLUDE MS, OHE FLEW OVER THE CUCKOO'S NESl AND mSHmLE.
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Letters
to the Editor
^
Medicare Cost Shifting To the Editor:
The article by Edward H. Kincaid, "The Medicare Pro- gram: Exploring Federal Health Care Policy," (NC Med J 1992;53:596-601) revealed an impressive understanding for the complexities of the system and how we got there. His comments, for the most part, were insightful and well balanced. However, I would like to take exception to one of his observa- tions.
He mentions, in a section entitled "Cost Shifting:" ". . .Fig- ure 2 shows a rapid decrease in hospital 'profits' from Medicare patients, ...a much slower decline in aggregate margin..." I disagree with his interpretation of what Figure 2 and Figure 3 reveal. If the Y ordinate was drawn on the same scale for both figures, it would clearly show that hospital overall margins have dropped much more precipitously than hospital PPS (Prospec- tive Payment System) margins.
I am especially pleased lo see a medical student publishing a comprehensive article addressing an area traditionally ig- nored in medical education. If we as physicians are to be part of the solution, we need to be able to grapple with the problem . Mr. Kincaid is well on his way.
Jack R. Page, M.D., M.B.A., Pres.
Coastal Emergency Services of the Carolinas, Inc.
3708 Mayfair Sl, Ste. 300
Durham, NC 27717
In Tribute To the Editor:
What a marvelous tribute to Dr. Davison in the November Journal (NC Med J 1992;53:604-5). As many of you know, words fall short in describing the magnificence and humility of this remarkable man. It is seldom that we have men of his quality in our midst.
Arthur B. Croom, M.D.
Former House Staff Officer
Duke University Medical Center
Radiology '54-'57
1311 Robin Hood Road
High Point, NC 27262
Continued on page 45
YOCON'
YOHIMBINE HCI
Description: Yohimbine is a 3a-15a-20B-17a-hydroxy Yohimbine-16a-car- boxylic acid methyl ester. The all<aloid is found in Rubaceae and related trees. Also in Rauwoltia Serpentina (L) Benth. Yohimbine is an indolallqdamine alkaloid with chemical similarity to reserpine. It is a crystalline powder, odorless. Each compressed tablet contains (1/12 gr.) 5.4 mg of Yohimbine Hydrochloride.
Action: Yohimbine blocks presynaptic alpha-2 adrenergic receptors Its action on peripheral blood vessels resembles that of reserpine, though it is weaker and of short duration. Yohimbine's peripheral autonomic nervous system effect is to increase parasympathetic (cholinergic) and decrease sympathetic (adrenergic) activity. It is to be noted that m male sexual performance, erection is linked to cholinergic activity and to alpha-2 ad- renergic blockade which may theoretically result in increased penile inflow, decreased penile outflow or both.
Yohimbine exerts a stimulating action on the mood and may increase anxiety. Such actions have not been adequately studied or related to dosage although they appear to require high doses of the drug Yohimbine has a mild anti-diuretic action, probably via stimulation of hypothalmic centers and release of posterior pituitary hormone
Reportedly, Yohimbine exerts no significant influence on cardiac stimula- tion and other effects mediated by B-adrenergic receptors, its effect on blood pressure, if any, would be to lower it: however no adequate studies are at hand to quantitate this effect in terms of Yohimbine dosage. Indications: Yocon ■ is indicated as a sympathicolytic and mydriatric. It may have activity as an aphrodisiac.
Contraindications: Renal diseases, and patient's sensitive to the drug. In view of the limited and inadequate information at hand, no precise tabulation can be offered of additional contraindications
Warning: Generally, this drug is not proposed for use in females and certainly must not be used during pregnancy. Neither is this drug proposed for use in pediatric, geriatric or cardio-renal patients with gastric or duodenal ulcer history. Nor should it be used in conjunction with mood-modifying drugs such as antidepressants, or in psychiatric patients in general. Adverse Reactions: Yohimbine readily penetrates the (CNS) and produces a complex pattern of responses in lower doses than required to produce periph- eral a-adrenergjc blockade. These include, anti-diuresis, a general picture of central excitatton including elevation of blood pressure and heart rate, in- creased motor activity, irritability and tremor. Sweating, nausea and vomiting are common after parenteral administration of the drug.^'^ Also dizziness, headache, skin flushing reported when used orally.'''' Dosage and Administration: Experimental dosage reported in treatment of erectile impotence. ' ■3'' 1 tablet (5.4 mg) 3 times a day. to adult males taken orally. Occasional side effects reported with this dosage are nausea, dizziness or nervousness. In the event of side effects dosage to be reduced to 'A tablet 3 times a day, followed by gradual increases to 1 tablet 3 times a day. Reported therapy not more than 10 weeks.3 How ^qiplied: Oral tablets of Yocon* 1/12 gr. 5.4 mg in bottles of 100's NDC 53159-001-01 and 1000's NDC 53159-001-10. References:
1. /v. Morales et al.. New England Journal of Medi- cine: 1221 . November 12, 1981 .
2. Goodman, Oilman — The Pharmacological basis of Therapeutics 6th ed., p. 176-188. McMillan December Rev. 1/85.
3. Weekly Urological Clinical letter, 27:2, July 4, 1983.
4. A. Morales etal.,TheJoumal of Urology128: 45-47, 1982.
Rev. 1/85
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NCMJ / January 1993. Volume 54 Number 1
A PIECE OF A NORTH CAROLINA DOCTOR'S MIND
The Road to Hell
New Rules to "Protect" Patients
From Being Infected with HIV by Their Doctors
Charles Ellenbogen, M.D.
Even when you think a law is bad, you still have to obey it.
In August 1992, the Commission on Health Services of North Carolina promulgated two public health rules (15A NCAC 19 A .0206 and .0207). These rules carry the force of law. These new rules — laws — are bad rules. They try to reduce the supposed risk that patients will become infected with the human immunodeficiency virus (HIV) from their health care provider should that provider be infected with HI V. But this risk may not even exist; at the outside, it is extremely small. Nevertheless, we still have to obey these new rules pending repeal. And obedi- ence— to rule .0206, at least — will be more complicated and difficult than most physicians or hospitals realize.
Rule .0206 specifies that hospitals and other health care organizations employing or granting privileges to health care workers infected with HI V or hepatitis B (HB), are obligated to prevent transmission of HIV or HB from these infected physi- cians to patients.
Rule .0207 specifies that individual health care providers whose practices include surgery, vaginal deliveries, or dentistry and who are infected with HIV or HB, are obligated to report themselves to the State Health Director. The Director will investigate each practitioner to determine whether the indi- vidual physician poses a danger to patients. If the Director decides that there is a danger, then the Director will: 1) report this to the appropriate State Licensing Board and 2) direct the physician to restrict his or her practice in specific ways designed to eliminate risks to any patient.
Here is why I think these rules are bad. We know that the risk of transmitting HIV infection from health care workers to patients is extremely small, if it exists at all. On May 15, 1992,
From Director, Internal Medicine, Fayetteville Area Health Edu- cation Center, Cape Fear Valley Medical Center, Fayetteville 28304.
two months before the stale Commission on Health Services promulgated its new rules, the National Centers for Disease Control (CDC) published findings on the risks of receiving care from HIV-infected health care workers.' The CDC reported HIV test results from 10,270 patients of 23 HIV-infected health care workers (including 1 1 dentists or dental students and six surgeons or obstetricians). The results were entirely negative. Among an additional 5,525 patients of nine HIV-infected health care workers, 84 patients were found to be HIV-infected. Forty-seven of the 84 had personal risk factors for HIV infec- tion; information on the remaining 37 patients is incomplete. So far this study has not demonstrated a single case of HIV transmission from a physician or dentist performing invasive or surgical procedures.
The editorial accompanying the MMWR report properly noted that more study is needed. But the bottom line is that, despite a vigorous search, no data support a risk of HIV transmission from health care workers (other than a single dentist) to their patients, and there is abundant evidence against it. The solitary instance of suspected transmission of HIV involves five patients of one dentist in Florida. The mechanisms of transmission in the case of this dentist are not clear, but the totality of scientific evidence indicates that the risk of HIV transmission from provider to patient is so minuscule that it cannot even be calculated based on the number of patients studied so far.^
But there is more to it. Another North Carolina Public Health rule (ISA NCAC 19a .0201 (b) (1)) states that, in attempting to preserve the public health, "control measures shall be those which can reasonably be expected to decrease the risk of transmission and which are consistent with recent scientific and public health information." Rules .0206 and .0207 cannot "reasonably be expected to decrease" a risk so small that it cannot even be computed.
NCMJ /January 1993, Volume 54 Number 1
Paragraph (e) of rule .0206 states: "In order to prevent transmission of HIV and hepatitis B from health care workers to patients, each health care organization that performs invasive procedures shall implement a written infection control policy* by July 1, 1993." This means that hospitals, surgical centers, nursing homes, our own office practices, and other organiza- tions are now institutionally responsible for keeping those of us who are infected from transmitting HIV or HB. The rule specifies some elements of policy. For example, "the health care organization shall ensure that health care workers in its employ or who have staff privileges are trained in the principle of infection control and the practices required by the policy*; require and monitor compliance with the policy; and update the policy as needed to prevent transmission of HIV and hepatitis B from health care workers to patients." But doing the listed things won't be enough unless they fulfill the overriding pur- pose specified in paragraph (e): prevention of transmission. Preventing transmission is the purpose of the rule and the policy must require whatever is necessary to achieve that. The listed activities are only minimal requirements.
Enforcement of rule .0206 is going to be com- plex . To begin with , the two rules ostensibly talk about the same infected health care workers and the same risks to patients, but they disagree with themselves on a major part of the basic definition of the cHnical procedures at risk. Both rules include sur- gery, obstetrical procedures,
and dental procedures, but
rule .0206 includes "use of
needles to puncture skin," while rule .0207 specifically ex- cludes "phlebotomy; administration of intramuscular, intrader- mal, or subcutaneous injections; needle biopsies; needle aspi- rations; lumbar punctures; angiographic procedures;..."
Furthermore, enforcing rule .0206 will be complex be- cause of the difficulty in identifying those who are infected. Neither of these rules, or any other for that matter, requires that physicians or other health care workers be tested. I cannot see how the State can pretend that these rules will protect patients, or can obhgate hospitals to do so, while leaving the choice of HIV or HB testing to the whim of the physicians who are supposed to be the sources of risk.
What kind of policy would allow a hospital to fulfill its legal obligation? First, the hospital must decide how to deter- mine what prevention requires. The answer is established by
rule .0207. It creates a standard of prevention, defined as an investigation of the practice of the infected health care worker by the State Health Director and restriction of the practice of the health care worker as specified by the Director. However, the State Health Director is not obligated to report his findings to the institutions who hire or grant privileges to an infected health care worker, only to the health care worker and to the State Licensing Board. So the health care organization can fulfill its institutional obligation, as defined by law, only by "finding out" in some unsj)ecified way that its health care workers have been tested and, if positive, reported the results.
Let me offer a specific example of a policy by which a hospital might comply with .0206. The hospital would require attestation in writing from each employee who has privileges to perform or assist in invasive procedures. At initial employment or granting of privileges and at each subsequent regranting of privileges, physicians and other providers would attest that they had been tested for HIV and hepatitis B and, if the results were positive, had complied with the requirements of 15A NCAC 19A .0207 by reporting themselves to the Slate Health Director.
Moreover, the attestation would further specify that, should the State Health Director's findings require limitation of any privileges, the physicians would confi- dentially report that to the Medical Director or the Chief of Staff and then com- ply with the restrictions.
If this kind of a policy sounds like illegal discrimi-
nation based solely on
HIV-infection, you are right. Both North Carolina and federal anti-discrimination laws are supposed to prohibit such discrimination, but in this case both permit it for the purpose of "protecting" other people, such as fellow workers or patients. In the case of health care providers who are hepatitis B antigen positive, there is some scientific basis by which such rules might be justified, because physicians and other providers do rarely transmit hepatitis B to patients.^ But there is nothing to justify such action with HIV-infected health care workers.
I think these are bad rules, but they are the law and, until repealed, have to be obeyed. By July 1, 1993, hospitals must develop policies to prevent transmission, and starting October 1, 1992, physicians who are HTV- or HB-infected must have reported themselves. Members of the Medical Society: beware the good intentions that have paved this road ahead of us. □
"I cannot see how the State can pretend that these rules W\\\ protect patients, or can obligate hospitals to do so, while leaving the choice of HIV or HB testing to the whim of the physicians who are supposed to be the sources of risk,"
* Italicized emphases above (this page, first column, paragraph) added by Dr. Ellenbogen.
first References
1 MMWR 1992;41:344-46.
2 Chamberland ME, Bell DM. HIV transmission from health care worker to patient: what is the risk? Ann Intern Med 1992;116:871-2.
NCMJ / January 1993. Volume 54 Number 1
[E Simple IdeaCan
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A single drop of water. It can effect change in a mass millions of times its size. In the same way, we believe our efforts should be far reaching. That's why we are dedicated to improving the quality of life through our medicines. And through our commitment to the community. To see the best ideas make waves.
Glaxo
A Pharmaceutical Research Company
MEDICINE IN THE TIME OF AIDS
Charles Ellenbogen, M.D.
Until 1 984, the incidence of active, clini- cal tuberculosis (TB) in the United States was falling. In 1984 the fall stopped, and the rate began to rise. By the late 1980s theU.S.caserateofTBwasl5.5%higher than its nadir. Through 1991 there were about 39,000 cases of TB more than had been expected,' nearly 26,000 cases of TB in 1990 alone. The resurgence of TB has occurred primarily — nearly 70% of new cases — among racial and ethnic mi- norities. More than half of all new cases and 86% of those in children under 1 5 years old were in blacks.
The increased frequency of infec- tion with Mycobacterium tuberculosis is due largely to the epidemic presence of the human immunodeficiency virus (HIV). HIV and its end-stage, AIDS, are greatly overrepresented among racial and ethnic minorities and so too is TB. Clini- cal TB occurs 100 times more often in HIV-infected (HI Vpositive) persons than in HTV-uninfected (seronegative) persons because HIV infection destroys the very cellular immunity that is the main im- munological defense against TB.
There is no firm evidence that HIV infection increases susceptibility to in- fection with A/. tuberculosishulUIW does increase the risk of disease among those who become infected.^ For example, 5% to 10% of persons in the general popula-
From Director, Internal Medicine, Fayetteville Area Health Education Cen- ter, Cape Fear Valley Medical Center, Fayetteville 28304,
tion who become infected with M. tuber- culosis develop acii\e disease within two years,' but 40% of HIV-positive persons develop TB within four months. About 15% of injectable drug abusers in New York City who were both tuberculin re- actors and HIV positive developed clini- cal TB within two years, while none of those who were tuberculin reactive but HIV negative did. As expected, the actual rate of clinical TB among HIV-positive persons varies depending on other con- tributory factors such as alcoholism , drug abuse, poverty, homelessness, and crowd- ing. These factors can combine, as when drug abusers crowd together in crack houses. The importance of these factors is shown by the fact that about 2% of middle class, gay, white males with AIDS in San Francisco had active clinical TB while 40% of homeless men with AIDS in New York City (most of whom are minorities, alcoholic, and drug abusers) did.
From the opposite perspective, 28% of patients with active TB cared for at the San Francisco Health Department in 1986-1988 were HIV positive,whiIe 57% of U.S. -bom TB clinic patients nation- wide were HIV positive and, in New York City, 90% of homeless men with active TB were HIV positive. In North Carolina in 1989-1990, 290 (22%) of 1,303 TB patients were tested for HIV and 26% were positive. This emphasizes the need to routinely test TB patients in North Carolina for HIV infection.
Geriatric Tuberculosis
HIV is not the only factor contributing to the increased incidence of TB. Even be- tween 1953 and 1984 when the incidence of TB was falling in other populations, it was rising among persons over age 65. In 1953, 1 3.8% ofnew cases of TB occurred in persons more than 65 years old; by 1979, this had risen to 28.6%, a change not explained by the increased propor- tion of aged persons in the population. In 1984-1985 the Centers for Disease Con- trol found 21.5 new cases of TB per 1(X),(X)0 community-dwelling elderly while the overall national incidence was 9.1. Among nursing home elderly, the rate was 39.2. Moreover, the death rate from TB in the elderly is 10 times higher than in persons aged 25 to 44 years.
In addition to being more frequent among the elderly, TB is often more occult. Miliary or disseminated tubercu- losis may be found only at autopsy be- cause the clinical presentation is more chronic, slowly progressive, and pro- tracted and the illness non-specific. Fe- ver may be absent, or even when present, virtually no other findings may point to- ward TB. Finally, the reactivation of old pulmonary TB may involve unusual sites in the elderly, such as the lower lung fields or even the anterior segment of an upper lobe, a site unknown in phthisiolog- ical lore. Unfortunately, due to age alone or to accompanying disease, tuberculin skin testing is less reliable in the elderly.
NCMJ / January 1993, Volume 54 Number 1 9
Diagnosis: The Tuberculin Skin Test
The intradermal injection of Purified Protein Derivative (PPD) by the Man- toux method is the best technique for identifying infection due to M. tubercu- losis. It is not a diagnostic test for disease due loM. tuberculosis. The tubercuUn skin test is adelayed-hypersensitivity reaction that takes 48 hours to 72 hours to develop, and is interpreted by measuring the di- ameter of the area of induration sur- rounding the injection site, if any.
Tuberculin tests may be negative for two reasons: 1) The person may never have been infected with M. tuberculosis, or 2) the person may have impaired cell- mediated immunity (cutaneous anergy). Anergic patients may have a negative skin test, even when infected. Cutaneous anergy is demonstrated by failure to respond to any of a group of skin lest antigens {Candida albicans, trichophy- ton, mumps, tetanus toxoid) known to produce nearly universal dclayed-hyper- sensitivity reactions. Demonstration of anergy to these skin test antigens and to PPD provides the most clinically rel- evant assessment of cell-mediated im- munity in HI V-positive persons apartfrom the direct measurement of the number of CD4-f lymphocytes (the "helper" cells invaded and destroyed by HIV). Less than 10% of HI V-positive Army person- nel with CD4-t- lymphocyte counts greater than 500/|jL (normal over 800) were anergic while two thirds of those with CD4+ counts less than 200 and 80% of those with counts less than 50 were. Of course, many serious illnesses other than HIV infection, or, treatment with immu- nosuppressive drugs such as corticoste- roids, may produce anergy.
CDC Recommendations for Skin Testing and Prophylaxis
PPD skin tests are read as positive or negative based on the area of induration induced in persons known to have TB compared to responses in persons known
not to have TB. An area of induration greater than 10 mm in diameter 48 hours to 72 hours after PPD injection is consid- ered a positive reaction in HIV-negative persons. These criteria are not absolute. For persons exposed by direct contact to TB, 5 mm of induration is considered positive. The CDC, taking into account alterations in skin test responsiveness created by impaired cell-mediated im- munity, has recommended that 5 mm of induration be the criterion for a posi- tive response in HIV-positive persons. The CDC recommends evaluating HIV- positive persons for anergy by injecting 0.1 mL of Candida, mumps, or tetanus toxoid antigens using the standard Mantoux method. Any amount of indura- tion rules out anergy, but erythema alone does not. Persons with a positive response
"North Carolina law mandates that HIV- positive persons be tested for PPD response. All those with a positive reaction should receive Isoniazid(INH)..."
to one or more of the anergy antigens , but less than 5 mm induration to PPD are considered not infected with M. tubercu- losis. However, these criteriaare not fool- proof and it may be that any induration should be considered positive in patients with very low CD4-t- counts. I suggest that you regard 2 mm of induration in response to intermediate strength PPD as positive in HIV-positive persons whose CD4+ lymphocyte count is less than 350/
North Carolina law mandates that HIV-positive persons be tested for PPD response. All those with a positive reac- tion should receive Isoniazid (INH) un- less toxicity is a problem. All contacts of such patients should also be treated, even if anergic or initially PPD negative. Other
persons at high risk for infection with M. tuberculosis (alcoholics, intravenous drug abusers, prison inmates, the homeless, migrant laborers, or those bom in high- risk countries in Asia, Africa, and Latin America) should be considered for INH prophylaxis if they develop 5 mm of induration to PPD, even if they are HIV negative. In 1988, 31% of migrant farm workers in North Carolina were PPD positive, reflecting the magnitude of the problem in that population.
Infection Control
The beginning of infection control is sus- picion of the diagnosis. Treating an in- fected person with an effective drug be- fore the infection becomes disease, can minimbx morbidity, mortality, and the risk of transmission. Patients infected with a susceptible strain of M. tubercu- losis and who receive 12 months of daily INH have a 90% reduction in the subse- quent rate of TB.' This same approach works in HIV-positive patients. Rifampin may be an acceptable alternative agent for INH-resistant organisms.'
HIV-positive TB patients pose a sub- stantial infection risk to their contacts. In a residential facility for HIV-positive persons in San Francisco, 1 1 of 3 1 (35%) residents exposed to a person with infec- tious pulmonary TB developed TB them- selves within four months.^ A recent study from Puerto Rico found that HIV-posi- tive patients without TB when admitted but who shared a room with a TB patient later developed TB themselves. Only 2% of those who did not have a TB patient as a roommate developed subsequent TB, an 11-fold increase in risk. Similarly, nurses working on an HIV ward are six times more likely to have a positive PPD than nurses on other hospital wards. Sixty percent of multidrug-resistant (MDR) TB patients had identifiable pastcontact with a known MDR TB patient through the HIV ward or clinic, although only 5% of control patients did. Cough induced by pneumonia (or by prophylaxis with aero- solized pentamidine) facilitates spread of organisms.
10
NCMJ / Jwuary 1993, Volume 54 Number 1
The CDC advises screening patients to rule out pulmonary TB before begin- ning prophylactic aerosolized pentami- dine. Since PPD skin testing will miss some cases, chest x-rays are necessary. Any abnormality on the chest film, not just those "typical" of pulmonary TB, should prompt study of the patient's spu- tum. Regrettably, severely immuno- compromised patients may have normal chest films in the presence of pulmonary TB. Nevertheless, the risk of dissemina- tion can be lowered if patients are detected and rendered non-infectious, or more realistically, isolated appropriately.
Recommended guidelines" for isola- tion include placement of the patient in a single room under negative air pressure to assure that all airborne organisms flow away from other patients and personnel. Patients should leave isolation rooms only for medically essential procedures that cannot be done in the room. When they leave, patients must wear a mask at all times, as should health care workers ex- posed to them. The CDC recommends particle and fume filtering masks specifi- cally manufactured to block droplets (not ordinary surgical masks). Unfortunately, such masks may be uncomfortable, may garble speech and cause respiratory dis- tress, and their effect! veness is not proven.
Once placed on precautions patients should remain so until the diagnosis of TB is excluded or the patient becomes non-infectious as demonstrated by clini- cal and bacteriological response to treat- ment— specifically, more than two spu- tum smears negative for acid-fast ba- cilli— and not just a predefined number of days on allegedly effective therapy. Even so, caution is needed because infec- tious persons with multidrug-resistantTB may have intermittently negative sputum smears.
The CDC found breaches of these precautions in hospitals that had epidem- ics of MDR TB. Delays in starting respi- ratory isolation and failure to maintain it long enough were frequent. Patients who should have been in isolation were found walking the corridors and using a public lounge.
Clinical TB: Comparing HIV-Negative and HIV-Positive Patients
The secret to antcmortem diagnosis is to think about the possibility of TB and to recognize its clinical variations. TB can be the first clinical manifestation of cel- lular immunodeficiency as it was in 88% of HIV-positive men with TB in San Francisco.^ These men were not yet se- verely immunodeficient, and it may be that clinical TB occurs at higher CD4+ lymphocyte counts than other infections associated with AIDS. Sometimes pul- monary TB is missed because the patient is found to have Pneumocystis and the
"The secret to
antemortem diagnosis
is to think about
the possibiiity of TB
and to recognize
its clinical variations.
TB can be the first
clinical manifestation
of cellular immunodeficiency as It was in 88% of HIV- positive men with TB in San Francisco. 2"
search for M. tuberculosis is abandoned despite the possible presence of multiple pathogens at the same time in these pa- tients.
Extrapulmonary TB is seen in up to 70% of AIDS patients with TB. The like- lihood of extrapulmonary TB rises as the CD4-H count falls so that the 70% rate of extrapulmonary TB occurs in severely immunocompromised patients (for ex- ample, those with AIDS). Looked at from the opposite perspective, patients with extrapulmonary TB are twice as likely to be HIV positive as those with only pul-
monary disease. Extrapulmonary TB in AIDS patients may take the form of tu- berculous brain abscesses, osteomyelitis including vertebral disease, pericarditis, gastric and peritoneal disease, and scrotal abscess." Clinical forms unique to HIV- positive patients include large tubercular abscesses of the liver, abdominal wall, psoas muscle, mediastinum, and para- pancreatic area.
Miliary Tuberculosis
The febrile illness that marks dissemi- nated or miliary TB can be easily misdi- agnosed, or just missed. Since blood cultures may be positive in such patients, their use, previously unusual in TB, is now of primary importance. In fact, blood may be the only source of positive cul- tures in 19% to 42% of cases. Blood culturesare best made using BacTec bottle number 1 3 A, which effectively supports growth of many acid-fast species, includ- ing Mycobacterium avium-intra- cellularae and can show positive growth in as little as two weeks to three weeks. Conditions predisposing to dissemi- nation in the HIV-negative population include alcohol and tobacco use, steroid therapy, and connective tissue or renal disease, conditions often present in HIV- positive patients. Among HIV-positive patients with disseminated TB, 90% are febrile and, as with HIV-negative pa- tients, many of their clinical findings are non-specific. Two thirds of the chest films show miliary orreticulonodular infiltrates. Sterile pyuria is found in one third of cases but does nor correlate with isolation of M. tuberculosis from the urine. Tuber- culin skin tests are usually negative (72% to 90% of cases are negative compared to 40% of HIV-negative patients with dis- seminated TB). Most, but not all, patients who are PPD negative are anergic.
Tuberculous Meningitis
TB meningitis is a slowly evolving disor- der and half of all patients present with an illness of more than two weeks duration.
NCMJ / January 1993, Volume 54 Number 1 1 1
When behavioral disturbances predomi- nate, diagnosis may be delayed for months. No cUnical findings distinguish TB meningitis from fungal meningitis or syphilis. Ocular palsies, particularly of the abducens nerve, are common (in 30% to 70% of patients). Lymphocytic pleo- cytosis, elevated CSF protein, and low glucose are found on the first lumbar puncture in only two thirds of patients. Repeated LPs may be needed to docu- ment meningitis, to culture the CSF and perform smears, and to measure crypto- coccal antigen and VDRL.
TB meningitis is five times more common in HIV-positive than in HIV- negative patients. Presenting symptoms of fever, headache, and altered mental status are often associated with signs of systemic TB such as lymphadenopathy, and hepatomegaly in HIV-positive pa- tients. Traditional meningeal signs are less common than in HIV-negative pa- tients with TB meningitis. Since HIV- positive patients often have other causes of fever, headache, and altered mental status, TB meningitis is easy to miss.
Diagnostic Studies
Chest radiographs should be obtained in all HIV-positive patients with any chest or constitutional symptoms. Even with pulmonary TB, these patients may have unusual patterns of x-ray findings that become more atypical, may even be "normal," as immunocompromise wors- ens. Patients with lower CD4-(- counts have more diffuse infiltrates, often mim- icking those due to Pneumocystis carinii pneumonia and about 25% of patients have intrathoracic adenopathy. Pleural effusion may be the sole "positive" find- ing. There may be lower lung field paren- chymal infiltrates, resembling primary TB. Focal consolidation is present in from 30% to 40% and a miliary pattern (nod- ules 1-3 mm in diameter with a few larger) in up to 50% of patients. Cavities are less frequent but similar otherwise to those found in HIV-negative patients.
For the most part, sputum smears and cultures are helpful in HIV-positive
patients but they are positive less often (as few as 30% of cases) as the CD4 count falls. Diagnosis of TB in extrapulmonary sites relies on culture of blood, lymph nodes, bone marrow, hver, cerebrospinal fiuid (CSF), or urine.
Among HIV-positive and HIV-nega- tive patients with TB meningitis, the CSF initially has normal glucose, protein, and lymphocyte count in more than 10% of cases. The CSF may even show a neutro- philic leukocytosis early in TB meningi- tis. TB smears of the CSF are insensitive (about 22% positive) and head CT scans, while abnormal in 69% of cases of TB meningitis, are non-specific. Chest x-rays suggest active TB in only 54%, and the PPD is positive in only 29% of cases of TB meningitis. Unfortunately, mortality of TB meningitis is high, even with ap- propriate treatment.
Mycobacterium Avium Intracellularae (MAI)
Infection with M. tuberculosis is more common in HI V-positive than HIV-nega- tive persons, but MAI is more common than TB in HIV-positive persons. Distin- guishing the two can be difficult until cultures are reported. Clues to the pres- ence of MAI include the fact that it is rarely a pulmonary pathogen, and that it is a disseminated disease, occurring only after severe immunocompromise has de- veloped. If a febrile HIV-positive patient with a low CD4+ count has anemia, diar- rhea, and fever, think MAI . Stool or blood cultures may grow the organism. M. tu- berculosis grows from the stool only when organisms in the sputum have been swal- lowed, but MAI involves the bowel di- rectly. In most cases, however, it is not possible to distinguish MAI from M. tu- berculosis on clinical grounds.
Treatment of HIV- Negative Patients
Six months of Isoniazid (INH) and Rifampin (RIF) therapy, using one or two additional drugs at the beginning, works
as well as nine months of INH and RIF alone.' HIV-negative patients with pul- monary tuberc ulosis whose sputum smear shows acid-fast organisms and whose culture is positive, can be placed on one of two alternate regimens of three or four drugs for six months (Table 1 , at right). Both have proven safe and effective. Un- fortunately, both are more expensive than the previous nine-month regimen. One regimen requires daily therapy for six months while the other switches from daily to twice-weekly therapy after two weeks.
On either regimen sputum cultures become negative in more than 90% of patients after 16 weeks of therapy and virtually all patients are ultimately cured. Relapse rates of 3.5% and 1.6% were noted with the daily and twice weekly regimens, respectively. Approximately 1 .9% of daily therapy patients died due to tuberculosis while 2.4% of twice -weekly therapy patients died. Hepatotoxicity was more common in the twice-weekly drug recipients (6% vs. 1.6%). The twice- weekly regimen costs less ($1 13 vs. $92) but has higher toxicity; the reason for selecting it is that patients may comply with it better than with the daily regimen. Otherwise, it is not possible to designate one of these two regimens as superior.
Smear-Negative,
Culture-Positive
Tuberculosis
If an HIV-negative patient is suspected of having TB but the sputum smear is nega- tive for acid-fast organisms, the diagno- sis is obviously less certain. In one study, four pre-therapy sputum culture speci- mens were obtained and the patient started on INH and RIF. When, after eight weeks, the sputum culture was found to be posi- tive, the combination of INH and RIF alone for a total of six months proved to be adequate therapy. Specifically, 300 mg of INH and 600 mg of RIF (may be taken together in the form of Rifamate) should be given once daily until the cul- ture report returns. If the culture is nega- tive, treatment can be stopfxjd; if posi-
12
NCMJ / January 1993. Volume 54 Number 1
live, treatment can be continued (or changed to 900 mg INH and 600 mg RIF twice weekly) for a total of six months. If patients are elderly, alcoholic, or poorly nourished, 50 mg of pyridoxine should be given with each dose. Overall success was 97% with arelapserateof 2.4% after a median of 45 months of follow-up.
Treatment of HIV-Positive Patients
Standard anti-tuberculous drug regimens ordinarily work as well against sensitive strains of M. tuberculosis in HIV-posi- tive or AIDS patients as in HI V-negative patients. However, some patients have failed the standard six-month regimen and therapy for nine months is preferred.^ Eitherof the two drug regimens described in Table 1 may be chosen and given for nine months, although ethambutol (E MB) may be superior in HIV-positive TB pa- tients.' Streptomycin (SM) is helpful but it, like pyrazinamide (PZA), should be used only for the first four to eight weeks to minimize toxic effects on the ear and kidney.
If an HIV-positive patient with TB has a cHnical relapse, remember to look for other opportunistic, HlV-related in- fections, not just more TB. In addition, two anti-fungal agents often used in HIV- positive patients — ketoconazole and fluconazole — can reduce serum levels of INH and RIF and ketoconazole can inter- fere with RIF absorption.
Multidrug- Resistant (MDR) TB
M. tuberculosis isolates from patients in large cities have shown increasing drug resistance for years. In 1991, 14.4% of tested isolates in the U.S. were resistant to at least one anti-tuberculous drug and 3.3% to both INH and RIF. North Caro- lina has a lower rale of resistant organisms, but in the first nine months of 1992, 17 of 406 isolates (4.2%) were resistant to one drug.
The rise in drug-resistant M. tuber-
Table 1. Two alternate drug regimens
.
Dally Regimen
Twice-Weekly Regimen
INH: 300 mg daily for 24 weeks
First Two Weeks— Dally Doses
RIF: 600 mg daily for 24 weeks
INH: 300 mg daily
PZA: 30 mg/kg daily for eight weeks;
RIF: 600 mg daily
dosage rounded to accommodate
PZA: 1 .5 g if weight ^ 50 kg;
500 mg tablet size
2,0 g if 51 to 74 kg;
2,5 g if 2: 75 kg.
If patient previously had INH,
SM; 750mglMdailyifweighti50kg
or emigrated from a country
1.0 g if > 50 kg
at high risk for MDR TB, add:
EMB: 15 mg/kg/day until sensitivity
Weeks Three Through Eight—
tests done.
Twice Weekly Doses
INH: 15 mg/kg/body weight
RIF: 600 mg
PZA: 3,0 g if weight ^ 50 kg
3.5 g if 51 to 74 kg
4.0 g if i 75 kg
SM: 1.0 g IM if weighty 50 kg
1.25 g if 51 to 74 kg
1 .5 g if i 75 kg
Weeks Nine Through 26 —
Twice Weekly Doses
INH: 15 mg/kg/body weight.
RIF: 600 mg.
Abbreviations:
INH = Isoniazid RIF = Rifampin PZA = Pyrazinamide EMB = Ethambutol SM = Streptomycin
culosis is mainly due to patients' failure to take drugs as prescribed. In the past two years, there have been at least eight outbreaks of TB due to organisms resis- tant to multiple, first-line, anti-tubercu- lous drugs.' All were resistant to INH and RIF. More than 200 cases of MDR TB were recognized among in-patients, 83 of whom were HIV positive and 76 of whom had AIDS; mortality was 72% to 83%. In North Carolina there were no cases of MDR TB during or before 1 99 1 , and only four of 406 (0.98%) cases were resistant to both INH and RIF in the first nine months of 1992.' One of these North Carolina isolates was initially fully sen- sitive and became resistant over time due to patient non-compliance.
Mortality among HIV-negative pa- tients or health care workers with MDR
All drugs given by mouth except SM, which is given intramuscularly.
TB was no different from that due to drug-sensitive M. tuberculosis. Median survival after diagnosis of MDR TB in HIV-positive patients was 2.1 months compared to 14.6 months with drug-sen- sitive strains.
Epidemic transmission of MDR M. tuberculosis among HIV-positive persons tended to occur in the HIV clinic or ward.' HIV-negative persons or HIV-px)sitive patients with MDR TB who had no con- tact with an in-patient ward or clinic developed MDR TB because they failed to comply with a prescribed anti-tubercu- lous drug regimen or because they con- tracted the disease in a country with a high prevalence of MDR TB.
The question of anti-tuberculous pro- phylaxis in HIV-positive personsexposed to MDR M. tuberculosis is perplexing.
NCM J / January 1 993, Volume 54 Number 1 13
INH and RIF are obviously useless and no other agents have been tested for pro- phylaxis. Two regimens are currently under consideration.' One is a combina- tion of PZ A (daily oral dose of 25-30 mg/ kg) and EMB (daily oral dose of 15-25 mg/kg). A dose of 15 mg/kg of EMB gives bacteriostatic levels of drug and minimizes the risk of retrobulbar neuri- tis. A dose of 25 mg/kg may be bacteri- cidal, and therefore is preferable for pro- phylactic use but it poses a shghtly higher risk of retrobulbar neuritis. The other proposed regimen uses PZA and a fluoroquinolone, either ofloxacin at 4(X) mg twice daily or ciprofloxacin at 750 mg twice daily. Sparfloxacin, an experimen- tal quinolone, appears superior but is not yet available in the U.S.
The clinical findings and course of patients with MDR TB are similar to those in HIV-positive persons with drug- sensitive TB. Only 54% of cases were PPD positive. Nine percent had extrapul- monary disease only and 25% had both pulmonary and extrapulmonary disease; 66% had pulmonary disease only. The sputum smear was negative in 42% of cases, although other reports found smears negative in about 25% of cases. Many
cases of MDR TB had atypical or incon- clusive radiographic findings thatdelayed timely diagnosis.
Only those patients with MDR TB who received more than three drugs to which the organism was sensitive siu"- vived longer than patients with MDR TB who received no effective drugs. Even in appropriately treated patients, mortality is high; most patients continue to have intermittently or persistently positivecul- tures for M. tuberculosis and none steril- ize sputum or other tissues. All MDR TB cases, even those with cUnical responses, remain infectious.
Delay or failure to recognize drug resistance contributes to the danger of the epidemic. New technologies are needed to speed both diagnosis and sensitivity testing. DNA probes specific for M. tu- berculosis and MAI can speed recogni- tion of the organism, and the combined use of radiometric cultures and DNA probes may shorten the time needed to recognize M. tuberculosis in a culture specimen to seven to 10 days.^ The radio- metric method can also reduce the time to identify drug-resistant organisms from seven weeks to three weeks.'
The U.S. Public Health Service (USPHS) Plan
The USPHS has published a plan to combat TB in high-risk populations such as minorities and the homeless.' Since MDR TB is prevalent in such popula- tions, the plan proposes direct observation of treaunent because non-comphance is a major reason for therapy failure. Non- comphance also contributes to the devel- opment of MDR TB. Finding the money to pay for this expensive program will be a challenge. Expansion of Medicaid, Medicare, Social Security, and even pri- vate insurance coverage are all consid- ered in the plan.
To limit the nosocomial spread of MDR TB in AIDS patients, the plan re- examines the effectiveness of respiratory isolation, the use of germicidal ultravio- let radiation, and respiratory protective devices and policies. Even the use of Bacillus Calmette-Guerin (BCG) vaccine in health care workers will be re-exam- ined. □
References
1 Centers for Disease Control. Recommen- dations and rejxirts. Prevention and control of tuberculosis in the U.S. communities with at-risk minority populations and pre- vention and control of tuberculosis among homeless persons. MMWR 1992;41:1-23.
2 Hopewell PC. Impact of human immuno- deficiency virus infection on the epidemi- ology, clinical features, management, and control of mberculosis. Clin Infect Dis 1992;15:540-7.
3 Centers for Disease Control. National ac- tion plan to combat multidrug-resistant tu- berculosis; meeting the challenge of
multidrug-resistant tuberculosis: summary of a conference; management of persons exposed to multi-drug resistant tuberculo- sis. MMWR 1992;41:5-71.
4 Centers for Disease Control. Guidelines for preventing the transmission of tuberculosis in a health-care setting, with special focus on HIV-related issues. MMWR 1990; 39:1-29.
5 Committee on Infectious Diseases, Ameri- can Academy of Pediatrics. Chemotherapy for tuberculosis in infants and cfiildren. Pediatrics 1992;89:161-5.
6 Small PM, Schecter GF, Goodman PC, et al. Treatment of tuberculosis in patients with advanced human immunodeficiency virus infection. N Engl J Med 1991; 324:289-94.
7 Snider DEJr, Roper WL. The new tubercu- losis. N Engl J Med 1992;326:703-5.
8 Beck-SagueC, DooleySW,HuttonMD,et al. Hospital outbreak of multidrug-resistant Mycobacterium tuberculosis infections: fac- tors in transmission to staff and HIV-infected patients. JAMA 1992; 268; 1280-6.
14
NCMJ //onuary 1993, Volume 54 Number 1
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MEDICINE IN THE TIME OF AIDS
AIDS Cholangiopathy as the First Sign of HIV Infection
John G. Lee, M.D., 'Paul Grech, MRCP, FRCP,
Paul Edwards, M.B., M.S., FRACP, and Joanne A. P. Wilson, M.D.
FACP
Gastrocnterilis, esophagitis, and hepati- tis arc common gastrointestinal manifes- tations of AIDS and may precede the formal diagnosis of AIDS by many months. On the other hand, the biliary tree is not often involved early in the course of human immunodeficiency vi- rus (HIV) infection. Cholangiopathy is usually found only in patients who have clinically obvious (CDC stage IV) AIDS. We report here the unusual case of a previously healthy man whose AIDS cholangiopathy was the first clinical mani- festation of HIV infection.
Our Patient
A 3 1 -year-old, previously healthy homo- sexual man complained of abdominal pain and diarrhea. Six days before admission, he had developed severe mid-abdominal pain, nausea, and diarrhea. Physical ex- amination was normal except for a low- grade fever. Alkaline phosphatase was 642 lU/L (normal range 30-1 10); aspar- tate aminotransferase, 140 lU/L (normal range5-35)andalanineaminotransferase, 155 lU/L (normal range 5-35). Blood cell counts, and total serum bilirubin, amy- lase, and lipase were normal.
Abdominal ultrasound revealed a thick-walled, distended gallbladder con- taining "sludge." The biliary system and the pancreatic duct were dilated. The
From the Department of Medicine, Divi- sion of Gastroenterology and the 'Depart- ment of Radiology, Box 3858, Duke Uni- versity Medical Center, Durham 27710.
walls of the extra hepatic and larger intra-hepatic bile ducts were irregularly thickened and a zone of hyperechoic tis- sue surrounded the larger intra-hepatic ducts (Figure 1 , at right).
Endoscopic retrograde cholangio- pancreatography (ERCP) demonstrated a dilated biliary system with an irregular lumen. The intrahepatic ducts contained areas of stricture and of focal dilatation (Figure 2, at right). There was delayed drainage of contrast agent from the bil- iary system, suggesting papillary stenosis. Following endoscopic incision of the sphincter of Oddi, the patient experi- enced relief of abdominal symptoms. A repeat abdominal ultrasound demon- strated resolution of the extrahepatic bile duct dilatation and gallbladder disten- sion. Focal intrahepatic biliary dilatation persisted and the bile ducts and the gall- bladder walls remained thickened.
Stool examination revealed the pro- tozoal parasite, Cryptosporidium, and HIV serology was positive. There were no other clinical manifestations of HIV infection. Based on our diagnosisof AIDS cholangiopathy and Cryptosporidium in- festation, he was discharged on zidovudine and trimethoprim — sulfa- methoxazole. Six months later he re- mained asymptomatic.
Discussion
In this case the diagnosis of AIDS cholangiopathy was suggested by bio- chemical evidence of cholestasis and by cholangiographic abnormalities. Gall-
bladder wall thickening is the most com- mon finding in AIDS cholangiopathy' but is non-specific. Bile duct wall thick- ening provides additional evidence of cholangitis. Such thickening may occur in primary sclerosing cholangitis, but then we would not expect generalized biliary dilatation. AIDS cholangiopathy is not associated with jaundice unless there is hepatocellular disease.^
Various infective and neoplastic causes have been implicated in the pathogenesis of AIDS cholangiopathy.^ In our patient, Cryptosporidium was presumably the etiological agent, but since bile was not cultured and the ampulla of Vater not biopsied, a definite causal relationship cannot be proven. Other agents might be involved as suggested by the report that eight of nine patients with Crypto- sporidium cultured from the biliary tract had other intestinal opportunistic infec- tions.'
The optimal treatment for AIDS cholangiopathy is not established. Cholecystectomy may relieve pain but symptoms may recur due to disease pro- gression." In the presence of papillary stenosis endoscopic sphincterotomy may be effective^ as it was in our patient. Spiramycin treatment of Crypto- sporidiosis does not seem to be effec- tive.'
The occurrence of AIDS cholan- giopathy in an otherwise asymptomatic person who has no other manifestations of HIV infection is highly unusual. We found only three previous reports of AIDS cholangiopathy in patients who did not
16
'HCUi IJanuary 1993, Volume 54 Number 1
have clinically obvious AIDS. One pa- tient had a history of drug abuse and tested positive for HIV antibody after ERCP.^ No details were given but the patient was noted to have had AIDS symp- toms for one month prior to the diagnosis of cholangiopathy. Another patient de- veloped AIDS cholangiopathy two months after a seroconversion illness as- sociated with primary HIV neuropathy and dermopathy.' The third patient had AIDS-related complex (ARC) and diar- rhea.' The largest series reported to date showed that patients had had known AIDS for a mean of 5.8 months (range: 1-23 months) at the time of diagnosis of AIDS cholangiopathy.^
Our case clearly illustrates that AIDS cholangiopathy may be the presenting manifestation of HIV infection in other- wise asymptomatic, apparently healthy persons. Given the increasing prevalence of HIV infection, AIDS cholangiopathy should be considered in patients who present with biliary symptoms, chole- stasis, and evidence of gallbladder and bile duct wall thickening especially when accompanied by irregular biliary dilata- tion. The absence of clinically advanced HIV disease should not dissuade the cli- nician from this diagnosis. □
References
1 Romano AJ, Van Sonnenberg E, Casola G, Gosink BB, Withers CE, McCutchan JA, et al. Gallbladder and bile duct abnormalities in AIDS: sonographic findings in eightpatients. JAR, 1988;150:123-127.
2 Cello JP. Acquired immunodeficiency syn- drome cholangiopathy: spectrum of disease. Am J Med, 1989 86:539-546.
3 Teixidor HS, Godwin TA, Ramirez EA. Cryptosporidiosis of the biliary tract in AIDS . Radiology, 1991;180:51-56.
4 lannuzzi C, Belghici J, Erlinger S, Menu T, Fekete F. Cholangitis associated with cholecystitis in patients with acquired im- munodeficiency syndrome. Archives of Sur- gery, 1991;125:1211-1213.
5 Mercey DE, Loveday C, Miller RF. Scleros- ing cholangitis rapidly following anti-HI V- 1 seroconversion. Genitourin Med, 1991 67;239-243.
6 Roulot D, Valla D, Vezinet-Brun F, Rey M-A, Clavel F, Degott C, et al. Cholangitis in the acquired immunodeficiency syndrome: report of two cases and review of the litera- ture. Gut, 1987:28:1653-1660.
r
■
•
m m
li
1
GT UNIT 2r/fi'
Figure 1 (above). Longitudinal scan of common hepatic duct (closed arrow) and right hepatic duct (open arrow)) demonstrating irregularity of the lumen and echogenic zone surrounding the duct wall (arrow heads). The common bile duct is dilated to 1 1 mm. PV-porlal vein, L-liver.
Figure 2 (right).
Cholangiogram showing dilated extrahepatic bil- iary system (nor- mal duct should be of smaller diameter than the endoscope shown in the fore- ground) with ir- regular luminal border. The intra- hepatic ducts are strictu red (arrow) with upstream di- latation (arrow head). These findingsarechar- acteristicof AIDS cholangiopathy.
tiCMJ/ January 1993, Volume 54 Number 1 17
MEDICINE IN THE TIME OF AIDS
Psychosocial Issues in Pediatric AIDS
Chris Weedy, M.S.W.
Two hundred North Carolina children were bom with antibodies to the human immunodeficiency virus (HIV) in 1991, a 42% increase over 1990! At Duke Uni- versity Medical Center we are following 167 children who are HFV-exposed or infected, and we have evaluated a total of 329 pediatric patients since 1986. All children bom to HIV-infected women are seropositive at birth. Ultimately, one third prove to be HIV infected; the rest have received maternal antibody (not vi- rus) and serorevert. Health care profes- sionals, as they provide medical care to the growing cohort of children with HIV, must be familiar with and address the psychosocial issues that surround this devastating illness. In this paper I distill what I have learned from my experience as a clinical social worker who for five years has helped in the care of the chil- dren and mothers who attend our clinic. Most of the patients seen in pediatric AIDS treatment centers have acquired their infection by perinatal transmission of the vims. Ninety percent of the active patients in our pediatric infectious dis- ease clinic were bom to HIV-infected women. In order to understand the in- creasing incidence of perinatal transmis- sion we must understand the women who give birth to HIV-positive children.
The Women
In general, HIV-infected women attend- ing our clinic are young, usually in their
Ms. Weedy is a clinical social worker in Pediatric Infectious Diseases at the Duke University Medical Center, Durham.
20s and 30s (Table 1). Most of them are poor and depend on food stamps and social assistance programs (AFDC, SSI, WIC) for survival. They are education- ally poor as well; they usually have not completed high school. Most are minor- ity women, are single, and have, on aver- age, two to three children. They most commonly have contracted HIV through unprotected sexual intercourse (Table 2), although intravenous dmg abuse plays a role, directly and indirectly.
Geographically, the women come from virtually all counties in North Caro- lina. Forty-one percent of the HIV-infected mothers acquired their in- fection in North Carolina.' Metropolitan areas tend to have higher sero-prevalence of HIV, but the rate in rural counties is rising (Table 3) so no area is safe from this epidemic.
Social Issues
Families are very aware of the social stigma of having HIV. When mothers are informed of their own or their child's positive HIV status, they know how it will affect their rela- tionships with family, lovers, friends, employ- ers, and colleagues. Social isolation is a problem but, for the most part, is self-im-
posed because of fear of discrimination, rejection, and persecution. Widespread negative publicity reinforces and justi- fies these fears.
Discrimination is most common among family members and in day care and school settings. In all cases, it is due to fear of contagion. A respected health care professional who is comfortable and confident in explaining transmission is- sues can greatly assist by educating fam- ily members and teachers. Once fears are resolved, normal relationships can be re- sumed.
Because a perinatally exposed child has, by definition, an HIV-infected mother, the problems are multiplied.
Table 1. Maternal
demographics
Average age:
26 years
Average income:
$391/month
Source of income:
78% social programs
Education:
58% < high school degree
Marital status:
78% single
Race:
86% African-American
Average # of child
en:
2.45
Table 2. Maternal risk factors for HIV
Unprotected sexual intercourse 62%
a) sexual partner risk factor — unknown 60%
b) sexual partner risk factor — IVDU 31%
Intravenous drug use 32%
18
NCMJ/ January 1993, Volume 54 Number 1
Table 3. Seroprevalenca rates per 1,000 deliveries In NC
Metropolitan Rural
2.32
1.72
Source: NC AIDS Control Program, Perinatal Conference, August 1992
Having mother and at least one child with HIV greatly influences the number and kind of social problems family members face. Hospitalizations, multiple medical appointments, treatments, and, finally, death all produce separations between family members. Some families cope by stretching their boundaries and allowing other family or non-family members to provide care. Other families disintegrate and social services must provide the nec- essary structure such as a foster home.
Because these families are poor, their resources are slim. Most families do not have a car to provide transportation to medical appointments. Thermometers are rare in the home, and most parents do not understand how to take or interpret a child's temperature. Telephones, even for emergency calls, may be unavailable for economic reasons. Acetaminophen costs $4 a bottle. When this represents about 1% of a family's monthly income it may be an expense they cannot afford.
Being the parent of a child with HI V requires follow-through. This ranges from adhering to complex medication sched- ules, to keeping medical appointments, to maintaining enrollment in social pro- grams, to watching for signs and symp- toms of Pneumocystis carinii pneumo- nia. The caregiving parent must be ever alert and focused on the child.
There is a high prevalence of illegal drug use in the home. This (and its con- comitant social issues) combine with poverty and erratic medical fol- low-through to make child protection is- sues a constant concern (Table 4). Abuse, neglect, and dependency (the inability to provide for a child) must, by law, be reported to the Department of Social Ser- vices. Dependency in families of chil- dren with AIDS may be due to
Table 4. Social conditions contributing to child protection Issues In children with HIV
1.
advancing HIV disease in the mother
2.
illegal drug use
3.
alcoholism
4.
poverty
5.
lack of family support
6.
homelessness, housing changes
7.
chaos/instability in home
8.
incarceration of parent/caregiver
homelessness, or death, incarceration, or hospitalization of a parent. The most fre- quent form of abuse I have seen is sexual abuse, which can be the means by which the child contracts HIV.^ Tragically, per- petrators may sexually abuse their victim without regard to the child's HIV status.' Other examples of neglect I've seen in- clude failure to give medicines or to keep medical appointments.
In my experience. North Carolina's 100 counties vary widely in how their social service departments respond to complaints of neglect, abuse, or dej>en- dency. Let me give you a recent example: two families had HIV-infected two-year- olds with an uninfected sibling. In both cases, there was severe neglect by the mother. One department of social ser- vices "followed" the children, document- ing the problems in the home; the other department put the two children in foster care and then worked intensively to help the mother get her life back together.
In another example from a third county, an infant was not fed for three days, while her mother binged on co- caine. The child was transported by heh- copter from the local hospital and was found to have a serum sodium of 171 upon arrival. Initially, social services re- fused to prosecute the mother, and when they did go to court, they argued to return the baby to her mother immediately be- cause both had HIV and therefore "had
little time left" Fortunately the judge in this case protected the child by ordering her into foster care where she lived for another year and a half. Health profes- sionals need to take an active role in educating social service staffs to advo- cate the safety of children with HIV. This may mean taking an unpopular stance with the department of social services, which has family unification as its goal, but it may make the world a little safer place for children with HIV.
Placement in Foster Care or with a Relative
Foster care, either temporary or perma- nent, is a likely outcome when the parent cannot improve a neglectful, abusive, or dependent situation. Until three years ago neglected, abused, or dependent children with HI V were either kept in their unpro- tected home situations or were put in hospitals. Fortunately, Lutheran Family Services, a statewide, private, non-profit foster care agency, began a specialized program for children with HIV in 1989. As of this date, they have been able to provide foster homes for all North Caro- lina children with HIV who have needed placement, but the need for foster homes is increasing as the number of HIV-exposed children rises and as chil- dren with HIV live longer. Children do exceptionally well in licensed foster care, in part because the family members who provide foster care have been extremely dedicated, strong, and compassionate people. The social and physical implica- tions of caring for a child with HIV pro- vides a self-screening of foster families. Consequently, those who do offer care tend to be excellent care providers.
Sometimes we see family members come forth to help care for a child whose parent is unable. Traditionally, maternal grandmothers and maternal aunts fill this role, often caring for the parent in addi- tion to the HIV-infected child and sib- lings. Their difficulties are multiplied by the substance abuse that is often wide- spread among members of these families and by the financial problems that are so
NCMl/ January 1993, Volume 54 Number 1 19
common. And their grief sometimes seems endless as they watch family mem- ber after family member succumb to AIDS.
School and Day Care Issues
North Carolina state law requires that children with HIV be reported to school authorities if: 1) the child is a fighter or a biter (although biting is not a proven route of HIV transmission), or 2) the child has open, oozing wounds or sores. The burden of reporting falls onthechild's attending physician." In all other circum- stances, the child's legal guardian may choose whether or not to disclose the diagnosis to school or day care authori- ties. Factors affecting whether to disclose are: 1) whether the school atmosphere is hostile or supportive, 2) the severity of the child's disease, 3) the nature of the medicine regimen, 4) the child's aware- ness of the diagnosis, 5) the legal guardian's own disease level, and 6) local community gossip. The family's con- cerns about their legally protected right to confidentiality must be addressed di- recdy. Unfortunately, both public and private schools may have self-devised HIV policies that are not consistent with North Carolina laws regarding confiden- tiality or disclosure to the school. Confi- dentiality is a legal as well as a profes- sional issue in this stale. Breach of confi- dentiality in North Carolina is punishable by up to two years in prison. Health care professionals should familiarize them- selves with the law and assist local school and day care boards in developing HIV policies consistent with the State's.' Poli- cies that protect the family permit disclo- sure to occur, ending the imposed isola- tion and benefitting the child.
Psychological issues
The psychological responses of the child and his or her family to an HI V diagnosis, to progression to AIDS , and eventually lo death, depends on many factors (Tables
5 and 6). The psychological tasks that children and their families face when confronted with HIV can be divided into four areas: 1) coping with the diagnosis; 2) coping with transmission issues; 3) coping with HIV as a chronic illness; and 4) coping with death.
Coping with the Diagnosis
Children with HIV are identified in one of two ways: 1 ) they develop a symptom- atic infection, or 2) their mother is iden- tified as HIV positive during routine screening while pregnant (HIV testing should be offered to all pregnant women). Many mothers learn of their own positive HIV status when they hear their child's, and most are shocked to learn of the diagnosis because they never considered themselves to be at risk for HIV. The shock soon leads to denial, which can persist for years. Accepting a diagnosis ofHIV is extremely difficult. Some moth- ers never do, and their denial can lead to medical neglect of the child. Other com- mon reactions to the diagnosis include anger, depression, guilt, blame, and shame. Psychological insight may be lim- ited by the lack of education, dearth of resources, and overwhelming environ- mental pressures such as problems with housing, finances, and transportation. Typically, mothers have no one to help them with these feelings and, conse- quently, resolution may be difficult.
A health care professional who is sensitive to the psychological issues siu- rounding diagnosis and their impact on the child's care will ask the mother how she is coping and will respond supportively as she works through these issues. Many times, listening itself pro- vides enough support to handle these difficult matters. When the mother's de- pression or denial obstructs the child's care (for example, by withholding the child's medication), then the health pro- fessional must intervene. North Carolina state law obligates health professionals to report this medical neglect to the De- partment of Social Services.
Table 5. Factors affecting children's psychological response to AIDS
1. their age, both chronologic and developmental
2. their awareness or knowledge of their disease
3. their understanding of death and possible afterlife
4. how their parents are coping
Table 6. Factors affecting maternal psychological response to AIDS
1.
substance abuse
2.
age and maturity level
3.
support network
4.
environmental stresses, such as poverty, homelessness, no day care
5.
her own HIV disease process
6.
sense of guilt or responsibility for transmission
7.
ability to confront reality
The mother's anger about having HIV and a child with HIV may be ex- pressed as hostility towards health care providers. This can impede building a relationship with health care profession- als as well as inhibit consistent care for the child. Understanding that the anger is projected and not personal is helpful. I recommend patience, but prolonged hos- tility needs to be addressed and the source of that anger explored in order to provide adequate care for the mother and child.
The mother's sense of guilt, shame, or blame can be seen in her sense of self-esteem. Does she herself accept HIV care? How does she care for herself in general (hygiene, nutrition, etc)? Does she tolerate abusive interpersonal rela- tionships? I have found that promoting the mother' s sense of self- worth and treat-
20
NCMJ / January 1993, Volume 54 Number I
ing her with dignity result in better care for the child.
Mothers struggle with how and when to reveal the diagnosis of HIV infection to their child. When the child asks ques- tions, the pressure builds. Some mothers prefer to handle this alone, while others want assistance or want the health care professional to reveal the diagnosis. Chil- dren often have a pretty good idea of what is going on even before they are "told," because they have overheard conversa- tions and pieced things together. Some mothers decide against informing their child or allowing them to be informed. This makes matters very difficult for the health care professional, the child, and the mother. The psychodynamics are com- plex and best handled by mental health professionals.
How the child copes with the diag- nosis differs from the mother. Younger children have specific questions ("How did I get it?," "Will I die before I'm grown?," "Will I go to heaven?"). Older children are aware of the social stigma of HIV and of their mortality, as well as their mother's. Their information about HIV may be based solely on what TV offers, both negative and positive. Some- times HIV is a family secret and the mother may be unable to discuss the diagnosis directly with her child. The health care provider then may be the sole source of information and support.
Honesty is important as the children ask questions. Answers do not have to include all technical details, but should be appropriate for the child's age. For example, I usually answer "Will I die from AIDS?" with "Yes, you will," and "Will I die before my mommy?" with "We don't know." If mother or child is obviously sicker, then note that out loud, but give no guarantee. If I am asked, "Does my brother have AIDS too?" I may answer, "Yes, he does." Answers need to be direct, uncomplicated, and tailored to the family situation. If asked, "Will my mother, brother, and I go to heaven when we die?" I find out what mother believes and generally can agree with her. Young children do not typically fear dying as most adults do. Rather they fear abandon-
ment Assure the child that someone will be there with them. Once questions are addressed satisfactorily and assurance is given, younger children may have no further queries.
Older children have more anxieties, so it's more important that the health care provider stay alert for signs of depres- sion, fear, and isolation. The health of the mother is often a major determinant of whether a child is anxious or not. I often recommend psychotherapy for olderchil- dren, including family therapy. Local mental health centers have been a good resource for me. Of course, good com- munication between health and mental health practitioners is essential. Families may be resistant to psychotherapy, offer- ing cultural and religious objections as well as concerns about the cost of mental health assistance. You may need to be creative in getting things started, such as by asking the mental health practitioner to meet the family in your office with you. After discussing the issues together, you can pass the baton of responsibility to the mental health professional.
Coping with Transmission Issues
Mothers have two concerns about trans- mission; 1) worry about where and how they contracted HIV; and 2) fear and guilt about passing the virus to their children (current and future) and to their sex part- ners (past, current, and future). Blame of or by a partner is common, but we some- times see an apparent lack of concern about the origin of the virus in the family. As mother or child get sicker, these wor- ries may resurface and become paramount family issues, especially among healthy family members looking for an explana- tion of why this tragedy has visited their family.
Most women are unaware of what puts them at risk for HIV. They therefore unwittingly pursue age-appropriate de- velopmental goals of women in their 20s and 30s, exploring their sexuality and bearing children. After a diagnosis of HIV, women feel pressured to refrain
from both. They may note a decrease in desire for sexual relations after learning of their diagnosis, probably due to low- ered self-esteem and the fear of transmit- ting HIV. Paradoxically, since bearing children is a way to "hold onto life," contraception may used infrequently or not at all. Since only 30% of fetuses become infected, many consider the pos- sible negative outcome small compared to the gains. Of course, additional anti- body-positive children result from this approach.
North Carolina state law requires that all persons infected with HIV inform their partners of that fact and that they use condoms during every sexual act. The state provides for partner notification for HIV-positive persons who do not want to directly tell their partners. Physicians in North Carolina are required by law to report known violations and those re- ported to them by their patients. All other professionals are allowed to report viola- tions, but are not legally obligated to do so. This is the only exception to confiden- tiality.
Women (and men) find it very diffi- cult to tell their sex partners that they are infected with HIV. They fear rejection and withdrawal of financial and psycho- logical support. Insisting on condom use, whether the partner is infected or not, is a good idea as well as the law. Condom use prevents acquisition of other sexual- ly-transmitted diseases and repetitive ex- posure to HIV. Negotiating condom use is an acquired skill. Women are aware that, for cultural and social reasons, many men refuse to wear condoms despite re- quests from their partners. Discussing condoms during sexual intercourse is too late. I recommend to women that they not discuss whether a partner wants to wear a condom, but simply have condoms ac- cessible (on the bedside table or in a basket under the bed), and apply the condom themselves. In all cases asserti veness is needed to initiate condom use and to combat resistance. Assert- iveness training can be helpful.
Older children have concerns regard- ing transmission that are similar to their mother's: how did they get HIV and can
NCM J / January 1 993, Volume 54 Number 1 21
they pass the virus on? Older children are aware from television that one acquires HIV from sexual contact and from shar- ing needles, but may not understand perinatal transmission. They are aware of the negative social position of people with HIV. When told they are HIV-positive they are initially confused about how they acquired it. I have found this a delicate issue to address. It is im- portant not to blame the child's mother, but also to be clear about perinatal trans- mission. Basic descriptions are usually adequate.
The impact of society's view of HIV can pose problems. Older children may have been exposed to and subjected to the use of gowns, gloves, masks, and the "special status" treatment they receive from health professionals and teachers. They usually become self-responsible for precautions about their own body fluids and remind adults when they violate uni- versal precautions. They are aware of the "secret of HIV" and its potential impact on friendships, school, and family. Their burden is a heavy one as society still remains ignorant and fearful. I've often noted their concerns expressed in ques- tions like "Who will play with me?" I see the health care professional as providing support to the child by educating the public about these matters.
Coping with HIV as a Chronic Illness
Without treatment, children with HIV typically live to be two to three years old. With treatment, this has been expanded to at least eight and a half years of age.' Adults, on the other hand, typically live eight to 10 years without symptoms be- fore progression into AIDS. If diagnosis occurs early, HIV can be managed as a chronic illness.
Pediatric HIV care involves frequent out-patient medical visits and multiple hospitalizations. Both increase in num- ber as time goes on. Fortunately, home health , pharmaceutical, hospice, and nurs- ing agencies can provide much of the child's care at home, including checking
on medicine compliance, pain manage- ment, total parenteral nutrition, intrave- nous medications, and vital sign monitor- ing. These community supports shorten hospitalization. For the most part, home care is less of a burden for families than hospital care, which disrupts family rou- tines, puts pressure on family finances, and causes siblings to be shuttled to fam- ily and friends. The goal of tertiary care centers is to hospitalize only as long as necessary and to build more and more resources into the community.
Community resources I've found to be helpful to families in the chronic stage are: AIDS service organizations; child service coordinators; drug abuse pro- grams; Ryan White funds and services administered through consortiums; re- spite and foster care (Lutheran Family Services); and financial assistance through disability programs such as SSI and SSD. Good communication among involved agencies helps to coordinate care and avoid repeat services. Involving too many agencies can overwhelm fami- lies, and not all families view service agencies as supportive, so it may be nec- essary to negotiate what services will be provided.
As HIV-positive children live longer, more and more enter day care and school. Schools and day care agencies know the diagnosis in about half of the HIV posi- tive children I see. It is important to work with the school, if possible, because the psychosocial aspects of HIV effect the child's success or failure at school. When schools know the facts about the child's and family's situation, support is usually forthcoming. Sometimes school nurses assist with transportation or teachers take food to the home as the mother gets sicker. Of course, this kind of support requires that there be no fear of HIV transmission and a recognition of the effect of the fragile family structure on the HIV-infected child. Knowing the child's HIV diagnosis finally explains and pulls together pieces of information that help the school understand the child. Schools need the help of health care pro- viders to understand the importance of universal precautions and to follow es-
tablished guidelines to prevent transmis- sion of communicable diseases at school.
As children with HIV live longer, it is increasingly likely that they will have a change of caregivers. This may be due to the course of maternal AIDS, to interfer- ing drug and alcohol problems, or to incarceration or death. I feel it is impor- tant to discuss with mothers their plans for the children should they be unable to care for them. Remember, typically moth- ers will not live to see their children graduate from high school. Planning for the future may be uncomfortable, but it is essential in assuring that the children are well taken care of. When no plans are made, then social services must intervene to establish one. Health care profession- als can help at this lime by educating family members about the child's emo- tional, medical, and developmental needs.
I believe that the patient's quality of life is the most important goal throughout the duration of HIV illness. Those things that are important to uninfected children are important to a child with a chronic illness such as HIV: going to school or day care; maintaining activities such as trick-or-treating, summer vacations, and school trips; receiving medical care in the home instead of at the hospital; having consistent and adequate care from the family; and contact with peers. Health care professionals need to advocate these quality of life issues.
Coping with Death
Depending on their age, children will be more or less aware of their dying. Hon- esty at this time can be difficult, but it is essential. As we discussed earlier, an- swering children's questions is a good place to start. In allaying anxiety about death, the health care professional may have to explain religious views. I try to express views that are consonant with those held by the family. A consistent message is important.
Allowing the child to talk about death is also important, but can be especially difficult for mothers who are struggling with grief and guilt. Designating some-
22
NCMJ / January 1993, Volume 54 Number I
one with whom the child can talk may be necessary. Encourage mothers to get help from clergy, family, friends, and profes- sionals. I recommend that children and their caregivers read Lifetimes^
Grandparents have a difficult role in the family. They watch their children and their grandchildren succumb to AIDS. They are called upon to pick up the pieces of their broken family and hold it together until death occurs. Then they are left alone, to raise the survivors.
During the last months of the child's life a mother's focus is entirely on the child. When the child dies, there is no
more focus. It is important to watch for drug and alcohol relapses by the mother at this time. I recommend designing ways for the mother and child to separate some- what before death. Respite care, provided by professionals or by family members, can assist with separation. Finding or maintaining employment, or volunteer work can help.
Watching a child die of a prevent- able disease is difficult for all involved, including health care professionals. Is- sues of blame and guilt again become prominent as death approaches. Health care professionals need to resolve any
angry feelings toward the mother, so that they can help with her grief Similarly, "feeling sorry" for the mother makes her feel even more out of control. Profession- als must explore their own feehngs to- ward the child and the family, and it helps to have a forum in which professionals can explore and express their feelings. Personal growth and better patient care result when professionals can discuss the impact that these psychosocial issues have on themselves, as they care for the grow- ing number of children and adults with AIDS. □
References
1 Grant C, McKinney R, Weedy C, Katz S, and Wilfert CM. The introduction of human im- munodeficiency virus into the North Carolina pediatric population. Pediatrics 1992; 90:174-177.
2 Gutman LT, St. Claire K, Weedy C, Herman-Giddens M, Lane BL, Niemeyer J, McKinney R. Human immunodeficiency vi-
rus transmission by child sexual abuse. Amer
JDisChildl991;145: 137-141.
Gutman LT, St Claire K, Weedy C,
Herman-Giddens M, McKiimey RE. Sexual
abuse of human immunodeficiency
virus-positive children. Amer J Dis Child
1992;146:1185-1189.
North Carolina Administrative Code 1/1 1/90,
Section .0209 Control Measures.
Someone at School has AIDS: A Guide to Developing Policies for Students and School Staff Members Who Are Infected With HIV, National Association of State Boards of Edu- cation, 1989.
Connors E. Manuscript in press. Mellonie, B, and Ingpen, R, Lifetimes: The beautiful way to explain death to children. Hill of Content Publishing Co., Australia, 1983.
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Health Watch
VOLUME 54 / NUMBER 1 / JANUARY 1993
Breast Cancer
EARLY DETECTION MAY MEAN CURE Margaret L. Bertrand, MD Annie L Hayes, RN, MPH
Breast cancer is the number-one female cancer, now striking nearly one out of every eight American women. Despite advances in surgery and chemotherapy, the death rate has changed little over the last forty years. Breast cancer is the leading cause of death in women ages 35-55.
Because there is no known prevention of breast cancer, emphasis must be placed on detecting it early. At this stage, breast cancer is highly treatable and in many instances is associated with normal life expectancy. The earlier breast cancer is discovered, the more options a woman has about surgery. Depending on size and location of the tumor, removal of the breast (mastectomy) may not be necessary.
Annie Hayes is a retired public health nursing consultant with the NC Department Environment, Health, and Natural Re- sources, Division of Adult Health. She resides at Route 5, Box 396 in WhiteviUe, NC 28472.
Dr. Bertrand is a radiologist with Bertrand Diagnostic Imag- ing & Breast Center, Inc., 1309-11 N. Ehn Sl, Suite 9, Greenboro.NC 27401.
Lesser surgery combined with radiation therapy may be recommended instead.
Defense against breast cancer involves a three-part pro- gram which each woman should maintain throughout her life: breast self-examination, routine physical, and mam- mography (breast x-ray).
Breast Self- Examination
Breast self-examination should become a habit practiced once a month. Women need to check themselves when they are least likely to be engorged; for men- struating women, one week after their period begins, and for women onreplacementhormone therapy, the first day of their estrogen medication. The exam should include inspection in front of a mirror and palpation lying down and sitting or standing.
NCMJ / January 1993, Volume 54, Number 1 25
Detailed information on this procedure is available free from the American Cancer Society.
There is evidence that the more experienced a woman is in self-examination, the smaller the tumor she is capable of feeUng. Women 20 years of age and older should perform a breast self-examination every month.
Physical Examination
Women age 20 to 40 should have a physical examination of the breasts every three years, and women over 40 should have a physical examination of the breasts every year. This can often be combined with a gynecological exam or regular check-up.
Mammography
Mammography is a low-dose x-ray of the breast which is capable of detecting many breast cancers two to three years earUer than they can be felt by patients or physicians. The size of a breast cancer at discovery, and whether or not nearby lymph nodes are involved, are two of the main determinants of survival. When diagnosed at 5mm(the size of a pea), the five-year survival rate is 98% and the 20-year survival rate is 93%. Most breast cancers (75%) are found by the woman herself, with an average size of 2-3 cm (the size of a pecan). At this stage, approximately half of the cancers have already spread to lymph nodes. Even without lymph node spread, the 20- year survival rate is only 62%, but once lymph nodes are involved, the 20-year survival rate is less than 25%.
Mammography is the most sensitive of the tests available in detecting breast cancer, with an 85-90% detection rate. Not only is mammography safe and accurate, but it is a proven life-saver based on three major studies. Two of these, one carried out in New York City in the 1960's and the other more recently in Sweden, reported 30-40% fewer deaths among women over 50 who had routine breast x-rays along with their annual physical exams. A third study, organized jointly by the National Cancer Institute and the American Cancer Society, demonstrated that 35.4% of breast cancers detected in women under 50 were found by mammography alone. Doctors in Sweden have just reported the 12-year follow-up on a very large group of women (in five separate
controlled trials), ages 40 to 49, who were receiving screening mammography. It has now been confirmed that a significant mor- tality reducuon of 13% was achieved in those women under- going mammography screening. Because of these encouraging results, the American College of Radiology and the American Can- cer Society as well as ten other leading medical organizations, have adopted guideUnes for the routine use of mammography.
It is important for all women to be aware of their personal risk factors for developing breast cancer. Until medical science develops a method of prevention, success in early detection of breast cancer is based on an aggressive three-part program of breast self-examination, physician breast exam, and x-ray mammography.
Who is at risk for breast cancer?
• All women are at risk. Only 1% of breast cancers occur in men. Seventy-five percent of women who get breast cancer have no risk factors other than being female.
• The risk increases with age. Two-thirds of breast cancers occur over age 50, but sadly, 12% of breast cancer occurs under age 40.
• A personal history of breast cancer increases the risk for a second breast cancer to one in six.
• Family history is a strong risk factor if mother or sister has had a breast cancer before menopause. The risk is higher if these relatives have had breast cancer in both breasts. Of less risk is a close relative having a breast cancer after menopause. If there are several relatives with breast cancer on the father's side of the family, that is also a significant risk.
• Other risk factors include never having had children, having had a first baby after age 35 , early menarche and late menopause.
Wfio stiould hiave a mammogram?
As currently recommended by the American College of Radiology and the American Cancer Society for asymptom- atic women:
• Age 40-49, a mammogram every one to two years
• Age 50 and over, a mammogram every year
Women at high risk should consult their personal physician because it may be necessary to begin screening at a younger age.
Today less than one third of women in the recommended age category for screening are getting their routine mammog- raphy. If your physician has not already recommended this test, ask about it soon.
How is mammograptiy performed?
The standard mammographic procedure is two x-ray views of each breast, one from the side and one from above.
26
NCMJ / January 1993. Volume 54, Number J
To increase accuracy of detection, and to decrease radia- tion dose, adequate compression is necessary. This may be slightly uncomfortable, but usually is not painful if per- formed at the same time of the cycle that breast self-exami- nation is suggested.
Is mammography safe?
Only a few years ago, doctors were fiercely debating whether this breast x-ray might cause breast cancer. Fortunately, now that these x-rays deUver one-tenth the radiation of former techniques, the conQ-oversy has been laid to rest. Mammog- raphy is now thought to pose virtually no increased risk for developing breast cancer.
In choosing where you will have this x-ray examination, it is important to know whether or not the facility has been accredited by the American College of Radiology. Having passed this strict evaluation ensures that modem low-dose technique is being used and that mammograms are inter- preted by board-certified radiologists interested in mammog- raphy.
Where is mammography performed and how and how much does it cost?
In North Carolina, there are several free-standing breast centers, most of them associated with out-patient radiology centers. Additionally, mammography is performed in most hospitals.
In this state, most mammography is priced at less than $100. Routine mammography (performed in patients with- out symptoms) is now covered by Medicare and most insur- ance companies.
Breast self examination —
early detection for breast cancer
The good news is that breast cancer can be cured, if it is detected and treated early. If you are a woman, do you do breast self exam (BSE) monthly? If you do, congratulations! You are among a growing number of American women who are doing BSE regularly, once a month.
The best weapon against breast cancer is early detection. By performing BSE, women detect 95% of cancers of the breast. B ut let me reassure you that most breast lumps are not cancer. After investigation, only about two out of 10 breast lumps turn out to be cancer.
What are the facts?
About one in every eight women will develop breast cancer sometime in her lifetime. An estimated 1 8 1 ,000 new cases of breast cancer were diagnosed during 1992; deaths were
estimated at 46,300. Up to 90% of women whose breast cancer is detected early and is treated, will survive. Early detection also means that less extensive surgery may be used, often saving the breast itself.
What are the warning signals?
Breast changes that persist, such as a lump, thickening, swelling, dimpling, skin irritation, distortion, retraction, sca- liness, pain, or tenderness of the nipple, are all causes for concern and should be checked out by your doctor. Remem- ber, most breast conditions are not cancer, but only a doctor can make the diagnosis.
What are the risk factors? All women are at riski
Some of the things that increase risk are:
• Age, risk increases with age
• Personal or family history of breast cancer (mother, sister, grandmother, aunt)
• Never had children
• Older than 30 years at birth of first child
Breast cancer does not seem to be associated with hormone use. Every woman should discuss her own risk with her doctor.
What can you do about early detection?
The American Cancer Society recommends for women:
• 20 years and older: Practice breast self exam monthly.
• 20-40 years: Have a cUnical breast examination
every 3 years or as recommended by your doctor.
• 40-49 years: Have a mammogram every 1-2 years,
as recommended by your doctor.
• 50 years and older: Have a mammogram every year.
• 40 years and older: Have a clinical breast examination
every year. A combination of mammograms, clinical breast exams, and breast self exams as recommended could reduce the number of breast cancer deaths by 50%.
Examining your breasts
A woman's breast has a special significance for her. Breasts represent femininity, womanhood, mothering and sexuahty. Most women do not practice breast self exam monthly because of fear of cancer and not knowing what they are feeling. It is difficult to tell the difference between normal and abnormal without training and practice. The most
NCMJ / January 1993, Volume 54, Number 1
27
important thing is to leam how your breasts feel and be able to detect changes over time. Training by a health care professional can help relieve your fears and increase your confidence in performing BSE.
Steps Of BSE
Adapted from the American Cancer Society booklet "How to Examine Your Breasts"
In the shower
Examine your breasts during bath or shower; hands glide more easily over wet skin. With fin- gers flat, move gently and firmly over every part of each breast Use the right hand to examine the left breast and the left hand for the right breast. Check for any lump, hard knot, or thickening, and changes over time.
Before the mirror
Inspect your breasts with arms at your sides. Next, raise your arms high overhead. Look for any changes in shape of each breast; any swelling, dimpUng of skin, or changes in the nipple. Then rest palms on hips and press down fmnly to flex (tighten) your chest muscles. Your left and right breast may not match exactly; few women's breast do. Regular inspec- tion shows what is normal for you and will give you confi- dence in the exam.
Lying down
To examine your right breast, put a pillow or folded towel under your right shoulder. Place your right hand behind your head; this distributes breast tissue more evenly on the chest With your left hand, fingers flat, press gently and firmly, following either the circle, vertical strip, or other methods shown. Choose the method easiest for you. A ridge of firm tissue in the lower curve of the breast is normal. Also you will feel "glands" throughout the breast, these should be similar in both breasts. Repeat the procedure on your left breast. The important thing to remember is to leam how your breast feel and what is "normal" for you, then be aware of any changes over time. In the sitting position, gently squeeze the nipple of each breast between your thumb and index finger. Any discharge, clear or bloody, or other suspicious finding should be reported to your doctor as soon as possible.
BSE is every women's first hne of defense against breast cancer. Ask your health care professional lo do a thorough breast examination demonstrating how to do BSE. Call your local American Cancer Society or 1 (800) ACS-2345 for more cancer information or training on how to do BSE.
What else can you do to protect yourself against cancer? Practice a healthy lifestyle, eat a variety of foods from the basic food groups, exercise, avoid obesity, cigarettes, and alcohol. Strive for a balance between work and play. Leam how to relax and enjoy life! Q
References
American Cancer Society: Cancer Facts and Figures-1992 How to Examine Your Breasts Taking Control
National Cancer Institute:
The Challenge of Breast Cancer, A Program Kit
1993
February Cancer Screening
March 1992-93 Roster Issue
28
NCMJ / January 1993, Volume 54, Number 1
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MODERN MEDICINE
Chronic Temporomandibular Joint Disease and Head Pain
Response to Surgery
Williams. Kirk, Jr., D.D.S.
Chronic headache can be caused by dis- ease of the temporomandibular (TM) joint. The symptoms of inflammatory or degenerative disease of the TM joint generally include myofascial pain (spasm of the muscles of mastication induced by factors such as malocclusion or bruxism). This myofascial pain is treated by reducing myospasm through the use of medication, physical therapy, and muscle relaxants. Unfortunately, advanced or severe in- trinsic TM joint disease can produce myofascial pain that remains refractory to such treatment Then siu^gery is needed. In this paper I present a four- year, follow- up of 76 such patients who underwent such surgery of the TM joint I focus specifically on headache symptoms, particularly pre-operative location of pain and the post-operative subjective percep- tion of reUef .
Methods and Materials
I sent questionnaires to 83 patients who had undergone surgery during a con- secutive three-year period from 1986 to 1988; 76 were returned for a response rate of 91.6%. The remaining seven pa- tients were followed post-operati vely , but
From 600 S. College St., Ste. 1 1 00, Char- lotte 28202.
their data are not included because no questionnaires were returned. All patients had intrinsic disease of the TM joint(s) documented by magnetic resonance im- aging (MRI). All non-surgical treatments had failed (physical therapy, occlusal management, orthotic appliances, anal- gesics, anti-inflammatory medications, joint injections of steroid, even vasoactive medication prescribed because the headache was thought to be migraine or vascular headache). All patients had negative neurologic evaluation pre-op- eratively.
The questionnaire asked about the patient's subjective recall of pre-operative and post-operative joint and/or headache pain dilation, frequency, character, and location. Four categories were used to determine frequency of pain: 1) constant; 2) one to three times per week; 3) one time per month; 4) no pain. Patients were asked to locate headache to the following regions: frontal; temporal; retro-orbital ("behind the eye"); midsagitlal ("top of the head") ; occ ipi tal ("back of the head") ; over the paranasal sinuses; over cervical region ("upper neck"). Patients were asked to localize facial pain to: temporo- mandibular joint, deep ear, temple, upper jaw, or lower jaw.
Subjects were asked how long the pain and joint dysfunction had been present before surgery: 1) zero to six months; 2) six months to one yean 3) one
to two years; 4) two to Tive years; 5) more than five years.
Patients were asked: "If you had two or more types of headache, could you distinguish other types of headache from those associated with joint arthritis?"
Finally, patients were asked whether they were using: 1 ) more; 2) the same; 3) less; or 4) no medication to control headache pain after surgery.
Results
Pre-operative Symptoms. The patients ranged in age from 1 8 to 57 years with a mean of 39 years. Pre-operative joint pain, joint dysfunction, and cephalalgia were chronic. Sixty-six of the 76 patients (89.5%) reported constant symptoms (pain, mastication dysfunction, inability to tolerate a chewing diet, jaw locking, and hypomobility secondary to joint dysfunction) for more than one year; 32 (42.1%) had symptoms for greater than five years. Only eight patients had symptoms for less than one year. Some patients had significant mandibular trauma (fracture, hyperextension joint injury) immediately prior to the onset of symptoms.
Seventy of 76 patients (92.1%) de- scribed constant pain, well-localized in the TM joint or otalgia associated with joint use. Only six patients described less
30
fiCMJ / January 1993, Volume 54 Number 1
frequent pain and dysfunction. Prior to surgery, 52 patients (68.4%) had constant headache and 18 more (23.7%) reported several significant headaches per week. There was no specific localization of reported headache. The most frequent sites were frontal (35 responses), retro- orbital (38) and temporal (53), but most patients identified two or more locations, and many had difficulty localizing their pain. In addition, there were 64 responses describing well-locahzed TM joint pain, 49 responses of otalgia, 43 responses of temporal pain, 36 responses of pain re- ferred to the maxilla, and 36 to the ramus and body of the mandible.
Post-operative Symptoms. Thirty-two patients underwent TMJ capsule and disc repair procedures when qualitative de- generative changes of these tissues were not severe. Forty-four patients had discectomy because destruction rendered repair impossible. No distinction was made between these two surgical mo- dalities as related to long-term pain re- sponse.
Four years after surgery, most pa- tients reported that headache and facial pain symptoms had improved (Table 1). Twenty-three (30.3%) reported episodes of weekly but milder headache, 27 (35.5%) reported monthly episodes of headache, and 16 (21.1%) had no head- ache. Five patients (6.6%) continued to complain of constant headache.
Twenty-nine of the 76 patients (38.2%) had occasional joint pain post- operatively; 27 (35.5%) experienced one episode per month; and 16 (21.1%) had no post-operative pain.
Sixty-nine patients provided re- sponses about whether they could dis- tinguish types of headache. Forty-nine respondents stated that they could distin- guish headaches arising from TM joint arthropathy or arthritis from other head- aches; 20 could not.
Most significantly, 55 of the 70 re- sponding patients (78.6%) indicated that they needed less medication or no medi- cation to control headache after surgery. Nine (12.9%) used the same amount, and six (8.6%) needed more medication.
Theories of Etiology
Physicians often see patients complaining of facial, head, or neck pain. The multiple po- tential causes of such pain make this a diffi- cult area of clinical practice. Clinical diag- nosis is often a diagno- sis of exclusion. Den- tistry and medicine share confusion over the "TMJ syndrome." The multiple theories of etiology may be diffi- cult to unravel, and of- ten there are no good diagnostic data to sup- port the multitude of potential treatment op- tions. However, mag- netic resonance imag- ing of the TM joint can document the presence of significant internal derangement or early osteoarthrius of this synovial joint system. This imaging modality now allows accurate diagnosis and differen- tiation of patients with headache due to TM joint disease.
Theories of patho- genesis of facial pain and headache associ- ated with TMJ dys- function have histori- cally focused on spasm of the muscles of mas- tication. Beginning as early as 1937, Costen,' Schwartz,^' and Las- kin* have indepen- dently emphasized masticatory muscle spasm as the primary factor causing pain. Psychological factors may contribute, but the use of arthrography' and of MRI have allowed a more rational approach to iden-
Table 1.
Pain characteristics and response patients with documented disease mandibular Joint
to surgery In 76 of the temporo-
1. Recalled frequency of pain (#of patients reporting)
A. TM Joint/Facial Pain
Before
After
1 , Constant
Surgery 70
Surgery
3
2. Weekly
6
29
3. Monthly
0
27
4. None
0
17
B. Headache
1 . Constant
52
5
2. Weekly
18
23
3. Monthly
3
27
4. None
3
21
II. Recalled pain location (total#of patient responses)
A. TM Joint/Facial Pain
Before
After
1 . TM joint itself
Surgery
64
Surgery
31
2. Ear
29
19
3. Temple
43
7
4. Upper jaw
36
12
5. Lower jaw
36
13
B. IHeadache
1 . Frontal
35
12
2. Temporal
53
21
3. Retro-orbital
38
19
4. Mid sagittal
21
4
5. Occipital
28
13
6. Sinus
32
20
7. Upper cervical
33
17
tifying arthropathy when it is the source of pain and disease.'*
Treatment of TMJ syndrome has generally relied on modalities successful
NCMJ / January 1993, Volume 54 Number 1 31
in treating myospasm (physical therapy, ultrasound, diathermy, transdermal elec- trical nerve stimulation (TENS), heat, ice, orthotic appliances, non-steroidal anti-inflammatory drugs, muscle relax- ants, etc). In some cases, non-surgical treatment has been successful for years at a time, but the mechanisms of pain in those patients must by quite different from the refractory cases studied here.'
How Could Localized Joint Dysfunction Cause Widespread Pain?
Vasoactive substances such as serotonin and substance P (SP) can directly stimu- late craniovasodilation and mediate pe- ripheral inflammation, histamine release, and increased vascular permeability. '"SP has been shown to be synthesized in trigeminal cell bodies and is transported to peripheral axons. SP, released from trigeminal innervations of pial vessels and large vessels, causes dilation of these cerebral vessels." Its role in the patho- genesis of TMJ syndrome is suggested by the observations of Anderson and col- leagues'^ who found significant intra- articular concentrations of SP in patients with internal derangement and injury of the TM joint. In addition, Godsby, Edvinsson, and Ectman'^ found mark- edly elevated levels of SP in the external jugular vein of patients who exhibited facial flushing during the post-stimula- tion period after undergoing ther- mocoagulation of the trigeminal ganglion for treatment of tic douloureux. Their observations suggest that SP mediates a complex neurovascular cephalalgia when peripheral inflammation or disease stimu- lates cerebral blood vessels that in some way are controlled by trigeminal path-
ways. This may explain why patients with TM joint dysfunction can be refrac- tory to modalities that decrease muscle spasm.
Who Gets TMJ Pain?
Severe intrinsic disease of the TM joint should be suspected in patients who have orthopedic dysfunction of the mandible consisting of hypo- or hypermobility, progressive alteration in the translatory glide sequence caused by disc locking, pain localized to the capsiJe of one or both joints and/or subjective complaints of otalgia. Head pain may begin after long periods of dysfunction and inflam- matory desuuction of disc tissues. Inten- sity and frequency of headache can vary and do not appear to show any daily pattern. Headache may intensify after eating or manipulation of the mandible. Pain intensity can be quite severe and generally reflects the severity of inflam- mation or peripheral ligament entrapment. Unilateral headache is often perceived to be retro-orbital or an tenor temporal. Fron- tal, midsagittal, occipital headache and neck pain can occur but I usually find that these are preceded by retro-orbital and anterior temporal headache. Headache can be bilateral when both TM joints are diseased.
The predom inance of TMJ syndrome in women may be theoretically explained by experimental data. Bereiter, et al have demonstrated that systemic estrogens in- crease the size of receptive fields of trigeminal mechano-receptors. This change occurs even after nerve root sec- tion, suggesting hormone-induced changes at the level of the peripheral nerve.'* The effects of domestic trauma, hormone-infiuenced inflammatory de-
struction of fibroelastic tissues of the TM joint system, osteoporosis-induced de- generative disease, and periodontal bone loss with posterior tooth loss may also contribute to the high incidence of this disorder in women.
Analysis of my patients who did not get well reveals principles found in other joint systems. Patients with long-stand- ing joint pain and obvious arthrosis carry a poor prognosis. Patients with severe disorders of occlusion are in a relatively high-risk category. Patients who have had long-standing internal derangement (greater than two years) and no response to non-surgical treaunent (three months) may improve but continue to have pain consistent with chronic arthralgia. This type of patient made up the majority of those who only had a fair result. In my experience patients with long-standing degenerative disease or arthrosis have pain syndromes that are difficult to man- age.
Goals and
Hopes for Treatment
My survey shows that surgery for chronic intrinsic disease of the temporomandibu- lar joint can relieve symptoms in some patients with significant and long-stand- ing degenerative disease. Improved im- aging modalities allow us to identify pa- tients with TMJ dysfunction and to dis- tinguish these patients from those with other kinds of chronic facial pain and cephalalgia. Early identification and early treatment may prevent the development of severe osteoarthritic destruction with its chronic unremitting head and facial pain. This should be the ultimate goal of treatment. □
References
1 CostenJB.Somefeaturcsofthemandibular articulation as it pertains to medical diagno- sis, especially in otolaryngology. J Am Dent Assocl937;24:1507-ll.
2 Schwartz L. Disorders of the Temporoman- dibular Joint: Diagnosis, Management, Re- lation to Occlusion of Teeth. Philadelphia; WB Saunders, 1959, pp. 3-44.
3 Schwartz L. A temporomandibular joint- pain-dysfunction syndrome. J Chron Dis 1956;3:284-93.
Continued on page 45
32
NCMJ / January 1993, Volume 54 Number 1
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A Challenge to Sometimes Readers of the Joutnal
Francis A. Neelon, M.D., Editor
With this issue, we come to another turn of the wheel. Jeanne Yohn and I have completed one year as your managing editor and editor, respectively. I hope that you arc satisfied with our first year at your service. We have provided a steady stream of papers on a diverse set of topics for our readers, papers and authors that reflect the great diversity of practice and opinion encompassed by our Medical Society. 1 have been especially pleased by the interest and response of rank-and-file Society members who have responded to our requests to review papers or to prepare editorial comments for publication. The Editorial Board, although diminished by the death of its long-time chairman, Charles Styron, has been reinvigorated by the fresh perspectives of our new chair, Margaret Marker, and the addi- tion of two new members.
With this new year I have a challenge for our readers. As you know, I try to encourage vigorous interaction between you, the readers, and us, the editors. We want you to send us letters, opinions, comments, research papers. But most of all, we want you to read ihe Journal. Not everyone thinks you do. One of our reviewers once suggested that we print a certain manuscript because, although it might not appeal to everyone, it would to some and he doubted that many (any?) of our subscribers read
every article in every issue. He's probably right, and pity that it be so. One of the great treasures of the world of medicine is that it is so broad and so endlessly fascinating and that it is (at least was) a community. The hallmark of the doctor is breadth and range of understanding and information at his or her fingertips. Information about the practice of our craft, the march of science in the service of patients, the moral and ethical choices we face in our work. The Journal should reflect that breadth and range. I challenge you, dear reader, to do what I do for the next year: read every word in every paper in \heJournal\ It's too easy to forget the real joy of casting the intellectual net wide, too easy to slip into the complacency of learning more and more about what you already know. Several years ago Sir Richard Asher wrote a paper, "Why are medical journals so dull?" We try to avoid dull and I would like to know whether sometimes readers think we do. Most subscribers get the Journal automatically, as a "perk" of Society membership; unless they read it faithfully, they miss the sense of community that constant reading fosters. If any of you are moved to pick up the gauntlet, try the whole Journal for a year (every page!), then write and tell me what you have found out by this process. We will publish the best responses (if we get any) in 1994. □
1993 North Carolina Medical Society, Spring Leadership Conference, Thursday-Sunday, February 25-28, 1993, Durham Omni Hotel
Writing Workstiops
Sunday, February 28, 1 993
Conducted by Francis A. Neelon, M.D., editor, and
Jeanne C. Yohn, managing editor,
North Carolina Medical Journal
Session 1—10:15 a.m. to Noon
On writing for the reader:
• • • • •
Medical communication How to find a subject How to structure a sentence How to structure on article The mechanics of publication
Session 11—2:15 p.m. to 4 p.m.
Case studies in wr'rting:
• Getting the idea on paper
• Detecting problems and pitfalls in writing
• Making effective transitions
• Creating an outline after you've written
• Rewriting what you've written
To attend, complete ttte workshop registration form In your Spring Leadership Conference registration packet, or call the Journal at 919-286-6410.
34
NCMJ /January 1993, Volume 54 Number 1
TOXIC ENCOUNTERS
The Night the Light Went Off in
Roundup® (Glyphosphate) Poisoning
Ronald B. Mack, M.D.
In this era of obscene divorce rates and infidelity it is heartening to read stories of true love. The story of Hero and Leander would bring a tear to your eye, had you any romance left in you at all. Leander was a young man who lived on the Asian coast of the Hellespont River.''^ His true love, Hero, (a girl — don't get any ideas, I saw you make a face!) lived on the oppo- site shore. Every night Leander swam at least a mile to this shore. When they would meet it was only to enjoy each other's company — no slap and tickle par- ties for these two. The young swain was guided by a torch that his maiden set upon a tower. One night a storm roughened the sea and blew out the torch, and Leander lost his way and drowned. His body washed ashore on the European coast of the Hellespont Hero found his body and in despair jumped from the tower and died — earning an 8.7 from the judges for her dive. She could have swallowed glyphosphate instead and made less of a mess.
I was very surprised, one evening, to see a television commercial for Round- up®, an herbicide with fairly frightening results if accidently or purposefully in- gested. The primary effects of swallow- ing this product are mucous membrane irritation, vomiting, abdominal pain.
From the Department of Pediatrics, Bow- man Gray School of Medicine, Wake Forest University, Winston-Salem 271 03.
hypotension, oliguria, and anuria. Esoph- ageal or gastric erosions are fairly com- mon; death is also a possible consequence. This potentially very toxic product is becoming popular as a suicide agent; if the patient does not perish from ingesting Roundup®, he or she can become very sick indeed.
Roundup® is composed of 41% glyphosphate and 15% polyoxyelthyl- eneamine surfactant. It is a very efficient herbicide. When sprayed on plant foliage it moves through the plant to the root system. Effects of the spraying are evident in two to seven days. This compound is considered an important non-selective, post-emergence herbicide for control of deep-rooted perennial plant species and some biennial grasses. It is allegedly very mobile in soil and water and is avidly translocated in plants. Glyphosphatebinds to soil and is inactivated, like paraquat,' and so should not be expected to persist from one growing season to the next. The major soil metabolite is aminomethyl phosphoric acid, which is non-toxic. (An important question remains: If I sprinkle enough glyphosphate on my lawn will it destroy it so it won't need mowing? Then I could paint the yard green and nobody would know the difference.)
Glyphosphate herbicides can affect multiple organs depending on the mode of exposure. If it is accidently or pur- posefully (mean, mean!) splashed in the eyes, a conjunctival irritation is possible, and usually clears in 48 hours. If conjunc-
tivitis is more than mild, referral to an ophthalmologist would be a good idea. Glyphosphate is considered to be only mildly irritating to most mucous mem- branes, however, erosions of the pharynx have been described following ingestion. Ingestion can also produce increased salivation and a burning sensation in the oral mucosa and the pharynx.^'' It is no surprise that nausea and vomiting can occur as well as abdominal pain and in severe cases melena and paralytic ileus. In some cases reported in the literature, melena and hemetemesis developed in patients who initially were without symptoms.'
S ignificant amounts of this herbicide can cause diarrhea, sometimes severe enough to produce dehydration and electrolyte disturbances. Chemical bums of the esophagus, stomach, jejunum, and ileum have been reported. Inhalation of Roundup® has produced irritation of the throat and upper respiratory tract and a "raspy" sound to the voice. Pulmonary edema and hypovolemic shock are dreaded consequences of ingestion of this product. Death is a very real possibility with exposure to Roundup®.
An analysis of 56 cases''^ of Roundup® toxicity show several clinical adversities. In these 56 cases the polyoxyethyleneamine surfactant was considered a toxic agent and intravenous injection in beagles caused a cardiac de- pression that was thought to be due to the surfactant:
NCMJ /January 1993, Volume 54 Number I
35
1) Sore throat, abdominal pain, and vomiting — common
2) Erosions of the esophagus, stomach, and pharynx — 7 cases
3) Pulmonary edema — 3 cases
4) Pneumonia — 2 cases
5) Oliguria, anuria, hypotension — com- mon
A toxic dose of Roundup® in hu- mans has not been established, however a mean of 104 mL of the concentrate has produced severe toxicity when ingested. In one series of nine fatal cases of pur- poseful ingestion with suicidal intent," the mean amount ingested was 206 mL. Another report of 67 cases showed a mortality of 7.5%.' (Ninety-five percent of the cases and all fatalities in this series were suicides). The manufacturer alleges that ingestions of 30 mL to 240 mL of
Roundup® concentrate have resulted in vomiting and diarrhea lasting two to five days without other symptoms. This con- tradicts the outcome in 47 patients where a mean ingestion of 104 mL produced toxicity.'
Glyphosphate is excreted quite rap- idly in the urine and leaves the body fairly rapidly. It is usually impossible to detect it in the urine by the second or third day after ingestion. Glyphosphate and its major plant metabolite can be measured by gas chromatography, high-perfor- mance liquid chromatography, gas chro- matography/mass spectrometry, and nuclear magnetic resonance spectroscopy. Any of these methods would be helpful in the ED, but they are generally unavail- able clinically.
Treating human ingestion of Roundup® involves symptomatic care only. Inducing emesis is not recom- mended,^ since esophageal erosions can occur after ingestions of the concentrated solutions. With large ingestions, emesis may occur spontaneously. You should administer activated charcoal followed by a dose of a cathartic such as sorbitol. Needless to say, if you suspect more than mild mucous membrane involvement, endoscopy may be indicated. In very large ingestions the threat of pulmonary edema is present and respiratory support may be life saving.
I find the story of Hero and Leander very inspiring. I dedicate this paper to my true love, Marcia, and hope the light never goes out. □
References
1 Hamillon, E. Mythology. New York: Pen- guin Books, 1969. p. 293.
2 Bullfinch T, Bullfinch's Mythology. New York: Modem Library, p. 88.
3 Roundup®. Poisindex, Micromedex Inc., Vol. 73, Exp. 8/31/92.
4 Amdur MO, Doull J, et al. Casarettc and DouU'sToxicology, 4th Edition. New York:
Pergamon Press, 1991, p. 885.
5 SawadaY, etal. The Lancet 1988;1:299.
6 Talbot AR. Glyphosphate Poisoning. Vet Hum Toxicology 1989;3 1:379.
"WELCOME TO THE COMPUTER AGE, DOCTOR"
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April 12-15,1993 Hilton Head Island, South Carolina
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world-famous island (classes end at 1 p.m. each day).
This course has been reviewed and is acceptable for 15 prescribed hours by the American Academy of Family Physicians.
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36
tiCMJ/ January 1993, Volume 54 Number 1
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INDICATIONS AND USAGE: For therelief of moderate tomoderatelyseverepain CONTRAINDICATIONS: Hypersensitivity toacetammophenorhydrocodone WARNINGS: RespiratoryDepression: At high doses or insensitive patients, hydrocodone may produce dose-related respiratory depression. Head Injury and Increased Intracranial Pressure; The respiratory depressant effects of narcotics and their capacity to elevate cerebrospinal fluid pressure may be markedly exaggerated in the presence of head iniury, other intracranial lesions or a preexisting increase in intracranial pressure Furthermore, narcotics produce adverse reactions which may obscure the clinical course of patients with head injuries Acute Abdominal Conditions: The admmistrationof narcotics may obscure thediagnosisorclinicalcourseof patients with acute abdominal conditions. PRECAUTIONS: Special Risk Patients: VICODIN/VICODI^ with caution in elderly or debilitated patients and those with severe impairment of hepatic or renal function, hypothyroidism, Addison's disease, prostatic hypertrophy or urethral stricture Cough Reflex: Hydrocodone suppresses the cough reflex, as with all narcotics, caution should be exercised when VICODIN/VICODIN ES Tablets are used postoperatively and m patients with pulmonary disease Drug Interactions: Patients receiving other narcotic analgesics, antipsychotics, antianxiety agents, or other CNS depressants (including alcohol) concomitantly with VICODIN/VICODINES Tablets may exhibit an additive CNS depression The use ol MAO inhibitors or tncyclic antidepressants with hydrocodone preparations may increase the effect of either the antidepressant or hydrocodone. The concurrent use of anticholinergics with hydrocodone may produce paralytic ileus. Usage in Pregnancy : Teratogenic Effects : Pregnancy Category C Hydrocodone has been shown to be teratogenic in hamsters when given in doses 700 times the human dose. There are no adequaie and well-controlled studies in pregnant women VICODIN/VICODIN ES Tablets should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Nonteratogenic effects: Babies born to mothers who have been taking opioids regularly prior to delivery will be physically dependent The withdrawal signs include irritability and excessive crying, tremors, hyoeractive reflexes, increased respiratory rate, increased stools, sneezing, yawning, vomiting, and fever Labor and Delivery: Administration of VICODIN/VICODIN ES Tablets to the mother shortly before delivery may result in some degree of respiratory depression in the newborn, especially if higher doses are used Nursing Mothers: It is not known whether this drug is excreted in human milk Because many drugs are excreted in human milk ana because of the potential for serious adverse reactions in nursing infants from VICODIN /VICODIN ES Tablets, a decision should be made whether to discontinue nursing or to discontmue the drug, taking into account the importance of ^ tothe mother Pediatric Use; Safety andeffectiveness in children have not been established. ADVERSE REACTIONS: The most frequently observed adverse reactions include light-headedness, dizziness, sedation, naus These
effects seem to be more prominent m ambulatory than in nonambulatory patients and some of these adverse reactions may be alleviated if the patient lies down Other adverse reactions include Central Nervous System: Drowsiness, mental clouding, lethargy, impairment of mental and physical performance, anxiety fear dysphoria, psychic dependence and mood changes. Gastrointestinal System: The antiemetic phenothiazines are useful in suppressing the nausea and vomiting which may occur (see above); however, some phenothiazine derivatives seem to be antianalgesic and to increase the amount of narcotic required to produce pam relief, while other phenothiazines reduce the amount of narcotic required to produce a given level of analgesia. Prolonged administration of VICODIN/VICODIN ES Tablets may produce constipation Genitourinary System: Ureteral spasm, spasm of vesical sphincters and urinary retention have been reported Respiratory Depression ; Hydrocodone bitartrate may produce dose-related respiratory depression by acting directly on the brain stem respiratory center Hydrocodone also affects the center that controls respiratory rhythm, and may produce irregular and periodic breathing. If significant respiratory depression occurs, it may be antagonized by the use of naloxone hydrochloride Apply other supportive measures when indicated DRUG ABUSE AND DEPENDENCE: VICODIN/VICODIN ES Tablets are subject to the Federal Controlled Substance Act (Schedule III) Psychic dependence, physical dependence, and tolerance may develop upon repeated administration of narcotics, therefore, VICODIN/VICODIN ESTablets should be prescnbedand administered withcaution. OVERDOSAGE: AcetaminophenSignsand Symptoms: In acute acetaminophen overdosage, dose-dependent, potentially fatal hepatic necrosis is the most serious adverse eHecl Renal tubular necrosis, hypoglycemic coma, and thrombocytopenia may also occur Early symptoms following a potentially hepatotoxic overdose may include nausea, vomiting, diaphoresis and general malaise Clinical and laboratory evidence of hepatic toxicity may not be apparent until 48 to 72 hours post-ingestion Hydrocodone Signs and Symptoms: Serious overdose with hydrocodone is characterized by respiratory depression (a decrease in respiratory rate and/or tidal volume, Cheyne-Stokes respiration, (cyanosis), extreme somnolence progress- ing to stupor or coma, skeletal muscle fiaccidity, cold and clammy skin, and sometimes bradycardia and hypotension. In severe overdosage apnea circulatory collapse cardiac an-est and death may occur
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COMPASSIONATE CAREGIVING
The Ministry of Caring, Part 2
Margot Hover, D. Min.
Editor's Note: The folbwing is excerpted from Caring For Yourself When Caring For Others by Margot Hover, D. Min., to be published by Twenty-Third Publications, Mystic, CT 06355, in spring 1993. Dr. Hover is chaplain and pastoral educator in Pastoral Services at the Duke University Medical Center in Durham. This is the second of three installments that offer a unique perspective on the many facets of caregiving. (The first installment appeared in the December Journal.) We summarize Dr. Hover's introduction here.
"Prayer and love are really learried in the hour when prayer becomes impossible and your heart turns to stone."
—Thomas Merfon
Caregivers know many of those moments. There comes a time when the old truism, "It's good to be needed," wears thin, and our world seems full of neediness that can't be fixed. Those times come to all kinds of caregivers — parents, health care workers, family members of the sick or disabled, and parish ministers. For example, my role as a parish minister of the Eucharist is a very important part of my spirituality and vision of the Church. Usually I am energized by visits to the sick — until that Sunday afternoon when everyone is at the beach and
the tabernacle key isn't where it's supposed to be. I've come to think of these moments as a chance to look at the underside of the diamond of caregiving, an opportunity to examine the often hidden facets. Borrowing Jesus' metaphor, I have come to think of these mediations are signposts for shepherds in the far pasture. These have helped me and I hope they will help to nurture and sustain you in your work of providing companion- ship, counsel, and consolation to those you care for.
"But the Lord answered her, 'Martha, Martha, you are worried
and distracted by many things; there is need of only one thing.
Mary has chosen the better part, which will not be taken from her."
—Luke 10. 41-2: New Revised Standard Version
When Mom was diagnosed, someone gave me Elisabeth Kubler- Ross's book. On Death and Dying, to read. Some of her fx)ints described how Mom was behaving, but most of them didn't. I kept telUng Mom that she should be angry , but she said, "What' s to be angry about?"
During the past few years, much has been written about human feehngs and processes. Death, grief, family functioning, abuse, and interpersonal communication models have become the focus of research, books, television programs, support groups, and various causes. One benefit of this social phenom- enon is that people aren 't quite so ready to label themselves and others as crazy or bizarre. For instance, we've come to expect
toddlers and teens to rebel, retirees to be ambivalent about their new "freedom," and the terminally ill or newly disabled to be angry or depressed.
In knowing more about how people may feel and react, however, we have come dangerously close to assuming that they should respond in those ways. Like Martha, we are "busy about many things," including how others feel. The unfortunate result is that we caretakers begin to see ourselves as orchestrat- ing others' processes. We assume that we have failed if they can't move through Kubler-Ross's stages of grief, for example, in proper sequence and "on time." I've listened to nurses' and physicians' sadness and regret about having been unable to lead
NCMJ / January J 993, Volume 54 Number 1 41
terminally ill patients to become angry over their situation. I've heard their frustration when, despite their most direct confron- tations, parents of critically ill children persistently talk in terms of "When she gets well..." and "When we take him home..." regardless of the odds against a happy outcome. The same nurse who says, "Of course, I knew I couldn't keep him from dying," adds in the next breath, "But I wonder what I should have said to get him past his denial."
The most obvious difficulty with this stance is that it usurps people's right to their own feelings and their unique ways of expressing them. One of my keenest recollections of grief came during one late night shift as I was pastoring the large family of an elderly and beloved matriarch who had just died. There were, of course, tears and embraces of support, those more easily recognized and socially acceptable expressions of sadness. In the midst of that, however, one son-in-law wailed, 'There ain't never going to be any more Apple Brown Betty ! " His statement was a profound, unique, and intensely personal way of express- ing his loss, although it hardly fit any clinical script.
There is a second problem in perceiving ourselves as directing the grieving process of those we care for. This stance prevents us from sharing in and being instructed and enriched — like Mary of the Gospel — by the process through which they do move. I listened to the mourner that night and offered my acceptance and comfort. But I've Hstened to that memory
countless times since; it has taught me how to grieve losses in my own life, and has enabled me to cry over things that "The Books" might deem insignificant, inappropriate, or irrelevant. Perhaps it has made me more sensitive to the importance of the "little things" that 1 might otherwise have passed over in my rush to honor the "big" or "right" events, realities, or feelings. Put another way, maintaining a certain reverence for those we minister to and care for will enhance our ability to cope with our own inevitable losses — of independence, of belonging, of self- sufficiency, of current relationships, and of earthly life itself. In that sense, we are ministered to by those we serve.
Dear Lord, you teach hard lessons. Be with me as I struggle to listen carefully and sensitively to your presence in those whom I serve and care for, and to your instructions for me as they emerge from their struggles. Sometimes circumstances occupy me with Martha's role. After all, someone has to pay the bills, make out the schedule, arrange for transportation, coverage, trips to the drugstore, and so on. As gently as you affirmed Mary's quiet listening, lead me to tolerate those times when I can listen to your voice in the words of those I serve, especially when I relinquish my control and expectations of how they should respond. You know how difficult that can sometimes be. Amen. □
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42
NCMJ / January 1993, Volume 54 Number 1
BOOK REVIEWS
Carolina Physician's Booksiieiff
Edward C. Halperin, M.D., Deputy Editor
Clinton, Bill, Gore, Al.
Putting People First: How We Can All
Change America. New York: Times Books,
1992, ISBN 0-8129-2193-3. $7.99.
Every four years, throughout our history, the American reader has been treated to a peculiar form of literature — books that extoll the virtues of the candidates for president of the United States and are generally called "campaign biographies." Nathaniel Hawthorne wrote one for the campaign of President Franklin Pierce and was rewarded, after Pierce's election, with a political appointment at the Boston customs house — a fact that played a role in Hawthorne's subsequent literary career. James Michener wrote the I960 campaign biography for John F. Kennedy.
The 1992 presidential election was characterized by a new literary invention: the campaign platform book. H. Ross Perot began the process with a paperback outlining his plans for the economy. This effort was followed, shortly thereafter, with Clinton and Gore's Putting People First — 232 pages of brief chapters outlining their views on the issues sandwiched between the texts of campaign speeches. These books made their debut against the backdrop of Senator Gore's best-seller. Earth in the Balance: Ecology and the Human Spirit.
President-elect Clinton has plenty of material in this book for the reader to consider, on issues ranging from children to national security, crime and drugs, and housing. I'll confine myself to his plans for health care policy — a linchpin of his campaign.
Any health care plan for the United States will have to address two fundamental problems: access and cost. It is estimated that 35 to 37 million Americans have no health insurance of any kind, and that millions more have minimal
From the Division of Radiation Oncology, Box 3085, Duke University Medical Center, Durham 27710.
insurance. The second problem is the effect of persistently rising health care costs on the nation's current and future economic condition. Health care payments are currently 15.3% of total federal expenditures and 11.4% of state and local budgets. In 1989 the U.S. spent 11.8% of its gross domestic product (GDP) on health. In comparison Canada spent 8.7%. These figures are all the more disturbing when we consider that the U.S. spent about 5% of the GDP on health in 1960, 7% in 1970, 9% in 1980, 1 1% in 1990, and an expected 16% to 17% by the year 2000. We spend 6% of the GDP on defense and 5 .8% on education.
About S217 billion of the financing for health care comes from private insurance, $136 billion from the patient's pocket. Sill billion from Medicare, S96 billion from other government programs, $75 billion from Medicaid, and $31 billion from other private sources. Most of our health care dollars are spent on hospitals — $256 billion. Physician services show up next at $ 126 billion followed by other personal expenses ($64 billion), medical supplies such as drugs and eyeglasses ($67 billion), other expenses including administration ($58 billion), nursing homes ($53 billion) , and $23 billion on research and construction of facilities. (These data come from the interesting article "Health Care Reform" by Harvard economist Rashi Fein in the November 1992 issue of Scientific An^erican.) The facts, sim- ply stated, are that we are paying an extraordinary amount for health care, the costs are rising very rapidly, and a lot of people are not getting access to the system.
We can all speculate on the causes of the current situation: the increasing complexity of medicine, the phenomenal growth of biomedical research and its attendant benefits, the ineffi- ciencies of third-party reimbursement, poor preventive health measures, corporate and individual avarice — the list goes on and on. What does Gov. Clinton think he's going to do about it?
The Clinton program calls for a National Health Board composed of providers and consumers. (Did they tell you, when you went to medical school that one day you ' d be a "provider?") Anyway, this board will be charged with setting a budget target
NCM J / January 1 993. Volume 54 Number I 43
for health care. Federal and state governments would enforce these targets. Clinton is not explicit as to what this means. It seems similar to the Canadian provincial government plans where the provinces set a yearly medical expenditure cap. Thus, the health care system must trade off expenditures (i.e. more for primary care, less for tertiary care) and restrain capital expen- ditures (i.e. buy fewer MR! machines). CUnton provides for the possibility that the health board might set rates, for example, specify the acceptable charge for a bronchoscopy, appendec- tomy, or complex psychiatric consultation.
All employers would contribute to improved access to health care, according to Clinton and Gore, with a "play or pay" program. Your business must either provide a health insurance program or you must buy into a government insurance program. Insurance companies would be prohibited from setting differ- ential rates based on loss experience. This means that a healthy 25-year-old would pay the same for health insurance as a diabetic, tobacco-abusing, obese 55-year-old. The euphemism for this is "community-based" rating — forcing insurance com- panies to base rates on the entire community, not on subsets. The Health Board would set a standard package of benefits that would have to be provided by all insurance plans.
The Clinton/Gore plan also includes some interesting sideline proposals: a standardized insurance claim form to reduce administrative costs, restraints on prices for drugs charged by pharmaceutical companies, and the use of computerized "smart cards" intended to contain the patient's medical history.
The problems with the Clinton/Gore plan are formidable. It will be absolutely crucial to set the price for government insurance at the correct level. Set it too low and employers will desert private insurance for a cheaper government program. Set it too high and small business will be punished by increased costs of operation. A Health Board setting rates for medical procedures is abureaucratic nightmare, besides the well-known factthatpricecontrolsdon'twork. (Don't take my word for it — remember the Nixon price control debacle?) A price control system may create artificial shortages, delays in capital im- provements, and long waits for procedures. (Part of the reason the Canadians get away with this is that most of Canada's population lives near the U.S. border. Can't wait for a semi- elective procedure? Cross the border and get it done in Seattle, Detroit, or Bangor.) The Clinton/Gore solution will also be extraordinarily expensive, and thinking that we'll pay for it by "getting tough with greedy insurance companies" is a pipe dream. (An excellent review of the Clinton and Bush proposals canhe(oundintheNew England Journalof Medicine'in:\090- 2 and 327:800-11.)
A proposal that will particularly annoy academic physi- cians is the plan to "reduce overhead on federally sponsored university research." This is commonly called "indirect costs." My research grants, for example, include a dollar amount to carry out the experiments proposed and a smaller amount to go to the university for the "indirect costs" involved in keeping up the laboratory building, utilities, administrative costs, general
maintenance, etc. There have been some well-publicized abuses of this system in recent years. Nonetheless, indirect costs are crucial to the conduct of the research enterprise. Clinton may be educable on this issue. It has been reported that he modified his position following an outcry from alarmed university officials. (See "Bill Clinton may be mellowing when it comes to overhead costs" in the October 21,1 992, issue of The Chronicle of Higher Education.)
What does all this mean for the individual practitioner? First, expect a big battle in Congress. The AMA, insurance industry, and hospital lobby are sure to weigh-in heavily in this debate. Second, taxes will surely rise on upper-income bracket physicians to pay for health policy as well as other expensive Clinton proposals. Third, American physicians will almost certainly be reminded that the ratio of physician's income to the average citizen's income is 5:1. This compares to 2:1 in En- gland and Australia, 3: 1 in Canada, and 4: 1 in the former West Germany. Some politician will figure out, pretty soon, that reducing physician payments will be one way to cut costs. In the words of the folk-song doctor. "Keep your hand upon the dollar, and your eye upon the scale! " Fourth, the Clinton/Gore propos- als, if enacted, are likely to significantly restrict equipment purchases and construction — look for a tightening of certificate of need approvals.
It will certainly be interesting. Stay tuned. Q
Frazier, Claude A, Brown, J.K.
Miners and Medicine: West Virginia Memories.
Norman and London: University of
Oklahoma Press, 1992, 131 pages.
Reviewed by Robert W. Prichard, MD., Department of Pathol- ogy, Bowman Gray School of Medicine, Wake Forest Univer- sity, Winston-Salem.
Asheville's Dr. Claude Frazier has most often written articles for the NCMJ in connection with his professional interest in allergies and insect stings. Now he brings his tales of medical life in the coal-mining areas into a slim volume, mostly dealing with West Virginia mining towns. His material comes from his own childhood as a coal-mine physician's son, and from over a hundred letters, photos, etc. solicited from those connected with coal-mining medicine. It is obvious from the text that he feels deeply about the trials of miners, their families, and their medical attendants.
Much of the book deals with coal-mining history, technical aspects of the mining procedures, the sociology of Appalachia, etc. The medical setting of the West Virginia coal miners was not basically different than that of people in other walks of life
44
NCMJ / January 1993, Volume 54 Number 1
among the hills of the western part of North Carolina. Poverty, ignorance, geographic isolation, the pressures of a harsh envi- ronment and the lack of what is now called a "social safety net" make the overall tone of Dr. Frazier's book dark. Due regard is given, however, to the camaraderie of those who shared times that probably look a lot harder to us than they did to those who lived through the era. When a coal-mine doctor's salary in 1 923 is noted as $4,200 it is necessary to consider its historical context — back then one could buy about six Fords for that sum , perhaps equivalent to $100,000 now.
For a contemporary medical student, this book could best be regarded as a snapshot of the lives of patients, doctors, and nurses in rural America between 1900 and 1945. The coal- mining details of the book seem most important as examples, perhaps extreme, of horrors seen in industrial medicine during the period. The continuing saga of the high-risk coal-mining industry, and the legacy of our poor understanding of the black- lung problem, give current pertinence to much of what is set out in the book.
Despite poor copy editing, this little period pieceof a book has its own charm and is well worth the short time it takes to read it. Those who doubt the reality or progress of coal-mining and industrial medicine would surely change their mind when they finish what Dr. Frazier and Mr. Brown have set down for them. □
"Chronic Temporomandibular
Joint Disease and Head Pain, " references
continued from page 32
4 Luskin DM. Etiology of the pain-dysfunction syndrome. J Am Dent Assoc
1969;79:147-53.
5 Wilkes CH. Stmctural and functional alterations of the temporomandibu- lar joint. Northwest Dentistry 1978;57:287-94.
6 Schellhas KP, Wilkes CH, et al. The diagnosis of temporomandibular joint disease: two compartment arthrography and MR. Am J Neuroradiology 1988;9:579-88.
7 ScheUhas KP. Internal derangement of the temporomandibular joint: radiologic staging with clinical, surgical, and pathologic correlation. Magnetic Resonance Imaging 1989;7:495-515.
8 ScheUhas KP. Wilkes CH, Baker CC. Facial pain, headache, and temporo- mandibular joint inflammation. Headache 1989;29:229-32.
9 Isacsson G, et al. Internal derangement of the temporomandibular joint: radiographic and histologic changes associated with severe pain. J Oral Max Surg 1986;44:771-8.
10 Lembeck F. Peripheral substance P Neurons: afferent, efferent or both
functions? In: Skrabanek P, Powell D (eds): Substance P. Dublin: Dublin Press, 1983, pp. 81-5.
1 1 Edvinsson L, McCuUough J, Uddman R. Substance P: immunohistochemi-
cal localization and effect upon cat pail arteries in vitro and in vivo. J Physiol 1981;318:251-8.
12 Anderson Q. Routine imaging strategies for detecting fractures and MRI
techniques to evaluate coincident TMJ injury. Lecture, Am Soc Temporomandib J Surg, Sea Is., GA 1991, unpublished data.
13 Godsby PJ, Edvinsson L, Ectman R. Release of vasoactive peptides in the
extracerebral circulation of humans and the cat during activation of the Irigeminovascular system. Ann Neur 1988;23:193-6.
14 Bereiter DA, Standord LF, Barker DJ. Hormone-induced enlargement of
receptive fields in trigeminal mechanoreceptive neurons. H. Possible mechanism. Brain Res 1980;184;41 1-23.
"I'm practicing medicine the \\'ay 1 think il should be practiced, sans the paperwork and administrative o\'erload."
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Letters to the Editor
continued from page 5
Prescription for Prose To the Editor:
I enjoyed Divyang Joshi's article in the November issue, "Why Do Practitioners Contribute to the Medical Literature," (NCMedJ 1992;53:608-610). My motivations for contributing to the medical literature include all of the reasons Mr. Joshi cited in his survey questionnaire. 1 think I might go mad if I did not write occasionally!
If Mr. Joshi ends up in one of the fine medical schools in North Carolina, or even elsewhere, I would be delighted if he would drop by for a visit sometime.
John R. Dykers, Jr., M.D.
P.O. Box 565
Siler City, NC 27344
Send all Letters to the Editor to:
Editor, North Carolina Medical Journal, Box 3910, DUMC,
Durham, NC 27710; or tax them to 919-286-9219.
^CMJ / January 1993, Volume 54 Number 1
45
New Members
Steven Arcangeli (RESIDENT), Coastal
AHEC, Dcpt. Ob-Gyn, P.O. Box 9025,
Wilmington 28402 Polly OlingcrBillips (RESIDENT), 9019
Landsburg Lane, Charlotte 28210 William RaymondBlythe (RESIDENT),
109 Celeste Circle, Chapel Hill 275 14 James Patrick Capes (RESIDENT), P.O.
Box 3286 1 , Carolinas Medical Center,
Charlotte 28232 Michael John Coffey (RESIDENT),
1660-S Woods Road, Winston-Salem
27106 David Peter Fedder (ORS), One Memo- rial Drive, P.O. Box 2000, Pinehurst
28374 Eric Matthew Gabriel, (RES1DENT),9 1 0
Constitution Drive, Apt. 411, Durham
27705 Tana Annette Grady (P), Box 3837,
DUMC, Durham 27710 Joseph Nihal Gunasekera (IM), 323 Third
St., SW.Taylorsville 28681 Keith Lawrence Hassan (RESIDENT),
2643-F MacGregor Downs Road,
Greenville 27834 Georgia Latham (RESIDENT), Rt. #1,
Box 269, P.O. Box 507, Glade Valley
28627 Lucie Marie Lauve (RESIDENT), 1826
Elizabeth Ave., Winston-Salem 27 103 Paul Arthur Lawrence (RESIDENT),
2201-B Anthony Drive, Durham
27705 Danielle Suzanne Malbasa (RESIDENT),
1212 W. 4th St., Apt. B, Winston- Salem 27101 Linda Meredith Nicholas (RESIDENT),
522 Colony Woods Drive, Chapel Hill
27514 George Louis Nichols, Jr. (STUDENT),
Box 2660, Bowman Gray, Medical
Center Blvd., Winston-Salem 27157 Sudhir Vinayak Raikar (AN), 318
Forsyth Medical Park, Winston-Salem
27103
Christopher Alan Sendi (RESIDENT), 3288 Colony Court, #616, Greenville 27834
Matthew Vinson Sheffield (RESIDENT), 7(X)5-E Brandemere Lane, Winston- Salem 27106
David Albert Smith (P), 248 Old Forest Creek Drive, Chapel Hill 27514
Mark Cooper Sturdivant (RESIDENT), 1 604 Kenilworth Ave.Charlotte 28203
Burke
Mark Hudson Davis (OBG), 403 S. King
St., Morganton 28655 Larkin Lee Selman (R), P.O. Box 38,
Rutherford College 28671
Columbus
Leroy Walker Rhein (OPH), 705 Jefferson St., Whiteville 28372
Durham-Orange
Justin J .G. Broughton (STUDENT), 1 39 A
Purefoy Road, Chapel Hill 27514 Patrick James Cawley (RESIDENT),
2610-H Camellia Sl, Durham 27705 Daniel Agee Coles (RESIDENT), 605
Jones Ferry Road, Apt. RR 10,
Carrboro 27510 William David Green (OBS), 1601
Glasgow St., Durham 27705 Jerry Eugene Patterson (MFS), 401
Providence Road, Chapel HiU 27514
Forsyth-Stokes-Davie ^
Martha Torrey Anderson (RESIDENT), 1 009 Kingstree Ridge Drive, Winston- Salem 27127
Joseph Madison Clark (STUDENT), 2055- A Academy St., Winston-Salem 27103
Lloyd P. Hitchings (N), 201 Executive Park Blvd., Winston-Salem 27103
Daniel Joseph Kennedy (RESIDENT), NC Baptist Hospital, Medical Center Blvd., Winston-Salem 27157
George Dave Robinette (RESIDENT), 2500 Jefferson Ave., Winston-Salem 27103
Venezela Ethel Bessie Thomas (STU- DENT), 5130 Ambercrest Drive, A- 10, Winston-Salem 27106
Mark Taft Thome (GS), Bowman Gray School of Medicine, Medical Center Blvd., Winston-Salem 27157
Gaston
Thomas Michael Florack (ORS), 902 Cox Road, Ste. A, Gastonia 28054
Vicki Weiss Light (OBG), Courtview Ob/Gyn, P. A., 2550 Court Drive, Ste. 204, Gastonia 28054
Greater Greensboro Society of Medicine
Keith Montgomery Clance (PUD), 520
N. Elam Ave., Greensboro 27403 Henry Fredrick Gregor (OBG), P.O. Box
10528, Greensboro 27404 Malcolm Truman Stark, Jr., (IM), 520 N.
Elam Ave. Greensboro 27401 Julius Nicolas Torelli (IM), 520 N. Elam
Ave., Greensboro 27403
Iredell
Frank Joseph Detrane (GE), 110-H Stockton Sl, Statesville 28677
Mecklenburg
Timothy Andrew Gajewski(U), 101 W.T. Harris Blvd., Ste. 2222, Charlotte 28262
Jeffrey S. Kneisl (ORS), Carolinas Medi- cal Center, Dept. of Orthopaedic Sur- gery, Charlotte 28226
Mark Hayden LeQuire (R), P.O. Box 36937, Charlotte Radiology, Charlotte 28236
Sheila Sawant Rondeau (IM), 7108 Pineville-Matthews Road, Nalle Clinic, Charlotte 28226
Continued on page 48
46
NCMJ / January 1993, Volume 54 Number 1
Continuing iViedicai Education
January 18-19 Mammography Minifellowship
Place: Winston-Salem Credit' 16 hours Category I, AMA Info: Division of Continuing Educa- tion, Bowman Gray School of Medicine, Winston-Salem 27103. 919/716-4450
January 18-22
Adult Echocardiography
Place: Winston-Salem Credit: 25 hours Category I, AMA Info: Division of Continuing Educa- tion, Bowman Gray School of Medicine, Winston-Salem 27103. 919/716-4450
January 20-22
Basic Food Service Plan Review
Place: Greenville
Info: OfficeofContinuingEducation, School of Public Health, CB# 8 165, Miller Hall, UNC, Chapel Hill 27599-8 1 65. 9 1 9/966-4032
January 21
North Carolina Health Law
and the Physician
Place: Research Triangle Park Credit 3 hours Category I, AMA Info: Kim Leadon, Director of CME,
Wake Area Health Education
Center, P.O. Box 14465,
Raleigh 27620-4465.
919/250-8030
January 21-22
Improving Clinical Education:
Teaching, Evaluation, and Feedback
Place: Chapel Hill Credit 12 hours Category I, AMA Info: Nancy Barnes, Office of CME, UNC School of Medicine, CB
#7000,231 MacNider Building, Chapel Hill 27599-7000. 919/962-2118
January 22 Neurology Day
Place: Greenville Credit 7 hours Category I, AMA Info: Mary C. Valand, Office of Con- tinuing Medical Education, Box 7224, Greenville 27835-7224. 919/551-5208
January 25-29
Peripheral Vascular Ultrasound
Place: Winston-Salem Credit 25 hours Category I, AMA Info: Division of Continuing Educa- tion, Bowman Gray School of Medicine, Winston-Salem 27103. 919/716-4450
February 3-4
Public Health Pest Management Workshop: Focusing on Food Service Vector Control
Place: Asheville
Info: OfficeofContinuingEducation, UNC School of Public Health, CB #8165, Chapel Hill 27599-8165. 919/966-4032.
February 8-12 Radiological Ultrasound
Place: Winston-Salem Credit 25 hours Category I, AMA Info: Division of Continuing Educa- tion, Bowman Gray School of Medicine, Winston-Salem 27103. 919/716-4450
February 12
Third Annual Public Health
Social Work Seminar Series
Place: Greenville
Info: OfficeofContinuingEducation,
UNC School of Public Health,
CB #8165, Chapel Hill
27599-8165.
919/966-4032.
February 15-17 Selected Topics for the Practicing Clinician
Place: Durham
Info: Office of CME, DUMC,
Durham 27710. 919/684-6485
February 17-19 Basic Food Service Plan Review
Place: Wilmington
Info: OfficeofContinuingEducation, School of Public Health, CB# 8165, Miller Hall, UNC, Chapel Hill 27599-8165. 919/966-4032
February 19 & 20
Pediatric Advanced
Life Support Course (PALS)
Place: Raleigh
Credit 16 hours Category I, AMA
Fee: $200
Info: Kim Leadon, Director of CME,
Wake Area Health Education
Center, P.O. Box 14465,
Raleigh 27620-4465.
919/250-8030
February 22-26 MRI Minifellowship
Place: Winston-Salem Credit 32 hours Category I, AMA Info: Division of Continuing Educa- tion, Bowman Gray School of Medicine, Winston-Salem 27103. 919/716-4450
tiCMJ / January J 993. Volume 54 Number 1
47
February 26
The Rafael C. Sanchez
Family Medicine Annual Update
Place: Greenville Credit: 7 hours Category I, AMA Info: Mary C.Valand, Office of Con- tinuing Medical Education, Box 7224, Greenville 27835-7224. 919/551-5208
March 1-4
The Alton D. Brashear Postgraduate
Course in Head and Neck Anatomy
Place: Richmond, VA
Credit- 40 hours Category I, AAGP/
AGD Info: Dr. HugoR.Seibel, Department
of Anatomy, Box 709, Medical
College of Virginia, Richmond,
VA 23298.
March 1-5
Ultrasound Principles and Instruments
Place: Winston-Salem Credit; 25 hours Category I, AMA Info: Division of Continuing Educa- tion, Bowman Gray School of Medicine, Winston-Salem 27103. 919/716^M50
March 5-6
Neurology for the Non-Neurologist
Place: Winston-Salem
Info: Division of Continuing Educa- tion, Bowman Gray School of Medicine, Winston-Salem 27103. 919/716-4450
March 8-9
Mammography Minifellowship
Place: Winston-Salem Credit 16 hours Category I, AMA Info: Division of Continuing Educa- tion, Bowman Gray School of Medicine, Winston-Salem 27103. 919/716-4450
March 8-12
Adult Echocardiography
Place: Winston-Salem Credit 25 hours Category I, AMA Info: Division of Continuing Educa- tion, Bowman Gray School of Medicine, Winston-Salem 27103. 919/716-4450
March 11-12
ACLS Provider Course
Place: Raleigh
Credit 16 hours, AAFP
Fee: $150
Info: Helen Creech, RN, Course
Coordinator, Rex Hospital,
4420 Lake Boone Trail
Raleigh 27607.
919/783-3161.
March 17
Fourth Annual Risk
Management Symposium
Place: Greenville Credit 7 hours Category I AMA Info: Mary C.Valand, Office of Con- tinuing Medical Education, Box 7224, Greenville 27835-7224. 919/551-5208
March 22-26 Obstetrical Ultrasound
Place: Winston-Salem Credit 25 hours Category I, AMA Info: Division of Continuing Educa- tion, Bowman Gray School of Medicine, Winston-Salem 27103. 919/716-4450
March 29-AprU 2 Radiological Ultrasound
Place: Winston-Salem Credit 25 hours Category I, AMA Info: Divisionof Continuing Educa- tion, Bowman Gray School of Medicine, Winston-Salem 27103. 919/716-4450
March 31 -April 2 Basic Food Service Plan Review
Place: Asheville
Info: OfficeofContinuingEducation, School of Public Health, CB# 8165, Miller Hall, UNCChapel Hill 27599-8 1 65. 9 1 9/966-4032
April 21-23
17th Annual Symposium of the
UNC Lineberger Comprehensive
Cancer Center — "Loss of Genomic
Integrity in Neoplasia"
Place: Chapel Hill
Info: Vickie McNeil, 919/966-3036.
New Members
continued from page 46
Michael Howard Rotberg (OPH), 1600 E.
Third St., Charlotte 28204 Brenda Austin Wells (FP), Nalle Clilnic,
1350 S. Kings Drive, Charlotte 28226
Montgomery
Charles Stephen Watras (FP), 508 Wood St., Troy 27371
Moore
William Vereen Terry, (RESIDENT), Pinchurst Surgical Clinic, One Memo- rial Drive, Pinehurst 28374
Onslow
John Leonard Almeida, Jr. (PTH), 1000 Summerbrook Place, Jacksonville 28540
Pitt
Johnny Stephen Howell (RESIDENT),
27 1 4 Mulberry Lane, Arlington Square,
Greenville 27858 Catherine Louise Johnson (STUDENT),
C-4 Doctors Park Apts., Bcasley Drive,
Greenville 27834 Randy Scott Lovelace (STUDENT), 507
Eleanor St., Greenville 27858 Robert Kepler Matlack, Jr. (STUDENT),
1535 Treybrooke Circle, Greenville
27834 Elizabeth Neel (STUDENT), 1642
Treybrooke Circle, Greenville 27834 William Russell (RESIDENT). 608
Cedarhurst Road, Greenville 27834 David Stuart Thompson (STUDENT), 101
Martinsborough Road, Greenville
27858
Rowan
Victor Manuel Rosado (P), P.O. Box 1718, Salisbury 28146
Scotland
Jeffrey David Seder (CD), 60 1 Lauchwood Drive, Laurinburg 28352
Surrey-Yadkin
Courtenay Salisbury Whitman, IV (ORS), 180-U Parkwood Drive, Elkin 28621
Wayne
Lawrence Jay Winikur (AN), Wayne Me- morial Way, Goldsboro 27530
48
NCMJ / January 1993, Volume 54 Number 1
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A GEM FOR SALE— 0.86 ACRES ZONED 0 & I: May be utilized as office or apartment site. Located on SunsetRoad off Blue Ridge Road near Rex Hospital and Kaiser Permanente in Raleigh. Priced $50,000 below tax value. Call today — This one's hot! 919/783-7911.
CHARLOTTE, NC: Five-M.D. general internal medicine group seeks BC/BE general internist to start after July, 1993. Send CV to Charlotte Internal Medicine Associates, 41 1 Billingsley Road,Suite 105, Charlotte, NC 2821 1.
DURHAM, NC: Four well-established and busy internists seek a BC/BE in- ternist to replace retiring senior part- ner. Attractive benefits. Salary nego- tiable. Send CV to Steven H. Hirsch, M.D., 2609 N. Duke St., Suite 205, Durham, NC 27704.
FAMILY PHYSICIAN OR GENERAL INTERNIST: needed to join the thriv- ing practices of two internists and one family physician, all board-certified and recently trained. Seek candidate of similar training to complement a recently formed group practice. With in an hour of Raleigh and the coast. Gen- erous income guaranteed. ContactPaul Edward Viser, M. D. , Woodside Medi- cal Associates, 603 Beaman St., Clinton, NC 28328.
FOR SALE— MEDICAL OFFICE COMPLEX: Morehead City location in medical community. 8,100 square feet. Inquiries: Ken Putnam, Realtor, P.O. Box 955, Morehead City, NC 28557. Tel. 919/726-2826; Fax 919/ 726-2829.
"HAPPINESS AND PROFESSIONAL SATISFACTION— Prevention of Physician Burnout": Two experienced physicians, a psychologist, and a fi- nancial advisor will facilitate at a coastal retreat. March 5-7, 1993, Seabrook Island, SC. CME credits. Room, meals, and tuition: $ 1 85. Write Donald E. Saunders, Jr., M.D., USC School of Medicine, 3555 Harden St. Ext., Columbia, SC 29208, or call 803/253-4214.
INTERNAL MEDICINE— Western North Carolina: BC/BE internist to join three internists. Pleasant moun- tain community of 75,000. Send CV to: P. A. Sellers, M.D., 510 7th Ave. West, Hendersonville, NC 28739.
OB/G YN PRIVATE PRACTICE: Great opportunity for physician to join well- established private practice. Excellent benefits and compensation. Ideal lo- cation in the "heart" of North Caro- lina. For details, call Melitta Kessner Monday-Friday 8:30a.m. to 5:30 p.m. at 1-800/476-2496, or fax inquiry/C V to same at 919/382-0227.
OUTSTANDING OPPORTUNITY: for a well-qualified general surgeon to join an established solo practice. Prac- tice has an excellent referral base and is located in a rural setting approxi- mately 20 minutes from Win- ston-Salem. A competitive compen- sation and benefit package is available with outstanding long-term growth potential. Please mail your resum6 to Locksley S. Hall, M.D., P.O. Box 68, Yadkinville,NC27055,orphone919/ 679-2041.
UNIQUE PROPERTY FOR SALE: Multi-use building located at the cor- ner of Barrett Drive and Six Forks Road just inside the Raleigh Beltline. This building has many "user" possi- bilities, and offers excellent location and visibility. The property is situated on an acre plus well-landscaped site with more than 50 parking spaces. At the entrance of North Hills Office Park with numerous medical and profes- sional goups nearby, the property is convenient to shopping centers, apart- ments,and densely populated residen- tial communities. The building mea- sures more than 13,000 square feet and is priced $60,000 below tax value with possible seller financing avail- able. Call today! 919/783-7911.
WANTED— PEDIATRICIAN: in Ra- leigh area. Group practice needs addi- tional physician, BC/BE. Send CV to Code #10, Duke University Medical Center, Box 39 10, Durham, NC 27710.
Classified Information
For NCMS members, rates are: $15 for the first 25 words, 25 cents for each additional word. For non-members, rates are $25 for the first 25 words, 25 cents for each additional word. Copy must be received by the 10th of the month preceding publication. Contact: NCMJ, Box 3910, DUMC, Durham, NC 27710; 919/286-6412; fax: 919/286-9219.
50
}iCMi IJanuary 1993, Volume 54 Number 1
Index to Advertisers
ACCESS
36
McGladrey & PuUen
1
Bristol-Myers Squibb Co.
52 & Cover 3
Medical Mutual Insurance Co. of NC
4
CompHealth
45
Medical Protective Company
15
CompuSystems
Cover 4
NC Practice Management Assn.
3
Crumpton Company
Cover 2
Palisades Pharmaceutir^ls
5
Eli Lilly & Company
29
U.S. Air Force
42
Glaxo, Inc.
8
U.S. Army
33
I.e. System
49
U.S. Army Reserve
49
Knoll Phannaceuticals
Insert after 36
Winchester Surgical Supply
33
Aphorisms off the l\/ionth
Daniel J. Sexton, M.D., Editor
Live as to die tomorrow. Learn as to live forever.
—Isidore of Seville 630 AD*
A dirty cook gives diarrhea quicker than rhubarb.
— Tung-su Pai**
Plurates non est ponenda sine necessitate (multiplicity ought not to be posited without necessity).
— Ockham
It is an axiom of a competitive society that is more powerful to give than receive.
— Sam Keen in "Fire in the Belly: On Being a Man"
I don't like money actually, but it quiets my nerves.
— Joe Louis***
Submitted by:
* Dr. Eugene A. Stead
** Dr. William Hathaway
*** Dr. E. Arthur Bolz
I have gathered a posy of other men's flowers; Nothing but the thread that binds them is my own.
— Montaigne
Everything has been said before, but since nobody listens we have to keep going back and beginning all over again.
—Andre Gide 1891
Men's maxims reveal their characters.
— Vauvenargues 1746
From the Editor: These three maxims help explain the reasons for this column. When I was asked to organize a monthly column on aphorisms I readily accepted since I had collected sayings on a wide variety of topics during the past 20 years. When Dr. Neelon became editor of the Journal he suggested that I solicit aphorisms from readers. This resulted in a number of responses, several of which are included in this month's column. We encourage all readers of this column to submit aphorisms. By sharing these bits of wis- dom important principles can be reaffirmed and empha- sized, and we may all have a bit of amusement in the process.
NCMJ / January 1993, Volume 54 Number J
51
PRA\ACHOL' (Pravastatin Sodium Tablets) CONTRAINOICAnONS
Hypefsensflivity to any comportenl of Uiis medication. Active l(\«r disease or unecplained. perststent ele«3tions in (ivef function tests (see WARNINGS). Pregnancy and lactation. Atherosclerosis is a chronic process and discontinuation ot lipid-lcwenng drugs during pregnarxry should have little impact on the outcome of long-term therapy ol pnmaiy hypercholesterctemia. Cholesterol and other products ol chotesteroi biosynthesis are essential components la fetal da^lopment Cincluding synthesis ot steroids artd cell membrar>es). Since HMG-CoA reductase inhibitors decrease chotesteroi synthesis and possibly the synthesis of other biologically acln^ substaix^s den\ed from chotesteroi. they may cause fetal harm wfien admristered to pregnant women Therefore, HMG-CoA reducla'^p mlTt >itif' . af '" rxitram- dicated dunng pregnancy arx3 n nursing nx)ther5. Pravastatin should be administered to women of child- bearing age only when such patients are highly unlikely to conceive and have been informed of the potential hazards. If the patent becomes pregnant while taking (his class of drug, therapy should be discon- Inued and tfie patent apprised of the potential hazard to the fetus. WARNINGS
Uver Enzymes: HMG-CoA reductase inhibrtors, like some other hpid-lcwering therapies, have been associated with bochemca) abnomialilies of li«r finction. Increases of serum transaminase (ALT, AST) values to more than 3 times the upper limit of nomial occumng on 2 or rnore (not necessarily sequential) occasions hae been reported in 1 .3% of patents treated with pravastatin in Vne U.S. over an average period of 18 months. These abnormalities were not associated with chdeslasis arxJ did not appear to be related to treatment duration. In those patients r\ v^iiom these abnomnalites were beliaed to be related to pravastatin and wtx) were discontrued from therapy, ttie transaminase levels usuaify fell slowly to pretreatment \e^\s. These biochemical findings are usually asymptomatic although worldwide expenence indicates that anorexia, v^eakress. arxJ/or abdomnaJ pain n^ay also be present m rare patents.
As with other lipid-bwenng agents, li\er function tests should be performed dumg therapy with pravastatin. Senjm aminotransferases, including ALT |SGFT). should be rrxxntored tjefore treatment begins, &ery six weeks for the Tirst three months, every eight weeks during the remainder of the first year, arxJ periodically thereafter (e.g., at atxxit six-month ntervals). Special attention should be given to patents v^fho dewtop increased transaminase levels. Uver function tests should be repeated to confirm an elevation and subsequently rrxxulored at more frequent nten/als. If increases in AST and ALT equal or exceed three times the upper limit of normal and persist, then therapy should be discontinued. Ffersistence of significant amrotranslerase ele^/atons lollcwing discon- tmuatton of therapy may warrant consideration ol liver biopsy.
Active liver disease or unexplained transaminase elevations are contraindications to the use ol pravastatin (see CONTRAINDICATIONS). Caution should be exercised when pravastatin is admimstered to patients with a history of liwr disease or heavy alcohol ingestion (see CLINICAL PHARMACOLOGY: Pharmacokinetics/MetaboJism). Such patients should be closely rronitored, started at the lower end of tfie recommended dosing range, and titrated lo the desired therapeutic effect.
Skeletal Muscle: Rhabdomyolysis with renal dysfunction secondary to myoglobinuria has been re- ported with pravastatin and other drugs in this class. Uncomplicaled myalgia has aiso been reported in pravastiiliii-lrrjtik-d ^kilteiilb i':** ADVERSE REACTIONS). Myopathy, defined as muscle aching or muscle v^eak- ness in conjunction with increases n creatine phosphoKnase (CPK) values to greater than 10 times the upper limit of normal was reported to be possibly due to prai/astalin m only one patient in clinical trials (<0,1%), Myopathy should be considered in any patient wflth diffuse myalgias, muscle tenderness or vk^akness. arxj/or marked elwation of CPK Ritpnts should be advised to report promptly unexplained muscle pain, tenderness or weak- ness, [>.irii< uLiiiy t I' ' ixnpaned by malaise or fe\er Pravastatin therapy should be discontinued if mark- edly elevated CPK levels occur or myopathy is diagnosed or suspected. Pravastatin therapy shoukl also be temporarily withheld in any patient experiencing an acute or serious condition predisposing to tt>e development of renal failure secorrdary lo rtiat>domyolysis, &g., sepsis; hypotension; major surgery; trauma; severe metat>olic, endocrine, or electrolyte disorders; or uncontrolled epilepsy.
Tfe rek ot myopathy dunng treatment with lovastalm is increased il ttierapy with eitfter cyclosponne, gem- fitxozil, erythromyan. or niaan is administered concurrently. There is no expenence with the use of pravostatn together with cyclosporine. Myopatfiy has not been observed in clinical Inals involving small numbers of patients wtx) were treated with pravastatin together with niacin. Or>e trial ol limited size rvolving combired therapy viflth pravastatin and gemfibrozil sfx?*ved a trend toward more frequent CPK elevations and patent vwttxjravrals die to musculoskeletal symptoms in the group receiving combined treatment as compared v^nth the grxips receiving placebo, gemfibrozil, or pravastatin mcnolherap^, Myopathy was not reported in this trial (see PRECAUTIONS: Drug Interactions)- One patient developed myopathy when clofibrate was added to a prwiously well tolerated regimen of pravastatin, the myopathy resolved when clofibrate therapy was stopped and pravastatin treatment continued The use of fibrates alone may occasionally be associated with myopathy. The combined use of pravastatin and fibrates should generally be avoided. PRECAUTIONS
General: Pravastatin may elevate creatine phosphokinase and transaminase la«ls (see ADVERSE REACTIONS). This shxxild te considered in the differential diagnosis ol chest pain in a patient on therapy with pra/astatin.
HbrTKtzygous Familial Hypercholestefciiemia. Pravastatin has not been evaluated m patents with rare homo- zygous familial hypercholesterolemta. In this group of patients, it has been reported that HMG-CcA reductase inhibitors are less effective because the patients lack functional LDL receptors.
R&ial Insufficiency: A single 20 mg oral dose of pravastatin was administered to 24 patents with varying degrees of renal impairment (as determined by creatinine clearance). No effect was obser\ed on the pharmacwki- netics ot pravastatin or its 3a-hydroxy sorreric metabolite (SO 31 .906). A small increase was seen m mean AUC values and hatt-lite (tV2) lor the [nacti\« enzymatic ring hydroxylatton metabolite (SO 31,945). Given this small sample size, the dosage administered, and the degree of andividual variability, patients with renal impairment w/ho are receiving pravastatin shxxjid be closety monitored.
Information for Patients: Patents should be advised to report promptly unexplained muscte pain, tenderness or weakness, particularty if accompanied by malaise or fei«r.
Drug Interactions: ImmLnosuppfBSsive Dnjgs. Gemfibmz}!. Niacii (Nicotric Aad). Erythmmydn: See WARN- INGS: Sketetal Muscle.
Anbpyme: Clearance by the cytochrome P450 system was unaltered t;y concomitant administration of prav- astatin. Snce pravastatin does not appear to induce hepatic drug- metabolizing enzymes, it is not expected that any significant interaction of pravastatin with other drugs (e.g., phenytom, quinidire} metabolized by the cyto- chrome P450 system will occur
Cftofesfyramfje/Cotesfi)x^. Concomitant administration resulted m an approximately 40 to 50% decrease in the mean AUC of pravastatin. However, when pravastatin was admristered i hour before a 4 hours after cholestyramine or 1 hour before colestipol and a slarxjard meal, there was no dimcalfy significant decrease m bioavailability or therapeutic effect. (See DOSAGE AND ADMINISTRATION: Concomitant Therapy.)
Vi^rfahn: in a study involving 10 healthy male subjects given pravastatin and warfam concomitantly for 6 days, bioavailability pararreters at steady state for pravastatin (parent compound) were not aftered. Pravastatr did not after the plasma protein- binding of warfann. Concomitant dosing did increase the AUC and Cmax of warfarin but did not produce any changes in its anticoagulant action (i.e., no ir>crease was seen in mean prothrombin time after 6 days ol concomitant therapy). However, bleeding and extreme prolongation of prothrombin time has been reported with anotfier drug in this class. Patients receiving warfann-type anticoagulants should have ther pro- thrombin limes closely monitored v^+ien pravastatin is initiated or the dosage of pravastatin is changed.
Cimetidine: The AUCo.,2hr 'o*" pravastatin when given with cimetidine was not significantly different from the AUC for pravastatin when gi\en alore. A significant difference was ot^seI^ed between the AUC's for pravastatin vrfen gi\en with cimetidire compared to when administered with antaad.
Dtgoxm: In a crossover trial involving 18 healthy male subjects gi\en pravastatin arxJ digoxin corxxirrently for 9 days, the bioavailability parameters of digoxn were not affected. The AUC of pravastatin tended to r>crease. but the overall bioavailability of pravastatin plus its metabolites SO 31 ,906 arxJ SQ 31 ,945 was not altered.
Gemfityozil In a crossover study n 20 healthiy mate volunteers given concomitant single doses of pravastatin and gemfibrozil, there was a significant decrease in unnary excretion and protein binding of pravastatin. In addition, there was a significant increase in AUC, Cmax, and Tmax tor the pravastatin metabolite SO 31,906. CombJiation therapy with pravastatin and gemfibrozil is generally not recommended.
in interaction studes with aspim. antaods { 1 hour prior to PRAVACHOL), ametidne. ntcotnic aad. or pfobucol. no statistically significant ditfererK::es in bioavailability were seen when PRAVACHOL (pravastatin sodium) was administered.
Other Drugs: Durng clinical trials, no noticeabte drug interactions were reported when PRAVACHOL was added tc diuretcs, antihypertensi\es. digitalis, converting-enzyme inhibitors, calaum channel blockers, beta- tilockers, or nitroglycerin.
Endocrine Function: HMG-CoA reductase inhibitors interfere vflth cholesterol synthesis and lower arculating cholesterol levels and, as such, might theoretically blunt adrenal or gonadal sterotd hormone production. Results of clinical tnals w/ith pravastatin in mates and post- menopausal females were inconsistent witfi regard to possibte effects of the dnjg on basal steroid honrtore levels In a study of 21 mates, the mean testosterore response to human chononic gonadotropin was significantly reduced (p<0.004) after 16 weeks of treatment with 40 mg ol pravastatin. Hovv^ver, the percentage of patients showing a >50% nse m plasma testosterore after human chorionic gonadotropin stimulation did not change significantly after therapy ri these patients, Tfie effects of HMG-CoA reductase inhibitors on spermatogenesis and fertility have not teen studied in adequate numbers of patents- The effects, if any, of pravastatr on the pituitary-gonadal axis in pre- menopausal females are unknown. F^tienls treated vwth pravastatin wUo display clinical andence ol endocrine dysfunction shxxjld be evaluated appropriately, Caution should also be exerased if an HMG-CoA reductase inhibitor or other agent used to lower chotesteroi tevels is administered to patients also receiving otter drugs (e.g.. ketoconazote. spirDfX)lactor>e. dmelidire) that may diminish the levels or activity of steroid hormones.
CNS Toxicrty: CNS vascular tesions. characterized by perivascular hemorrhage and edema arxl nxxionuctear cell infiftration of perivascular spaces, w/ere seen in dogs treated writh pravastatin at a dose of 25 mg/kg/day, a dose that produced a plasma drug tewel atxxit 50 times higher than the mean drug level m humans taking 40 mg/day. Similar CNS vascular lesions have been observed with several other drugs n this class.
" A chemically similar drug r this class produced optic nerve degereration (WaHenan degereralion ol reti- nogeniculate fiters) m clinically normal dogs m a dose-dependent fashcn startng at 60 mg/kg/day, a dose th^at produced mean plasma dnjg teveb about 30 times higher thian the nean drug level ri humans lakrtg tfe highest recommerxled dose (as measured by total enzyme inhitxtory activity). This same drug also produced ves- tibuiocochtear \ftfallenan-like degeneration arx) relral ganglion cell chromatotysis in dogs treated lor 14 weeks at 180 mg/kg/day, a dose wtiich resulted in a mean plasma drug tevel similar lo that seen with the 60 mg/kg dose. Carcinogenesis, Mutager>esls, Impairment of Fertility: In a 2-vear study n rats led pravastatin at doses ol 10, 30, or 1 00 mg/kg tx)dy weight , there was an increased inadence of hepatocellular carcinomas in males at ttie highest dose (p<O.0i)- /\Jthough rats were given up to 125 times the human dose (HD) on a mg/kg IxxJy weight basis, their serum drug levels were only 6 lo 10 limes higher than those measured in humans gi\«n 40 mg pravastatin as rreasured by /^C
The oral administration of 10. 30. or 100 rrtg/kg (producing plasma drug i&«te approximately 0 5 to 5.0 tines hujman drug tevels at 40 mg) ol prspi/astatn lo mice lor 22 nxrths resulted in a statistically signrficant irx^Base in the inciderKe o( mafignant lymphomas r treated femates vrfen all treatment grocps were pooted arxl compared to controls (p<0.05). The ixxtence was not dose-retaled and mate mice were not affected.
A chemically simitar dnjg in this dass was administered lo mice for 72 weeks at 25. 100. and 400 mg/kg body weight, which resulted m rrean serum drijg tevels approximately 3, 15. and 33 times higher thian thie mean human senjm dnjg corKentraton (as total inhibitory activity) after a 40 mg oral dose \jn& carcinomas were significantly increased in high-dose femates arxJ mid- arxl high-dose males, with a maximum irodence of 90 percent m mates. The rodence of adenomas of the li\er was significantly ncreased m mid- and high-dose femates. Drug treatment also sigmficantty increased tte incidence of lung adenomas ri mid- and high-dose mates and females. Adenomas of tfe eye Hardenan gland (a gland of the eye of rodents) v^ere significantly higher m high- dose mice than in controls.
fsio e/idence of mutagenicity was observed in vrtro. with or without rat-liver metatxilic activation, n tfie folkxving studes: mcrobial mutagen tests, usmg mutant strains of Salmonella typhimunum or Eschenchia coii. a forward mutation assay n L51 78Y TK + / - mouse lymptxxna cells; a chromosomal aberration lest n hamster cells. arxJ a gere conversion assay using Saccharomyces cerBvtsiae. In addition, there was no evidence of mutagencity in either a dominant tettial test m mice or a mcronucteus test in mice.
In a study m rats, w^th daily doses up to 500 mg/kg, pravastatin did not produce any adverse effects on fer^l- ity or general repnDducti\e performarx:e. However, m a study with another HMG-CoA reductase inhibitor, there was decreased fertility in mate rats treated for 34 weeks at 25 mg/kg body weight, although this effect was not observed n a subsequent fertility study when the same dose was administered for 11 vreeks (the entire cycte of spermatogenesis, including epididymal maturation). In rats treated wnth this same reductase inhibitor at 180 mg/kg/day, seminiferous tubute degeneration (necrosis and loss of spermatogenic epithelium) was ob- served. AJthou^ not seen vwth pravastatin, two similar drugs in this class caused drug-related testicular atrophy. decreased spermatogenesis, spermatocytic degeneration, and giant cell formation in dogs. The clinical significance of these findings is inctear Pregnancy: Pregnancy Category X: See CONmABsOGATlONS
Safety in pregnant women has not been established. Pravastatin was not teratogenic n rats at doses up to 1000 mg/kg daily or m rat)bits at doses of up to 50 mg/kg daily- These doses resulted in 20x (rabbrt) or 240x (rat) tfe human exposure tased on surface area (mg/meter2). Howiever, r studies w/rth anotfer HfvlG-CoA reductase nhibitor, sketetal malformations were observed in rats and mice, PRAVACHOL (pravastatin sodium) should be administered to women of child-Ceamg potential only w/hen such patients are highly unfikely to conceive arxi have tseen intorrred of the potential hazards. If the vwxnan becomes pregnant white lakng FTIAV/VDHOL (prav- astatin sodium). It should tie discontinued and tfe patient advised again as to tfe potential fiazards to the fetus. Nursing Mothers: A small amount of pravastatin is excreted in human breast milk. Because of tfe poten- tial for senous adverse reactions in nursing infants, women taking PRAVACHOL should not nurse (see CONTRAINDIG^TIONS),
Pediatric Use: Safety and effectiveness in individuals tess than 18 years old ha* not been estatJlished. Hence, treatn-ent m patents less than 18 years old is not recomrrended at this tine. (See also PRECAUTIONS: General.) ADVERSE REACTIONS
Praiastatin is gererally vrell loterated; adverse reactions tiave usually been mikj and transent. In 4-month long placebo-controlled tnals, 1 .7% of pravastatin -treated patients and 1 .2% of placebo-treated pattenis were discon- trued from treatment because of adverse expenerx:es attributed to study drug therap/; this difference was not statistically signrficant. In long-term studes. the most common reasons for discontinuation were asymptomatic serum transaminase increases and mild, non-specific gastrointestinal complarts. During clinical tnate the o\erall incidence of adverse events m the elderty was not dtfferent from the inadence obsen/ed m younger patents. Adverse Clinical Events: All adverse clinical events (regardless of attribution) reported n more than 2% of pravastatin- treated patents ffi the placebo-controlted trials are identified in the tabte tjelow; also shxMn are the percentages of patents in whom these medical events were beliaed to be related or possibly related to the drug:
All Events %
Events Attributed lo Study Drug %
Praastatm
Placebo
Pravastatin
Placebo
Body System/Event
(N = 900)
(N = 411)
(N = 900)
(N = 411)
Cardk>/3scuter
Cardiac Chest Ftir
4.0
3.4
0.1
0,0
Dermatologic
Rash
4X)*
1.1
1,3
0.9
Gastrointestina]
NBLeeaA/omlling
7.3
7.1
2,9
3.4
Diantiea
6.2
5.6
2,0
1.9
AbdomnalF^
5.4
6.9
2,0
3,9
Constipation
4.0
7.1
2,4
5,1
Flatulence
3.3
3.6
2,7
3,4
Heartburn
2.9
1.9
2,0
0,7
General
Fatigue
3.8
3.4
1,9
1.0
Chest F&jn
3.7
1.9
0,3
0.2
Influenza
2.4-
07
0,0
0.0
Musculoskeletal
Localized F^
10.0
9.0
1,4
1,6
Myalgia
2.7
1.0
0,6
0,0
Nervous System
Headache
6.2
3.9
17'
0.2
Dizziness
3.3
3.2
1,0
0.5
Ftenal/Genitounnary
Urnary Abnormality
2.4
2.9
0-7
1.2
Respratory
Common Cold
7.0
6,3
0.0
0,0
Rhiiitis
4.0
4.1
0,1
0,0
Cough
2.6
17
0 1
00
5 1992 E. R. Squibb & Sons, Inc.. Princeton, r^
0542-507B
'Statisticalfy signrficantly drfferent from placetxa.
The fdlcwing effects have been reported v^nth drugs in this dass:
Stetefa/. myopathy, ihatxJomyolysis.
Neur^ogical dysfunction of cedan cranial nen/es (including alteration of taste, impairment of extra-ocular mcwement, facial paresis), tremor, \ertigo, memory loss, paresthesia, penpteral neuropatfiy, peripheral nerve palsy.
Hyp&sensitjvfty ReactKms: An apparent hypersensitivity syndrome has been reported rarely w/hich has in- cluded one or more of the following features: anaphylaxis, angioedema. lupus erythematous-like syndrone, polymyalgia rheumatca, vasculitis, purpura, thrombocytopenia, teukopenia. henx)fytc anemia, positive ANA, ESR increase, arthrrtis. arthralgia, urticana, asthenia, photosensitiviry, leser, chills, flushing, malaise, dyspnea, toxic epidermal necrofysts, erythema multrfonre, including Stevens -Johnson syixJrome-
Gasfrorfesfna/- pancreatitis, hepatitis, including chronic active hepatitis, chotestatic jaundice, fatty change in liver, and. rarely, orrtiosis, fulminant hepatic necrosis and hepatoma: anorexia. «xniting.
R^DTOducfrie gyrecomastia, loss of libido, erectite dysfunction.
Eye: progression of cataracts (tens opaates), ophthialrrxptegia. Laboratory Test Abnormalities: Increases in serum transaminase (ALT AST) values and CFK have been observed (see WARNINGS)
Transent, asymptomatic eosrophilia has been reported. Eosnophil counts usually returred to normal despite continued therapy. /Vnemia. thrombocytopenia, and teukopenia ha\e been reported wrtth other HMG-CoA reduc- tase inhibitors.
Concomitant Therapy: Pravastatn has teen administered concurrently wflth cJxjtestyramine. colestipol, nico- thic aad, probucd and gemfibrozil Preliminary data suggest that the addition of either probucol or gemfibrozil to therapy' with lovastatn or prarastatm is not associated with greater reduction in UX-chotesterol than that achi&ed w^th lovastalm or pravastatin alone. No adverse reactions uiique to the combnation or r addition to those previously reported for each drug alone hae been reported, fvlyopathy and rtiabdomyolysis (with or without acute renal failure) have been reported when another HfyiG-CoA reductase rhibitor was used in combi- r^tion with immtnosuppressive dnjgs, gemfibrozil, erythromyan, or lipid-lcMering doses of nicotinic aad. Con- comitant therapy with HfvlG-CoA reductase nhibitors and these agents is generally not recommended. (See WARNINGS Skeletal Muscle and PREOiLmONS: Drug Interactions.) OVERDOSAGE There have teen no reports ot overdoses w/ith pravastatin.
Should an accidental overdose occur, treat symptomatically and rstrtute supportive measures as required.
^/K {J4-422A)
Issued September 1992
^P Bristol-Myers Squibb Company
^ choleSteftxDT cpritrol
Consistently and significantly reduces total C and atherogenic LDL-C; positively affects other key lipids
»v-
/H- .
Mean percentage change from baseline after
8 weeks of treatment with 10 to 40 mg of pravastatin"
Total C Triglycerides
'Each arrow represents a range of means derived from a single placebo-controlled ^
study that included 55 patients treated with pravastatin. • ' ' ^'
PRAVACHOL* (pravastatin sodium) is indicated as an adjunct to diet for the reduction of elevated total and LDL-cholesterol levels in patients with primary hypercholesterolemia (Types Ila and lib) when the response to diet alone has not been adequate.
Active liver disease or unexplained transaminase elevations, pregnancy and lactation are contraindications to the use of pravastatin.
Reference: 1. Jones PH, et al. Once-daily pravastatin in patients with primary hypercholesterolemia: a dose-response study. C//nCard/o;. 1991;14:146-151. ., ,^
^---^A-
pravastatin sodium &
Please see CONTRAINDICATIONS, WARNINGS, PRECAUTIONS, and ADVERSE REACTIONS in the brief summary of prescribing information on the adjacent page.
Bristol-Myers Squibb Company
*r
¥
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OF NORTH CAROLKM
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FEB i 0 1393 I
North Carolina Medical Journal
For Doctors and their Patients
SPECIAL ISSUE
Tiirning Pointe:
Arts Medicine
Patrick D. Kenan, M.D., Guest Editor
Health Care of Artists Arts in Healing Arts in Stress Management Arts in Education
Contents 54
jlW THERE IS
^ SOMETHING
IN OUR NAME
THAT BRINGS YOU
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NORTH CAROLINA MEDICAL JOURNAL
For Doctors and their Patients
Published Monthly as the Official Organ of the North Carolina Medical Society
February 1993, Volume 54, Number 2 (ISSN 0029-2559)
EDITOR
Francis A. Neelon, M.D. 919-286-6409
DEPUTY EDITOR
Edward C. Halperin, M.D.
CONSULTING EDFTOR
liugene A. Stead, Jr., M.D.
ASSOCIATE EDITORS
Eben Alexander, Jr., MX).
Winslon-Saiem William B. BIythe, M.D.
Chapel Hill F. Maxlon Mauney, Jr., M.D.
Asheville Walter J. Pories, M.D.
Greenville
MANAGING EDFTOR
Jeanne C. Yohn
919-286-6410
fax:919-286-9219
EDITORIAL ASSISTANT
Jane Whalen
SECTION EDITORS
Eugene W. Linfors, M.D. Daniel J. Sexton, M.D.
BUSINESS MANAGER
George E. Moore Raleigh
EDITORIAL BOARD
CHAIR
Margaret N. Harker, M.D.,
Morehead City MEMBERS Jay Arena, M.D.
Durham William B. BIythe, M.D.
Chapel Hill Jack Hughes, M.D.
Durham Timothy W. Lane, M.D.
Greensboro Walter J. Pories, M.D.
Greenville Robert W. Prichard, M.D.
Winston-Salem Mary J. Raab, M.D.
Greenville
The Society is not to be considered as endoising the views and opinions advanced by authors of papers delivered at the Annual Meeting or published in the official publication of the Society. — Constitution and Bylaws of the North Carolina Medical Society. Chap. IV. Section 3, pg, 4.
NORTH CAROLINA MEDICAL JOURNAL
Box 3910, Duke University Medical Center, Durham NC 27710, (919-286- 6410/fax: 919-286-9219), is owned and published by The North Carolina Medical Society under the direction of ii5 Editorial Board. Copyright© 1993The North Carolina Medical Society. Address manuscripts and communications regarding editorial matters, subscription rales, etc. . to the Managing Editor at the Duiham address listed above. All advertisements are accepted subject to the approval of the Editorial Board of the North Carolina Medical Journal. The appearance of an advertisement in this publication does not constitute any endorsement of the subject or claims of the advertisement.
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Annual subscription: $17 (plus 6% laxinNC). Single copies: $2. Second-class postage paid at Raleigh NC 27601 , and at additional mailing offices. Postmas- ter: Send address changes to the North Carolina Medical Society, 222 N. Person St., Raleigh NC 27601 .
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NCMJ / February 1993, Volume 54 Number 2
53
orth Carolina Medical Journal
FOR DOCTORS AND THEIR PATIENTS
Contents / February 1993, Volume 54, Number 2
On the cover: Dr. Lewis S. Rathbun of Asheville, one of this special issue's contributors, painted "Hibiscus" (watercolor, 199 1 ) after first photographing it from several positions. He describes his technique, and his involvement in the visual arts, in his article on page 115.
FROM THE GUEST EDITOR
59 Arts Medicine Patrick D. Kenan, MD.
HEALTH CARE OF ARTISTS
67 Dance Medicine: An Orthopaedist's View William T. Hardaker, Jr., M.D., and Lynn M. Vander Woude, PA-C
74 The Role of Somatic Education in Dance Medicine and Rehabilitation Glenna Baison, MA., PT
79 Medicine in the Vocal Arts James A. Kaufman, M.D.
HEALTH WATCH
87 Prostate Cancer M. Robert Cooper, MD.
ARTS IN HEALING
91 Music Therapy in Medical Settings Barbara C. Memory, PhD., RMT-BC, and Martha A. Bellamy, B.M.Ed., RMT-BC
96 Medicine and Literature William G. Porter, M.D.
101 Taking Shape: Environmental Art in Health Care Janice B. Palmer and Florence Nash
COMPASSIONATE CAREGIVING
105 The Ministry of Caring, Part 3 Margot Hover, D. Min.
ARTS IN EDUCATION
106 Drama in the Medical School Classroom: The Actor as Patient JoanTetel-Hanks,M.S.
ARTS IN STRESS MANAGEMENT
110 The Role of the Arts in Physician Stress Management Stephen I. Kramer, M.D., and Doreen L. Hughes, M.D.
115 The Visual Arts: The Door to a Fuller Life Lewis S. Rathbun, MD.. FACS
LETTERS TO THE EDITOR BULLETIN BOARD
56 The Risks of HTV Infection, The Editor Takes a Bow, 64 Instructions for Authors Ujjper Respiratory Disease in Asthmatics 119 Continuing Medical Education
120 New Members
57 Writing Workshop, More on "Aphorisms," 122 Classified Advertisements Two Suppwrt "Up Front" Fees 123 Aphorisms of the Month
123 Index to Advertisers
58 Physician Referral Policy
54 NCM J / February 1 993 , Volume 54 hi umber 2
WHAT HAVE OVER 2000
NORTH CAROLINA PHYSICIANS
DISCOVERED ABOUT THEIR PRACTICE?
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Letters to the Editor
The Risks of HIV Infection To the Editor:
Dr. Daniel J. Sexton has gingerly approached the key metaphor in compar- ing restrictions on HIV infected health care workers with driving an automobile ("Risks, Reactions, Regulations, and Reality: Health Care Workers with HIV Infection," NC Med J 1992;53:650-1).
Certainly, the risks are "small" when viewed as he chooses to view them, but one in a miUion doesn't make a damn if you're the one. Would Dr. Sexton "vol- unteer" to have his own hip replacement done by an HIV-positive orthopaedic surgeon? And would he do so "know- ingly"?
The equal or greater risk that HI V be transmitted from patient to health care worker is also equally abominable when it is done involuntarily and unknowingly. '
The risks we take driving are also risks that we constantly strive to reduce. We require licensing for drivers. We try to remove drunk drivers from the high- way.^ We wear seat belts and pay for air bags in our cars.
The bottom line is that we should all be tested so often that we know our HIV status. Only then can we begin to con- struct a society with a livable contract between those of us who are uninfected and those of us who are infected.
John R. Dykers, Jr., M.D.
P.O. Box 565
Siler City, NC 27344
References
1 Dykers JR, Jr. AIDS: discrimination and justice. NC Med J 1987;48:661-3.
2 Dykers JR, Jr. Chaos, alcoholism, and DWI. NC Med J 1991;52:394-7.
The Editor Takes a Bow To the Editor:
Several months ago, the venerable William Shawn, editor emeritus of The New Yorker, died at age 85 in his home in New York.
One of the plethora of panegyrics flooding the press extolling Mr. Shawn's virtues and his influence on American journalism impressed me the most. It was written by columnist Richard Reeves: ". . .magazines at their best are the exten- sion of one intelligence;" needless to say it is the intelligence of the editor. I recall once Dr. Eugene Stead, former editor of \heNorlh Carolina MedicalJournal, said something similar to this that the shadow of the editor is cast on every page of a publication.
We are now one year into the editorship of Dr. Francis A. Neelon who is obviously doing some shadow-casting of his own. It feels cool and comfortable. The magazine's quality is impressive, and the mission of the Journal as an instrument of communication among North Carolina physicians is being well fulfilled.
Assad Meymandi, M.D.,
Medical Director
Cape Fear Neuropsychiatric Associates
1212 Walter Reed Road
FayetteviUe, NC 28304
Upper Respiratory Disease in Asthmatics To the Editor:
Dr. Rubin F. Maness's "Managing Pediatric Asthma in NC" (NC Med J 1992;53:633-43) was most informative. Neglected in the article, however, was
the problem of upper respiratory disease in both pediatric and adult asthmatics.
With modem imaging and endo- scopic diagnostic capabilities, it is appar- ent that a large number of asthmatics suffer from chronic sinusitis. Aggressive medical therapy to control sinus disease can have an impact on asthmatic symp- toms. If the sinus disease cannot be con- trolled medically, effective surgical al- ternatives are available. Endoscopic surgical techniques in experienced hands can go a long way in controlling sinus disease that may be a contributing factor in asthma. These newer imaging and sur- gical techniques are being applied more and more to the pediatric population with good results. I believe it is imperative that an examination of the upper airway and sinuses be included in the evaluation of an asthmatic patient.
H. Clifford Baggett, M.D., FACS
Carolina Otolaryngology Consultants
901 N. Winstead Ave., Suite 210
Rocky Mount, NC 27804
From the Author:
I agree wholeheartedly with Dr.
Baggett in that sinusitis is a major trigger
for pediatric asthma. Any patient who is
not responding to appropriate asthma
therapy should have sinus x-rays obtained
and vigorous treatment instituted when
sinusitis is documented. A recent study
published in ihs. Journal of Allergy and
Clinical Immunology showed that 60%
of pediatric patients admitted to hospitals
due to asthma had abnormal sinus x-rays.
Rubin F. Maness, M.D.
Goldsboro Pediatrics, PA
2706 Medical Office Place
Goldsboro, NC 27534
56
NCMJ / February 1993, Volume 54 Number 2
Writing Workshop To the Editor:
While attending the annual meeting of the North Carolina Medical Society last November, 1 had the opportunity to participate in a workshop conducted by Dr. Francis Neelon and Ms. Jeanne Yohn, editor and managing editor, respectively, of the Journal. I thought that the work- shop was extremely well conducted and added tremendously to my somewhat scanty knowledge of writing for a medi- cal journal.
I would heartily recommend that this workshop be repeated at appropriate times in the future. It might also be expanded in format and content I, for one, would be interested in attending such a workshop again.
Charles E. Trado, M.D.
Hickory Psychiatric Center
24 Second Ave., N.E., Suite 201
Hickory, NC 28601
From the Editor:
The Journal staff will offer its sec- ond writing workshop on Sunday, Febru- ary 28, at the Durham Omni Hotel during the Medical Society's Spring Leadership Conference. See page 64 for details.
More on "Aphorisms" To the Editor:
I continue to be impressed with the wit, humor, and wisdom frequently con- tained in the quotes in Dr. Sexton's fea- tured item, "Aphorisms of the Month." I frequently save these in a file and use them either for humor or to make a point when teaching the students and residents.
I choose to disagree with Dr. Taylor's comments. (NC Med J 1992;53:504). We as physicians need lo be able to laugh at ourselves as well as others. We must always be careful to avoid inappropriate ridicule, but the aphorisms have never reached that point.
Keep up the good work for a feature that I look forward to each month in the Journal.
Dale A. Newton, M.D.
Associate Professor of Pediatrics
East Carolina University
GreenvUle, NC 27858-4354
Two Support "Up Front" Fees To the Editor:
1 would like to respond to Dr. Claude A. Frazier's comments in the December Journal (NC Med J 1992;53;621) and address the concept of'up front" fees. As a naive initiate to the practice of medicine in 1985, 1 frequently cared for obstetrical patients who were unable to pay "up front" for care. Unfortunately, after they went home as healthy mothers with healthy babies, they had little impetus to pay for obstetrical services. While an allergist is able to work up a patient in the office during scheduled hours, it is not unusual for me to be in the hospital caring for one patient in labor for 1 2 to 1 5 hours. This is generally at the expense of sleep and family responsibilities. My commit- ment in time and stress is worth adequate compensation, and at this time up front payment of co-payments, deductibles, or an entire fee for uninsured patients is my only guarantee for financial solvency.
A separate but related issue Dr. Frazier raises regards care provided by county health departments. There is the insinuation that an obstetrical patient would receive a lesser quality of care if she used the "public system." This is simply not true. In fact, there is evidence that some patients may have better out- comes when they receive care through the public sector, possibly due to the social and educational support that finan- cially stressed patients often require but private practice is unable to provide. Pri- vate practice differs because it often pro- vides amenities that are desirable but not critical to fetal or maternal well-being.
Our society is clearly expressing its desire for health care for all. As we work through the next decade, we must decide on the components of good health care with the recognition that many aspects of "private" care are luxuries provided to our patients at oiu" expense and for which we expect compensation. As long as the current paradigm for private practice re- mains viable, "up front" payments are a necessity for the business of medicine. William M. Callaghan, M.D. Asheville Women's Medical Center Asheville, NC 28801
To the Editor:
1 am responding to a letter to the editor by Claude A. Frazier, M.D., (NC MedJ1992;53:621)regarding"upfront" fees.
He was complaining that an indi- vidual patient of his who was pregnant was told by an obstetrician that if she could not pay S 1 ,8(X) "up front" then she should go to a public clinic. He then said if "this is what medicine has become, it is disheartening." 1 agree that medicine has become disheartening but fiscal realities and the medical legal environment have significantly reduced the opportunities for physicians to be benevolent and chari- table. Sitting on my desk is the malprac- tice bill for our two-physician group in the practice of obstetrics that exceeds $1 15,000. We have 2,500 square feet of rental office space, nine full-time em- ployees, and an overhead of nearly S60,0(X) per month. We have calculated our costs to perform an uncomplicated vaginal delivery to be at approximately $ 1 ,1(X), and that is before my partner and 1 receive any financial remuneration. The MAHEC Clinic here in Asheville is staffed by four full-time Ob-Gyn physi- cians who are funded by legislative tax dollars to provide care to indigent pa- tients. This is certainly not an unreason- able alternative for the patient who can- not afford a private physician.
Dr. Frazier has asked us to remem- ber "that each patient who comes to us is a human being in need of help." I heartily agree with this and am trying harder each day to remember it, but I would also ask Dr. Frazier this question: Who is going to pay my S115,0(X) malpractice premium for next year? These are fiscal costs that I cannot control and so, to insinuate that physicians are demanding "up front" fees because they are less charitable or be- nevolent, I believe, is unfair. The bills simply have to be paid. If Dr. Frazier can come up with some other way to pay these bills, I would be happy to hear from him.
R. Bruce Councell, M.D.
Sandridge & Councell Ob-Gyn Assocs.
50 Doctors Drive, Suite 120 West
Asheville, NC 28801
NCMJ / February 1993, Volume 54 Number 2
57
Physician Referral Policy To the Editor:
We appreciate the good intentions of the North Carolina Medical Society's Ethics Committee. [Drs. Spudis and Carlson are referring to the Society's recent adoption of the American Medical Association's policy on physician self referral. The AMA's policy states that physicians should not refer patients to a health care facility outside their office practice where they do not directly pro- vide care or services when they have an investment interest in the facility. The policy does allow for physicians to invest in and refer to an outside facility, whether or not they provide direct care or services there, if a demonstrated need exists in the community for the facility and alterna- tive financing is unavailable. In this case, certain requirements must be met. — ed.]
We feel, however, that the net result of their resolution concerning self refer- ral of patients for laboratory tests is the implication that we are confessing to a greedy practice that is easily identifiable
and intrinsically wrong. Statistical stud- ies do show that physician owners/inves- tors frequently order more procedures than non-owners/investors. This fact should not be surprising. It does not, however, justify public flagellation.
It seems to us that it would be better to point out that much, or perhaps most, of the medical education of each physi- cian is devoted to the evaluation of diag- nostic tools. These tools have evolved from rubber hammers to PET scans and DNA sequencing. This education is diffi- cult to obtain and must be constantly updated. The ownership or investment in a medical laboratory is not categorically unethical. We are constantly exposed to potentially unethical decisions. If patient A wants to chat for 15 minutes, does patient B get a short visit for the same charge? Is there a tendency to prescribe medication from a drug manufacturer that pays dividends to your wife? Would radi- ologists be hamstung by a system that required separate authorizations for fluo- roscopy, sonics, each contrast agent, or
each additional arterial injection?
The Ethics Committee should have stated that there appears to be an excessof inappropriate referrals from a small per- centage of physicians for diagnostic mon- etary investments. However, there may be an expression of excess caution evoked by a litigious society and by the reliable conclusion that more data usually leads to belter diseases management.
We should continue to study physi- cian referral patterns in light of these questions. The goal of the Medical Soci- ety is to eliminate both excessive and inappropriate referrals regardless of what facility performs the tests. Agencies such as Medicare are presently monitoring patterns and quality of care. Rather than create new legislation, we should use what is already in place and audit practice patterns that seem to be abusive.
Edward V. Spudis, M.D.
Kenneth P. Carlson, M.D.
Lyndhurst Urological Associates, P.A.
2932 Lyndhurst Ave.
Winston-Salem, NC 27103
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58 NCM J / February 1 993, Volume 54 Number 2
FROM THE GUEST EDITOR
Arts Medicine
Patrick D. Kenan, M.D.
All my life I have loved music. All kinds, really — classical, pops, grand opera, country and western, sacred, and a special love for Gilbert and Sullivan. I have listened to music, sung it, and learned to play several musical instruments. As an adult I undertook the serious study of music, and, at present, I continue with voice lessons, recitals, and choral performances. Medicine has been my profession and music, my avocation. Musicians, especially vocal artists, often seek my services as an otolaryngologist because I understand their voice and health problems. The natural blend of a scientific interest in laryngology and an awareness of the special needs of vocal artists and other professional voice users provided my personal entree into the medical care of artists.
Some 30 years ago, 1 developed my first concept of "Arts Medicine" and until the 1980s it remained the same. My primary contribution to the performing arts community was to provide for the health care needs of singers and other voice users. Of course, my personal enjoyment of music and the arts gave a much needed change of pace from the often frenetic activities of medical practice and represented a very important humanizing part of my life. And then I read a book that had a profound impact on my concept of medicine, arts, and the humanities.
In 1979, Norman Cousins, long-time editor of The Satur- day Review, published Anatomy of an Illness as Perceived by the Patient. In his book Cousins describes how he mobilized and used his own hidden resources to overcome a painful collagen disease. A recurring theme in the book is the value — indeed the necessity— of arts and entertainment, of laughter and mirth, and of creative expression in recovery from ill health. Cousins repeatedly emphasized the importance of the arts in maintaining the health of the patient and the provider as well.
From the Division of Otolaryngology, Department of Surgery, Box 3805, Duke University Medical Center, Durham 27710.
Anatomy of an Illness changed my philosophy of health care delivery. For reasons still not clear to me, my earliest ideas of the doctor-patient relationship involved physicians of great seriousness and dignity, usually unsmiling though kind, who approached problem-solving in ways that were totally objective and scientific but aloof from personal involvement in the lives of their patients. In fact, some of my role models in medical school were so serious and so demanding of high levels of knowledge and excellence that they frankly intimidated us students. We learned little of the "human" side of medicine, of the importance of friendship, of how a smile, a sense of humor, a warm handshake, or touch could put patients (and medical students!) at ease and gain their trust Norman Cousins made me realize the need for a major change in my approach to patient care. My personal involvement in vocal medicine became a useful vehicle for "rehumanizing" my approach to health care delivery.
My long-time interest in the arts took on a new meaning as I realized how essential the arts were to my own good health, particularly in areas of stress management. The relationship between arts and medicine became not only an ongoing study for me, but an obsession, even a passion, as I realized the broad impact of the arts and humanities on health maintenance, stress reduction, and the doctor-patient relationship, in addition to the responsibility we physicians have for the speciahzed health care needs of artists.
This edition of the North Carolina Medical Journal is devoted to a rather broad look at the arts and their interface with medicine. The reader will see the term "Arts Medicine." 1 am often asked, "What does it mean?" Few people, lay or profes- sional, have the slightest difficulty understanding a parallel term, "Sports Medicine," which of course involves (but is not restricted to) the delivery of health care targeted to the special needs of the athlete. An easy-to-understand extension of Sports Medicine to Arts Medicine is illustrated by the medical needs of the dancer. Is not the dancer an athlete as well? Many argue that dancers are the ultimate athletes. (See "Dance Medicine: An Orthopaedist's View" on page 67.) They have special
NCMJ / February 1993. Volume 54 Number 2
59
management needs for the treatment — and prevention — of dance-related injuries, but Sports Medicine clinics cannot ad- dress them with the expertise that the Dance Medicine specialist provides.
A major difference between Sports Medicine and Arts Medicine relates to the many facets of the latter. The problems of the vocal artist are obviously different from those of the dancer. Graphic and visual artists have still different problems related to exposure to pigments, solvents, and toxic agents. Then there are the repetitive movement problems of instrumen- talists. Arts Medicine therefore demands the services of profes- sionals from many disciplines: orthopedists, laryngologists, physical therapists, occupational medicine specialists, psy- chologists, generalists, orthodontists, environmentalists, dieti- cians, and others.
But Arts Medicine goes far beyond the delivery of health care to artists. In the words of Dr. Richard Lippin, president of the International Arts Medicine Association (lAMA), "Arts Medicine studies the relationships between human health and the arts. Artists and performing artists are among our world's most important human assets whose health must be increasingly protected and promoted. Arts have enormous healing power for individuals, institu- tions, and society as a whole. Arts can play a significanlroleinrehum- anizing health education and health care institu- tions. There must be co- operation between the performing Arts Medi- cine community, and those health educators
and administrators involved in the transition to rehumanize health education and health institutions around the world."
I believe that the scope of Arts Medicine encompasses four basic subsets. Articles in this issue of the Journal will address all four: 1) health care of artists; 2) the role of the arts in the healing process; 3) arts in stress management for health profes- sionals; and 4) arts in medical education.
Numerous professional organizations have emerged to underscore the alliance between medicine and the arts. Besides lAMA mentioned earlier, the list includes MEDART Interna- tional, The Voice Foundation of America, The National Asso- ciation for Music Therapy, Society of Health Care Arts Admin- istrators, American Art Therapy Association, The International Association for Dance Medicine and Science, Performing Arts
'Tm glad I can laugh at myself,
that I can take time to enjoy
the aesthetics as well as simple
pleasures of life, and that my career
in medicine has been mode more
fulfilling by the humanizing effect
of the arts in my life. I wish each
reader a comparable experience."
Medicine Association (PAMA), and American Physicians Art Association. These organizations provide newsletters, scien- tific meetings, and a variety of educational material for their constituencies. There are journals as well {Medical Problems of Performing Artists, Voice, International Journal of Arts Medi- cine), and a classic Textbook of Performing Arts Medicine, edited by Drs. Robert Sataloff, Alice Brandfonbrener, and Richard Lederman that provides a most comprehensive look at Arts Medicine.
The Performing Arts Health Resource Directory is avail- able to performers, agents, managers, directors, and other members of the performing arts and medical communities around the country. Various forms of Arts Medicine clinics have been established to meet the health needs of artists. At Duke we have an Arts Medicine "hotline," widely advertised through the performing arts community. A telephone call provides the mechanism for immediate triage, referral, and access so that performing artists, be they students or touring professionals, receive competent and prompt services.
This issue of the North Carolina Medical Journal brings
together a number of con- tributing authors who are widely dispersed geo- graphically in North Caro- lina, and who each ad- dress Arts Medicine from a different perspective. Not all the authors are physicians, but each has his or her own experience and expertise to share with the reader. As guest edi- tor I sincerely hope that
everyone who reads this
issue will derive a healthy respect for Arts Medicine, but more than that, a recognition of the necessity of the arts to the physical and mental health of all.
In closing, I want to share a personal experience I had last year with one of the true "giants" of medicine, a man who was my teacher at Duke and with whom I developed in later years a close collegial relationship. I asked him if he had it to do again, what if anything, would he have done differently. He re- sponded, "I wouldn't have been so serious."
I thank him for his advice, and I thank the arts for keeping my own life and career in perspective. I'm glad I can laugh at myself, that I can take time to enjoy the aesthetic as well as simple pleasures of life, and that my career in medicine has been made more fulfilling by the humanizing effect of the arts in my life. I wish each reader a comparable experience. □
60
NCMJ / February 1993, Volume 54 Number 2
TWO lANDMARK STUDIES, '-' PRESENTED AT THE 1 992 AMERICAN COLLEGE OF CARDIOLOGY MEETING,
FINALLY RESOLVED
A 200-YEAR-OLD CONTROVERSY...
LANOXIN JS EFFECTIVE IN CONGESTIVE HEART FAILURE MTIENTS IN NORMAL SINUS RHYTHM, WITH OR WITHOUT AN ACE INHIBITOR. ''
"The RADIANCE — Randomized Assessment of Digoxin on Inhibitors of the ANgiotensin Converting Enzyme — study was a multicenter, randomized, double-blind, placebo-controlled study of digoxin in CHE patients receiving diuretics and ACE inhibitors.
The PROVED — Prospective Randomized study of Ventricular failure and the Efficacy of Digoxin — study was a multicenter, randomized, double-blind, placebo-controlled study of digoxin in CHE patients receiving diuretics.
In early CHF.
LANOXIN
(digoxin) Tablets i
25 (ig (0.125 mg) 250 ng (0.25 mg) 500 ng (0,5 mg)
EFFECTIVE THERAPY... WITH OR WITHOUT AN ACE INHIBITOR.
Please see brief summary of prescribing information below.
LANOXIN® (DIGOXIN) TABLETS
Before prescribing, physicians should be thoroughly lamiliar with all aspects of this cardiac (or digjlalis) glycoside as discussed in the lull prescribing inlorrtiation.
Brief Summary
CONTRAINDICATIONS:
(1) venlficular libiillalion, (2) an untoward ellecl requiring ijisconlinualion ol other digitalis prepara- lions. and (3) a hypersensitivity or allergy to digoxin,
WARNINGS: The use ol digoxin lor the treatment ot obesity is dangerous since it may cause polenlially lalal arrhythmias. Anorexia, nausea, vomiting and arrhythmias may be indicalions ot digitalis toxicity: il so. digox- in should be temporarily withheld when possible Patients with renal insulliciency require smaller than usual maintenance doses ol digoxin Heart failure accompanying acute glomerulonephritis requires extreme care in digitalization and careful monitoring. Relatively low loading and maintenance doses and concomitant use ot antihypertensive drugs may be necessary Digoxin should be discontinued as soon as possible in tliis set- ting Patients with severe carditis are especially sensitive to digoxin-induced rhythm disturbances Newborn infants display considerable variability in their tolerance to digoxin with premature and immature inlanis being particularly sensitive, reduce and individualize dosage accordingly Note Digoxin is an important cause ol accidental poisoning in children
PRECAUTIONS: Digoxin toxicity develops mote Irequently and lasts longer in patients with renal impair- ment because ot the decreased excretion ot digoxin Normal potassium and magnesium levels should be main- tained in patients treated with digoxin Calcium, parlicularly when administered rapidly by the intra- venous route, may produce serious arrhythmias in digitalized patients Hypercalcemia predisposes the patient to digitalis toxicity, whereas hypocalcemia can cause digoxin to become ineltective. Patients with acute myocar- dial inlarction or severe pulmonary disease may be unusually sensitive to digoxin-induced rhythm disturbances Atrial arrhythmias associated with hypermelabolic states are particularly resistant to digoxin treatment Large doses ol digoxin are not recommended as the only treatment ol Ihese arrhythmias: il targe doses are required, be careful to avoid toxicity In hypothyroidism, digoxin requirements are reduced i^eduction ol digox- in dosage may be desirable belore electrical cardioversion to avoid induction ol ventricular arrhythmias II digitalis toxicity is suspected, elective cardioversion should be delayed Patienis with incomplete AV blocl<s may progress to advanced or complete heart block when given digoxin, especially in patients with Stokes-Adams allacks Digoxin may worsen sinus bradycardia or sinoatrial block in patients with sinus node disease Digoxin may cause rapid ventricular rales and ventricular librillation in patients with Wolll- Parliinson-White Syndrome and atrial librillation Because il may worsen Ihe outllow obstruction in patienis with idiopathic hypertrophic subaortic stenosis (IHSS), digoxin should only be used in severe car- diac lailure in this setting Patients with chronic conslrictive pericarditis may tail to respond to digoxin Slowing of Ihe heart rale by digoxin in some patients may lurlher decrease cardiac output Patients with heart lailure from amyloid heart disease or constrictive cardiomyopathies respond poorly to digoxin (See DRUtS INTERACTIONS section)
Laboratory Tests: Serum electrolytes and renal lunclion should be assessed periodically Drug Interactions Potassium-depleting cort/cos/ero/rfs and d/ure//cs may be major contributing lactors to digitalis toxicity Calcium, particularly il administered rapidly by the intravenous route, may produce seri- ous arrhythmias in digitalized patients Quinidine. verapamil, amiodarone. and propafenone cause a rise in serum digoxin concentration, with the implication that digitalis intoxication may result Certain antibiotics increase digoxin absorption in patients who inactivate digoxin by bacterial metabolism in the lower intes- tine, so that digitalis inioxlcation may result Propantheline anii diphenoxylate, by decreasing gut motility, may increase digoxin absorption Antacids, kaolin-pectin, sullasalaiine. neomycin, cholestyramine, certain anticancer drugs 5i\il metoclopramiderusy reduce intestinal digoxin absorption, resulting in unexpected- ly low serum concentrations There have been inconsistent reports regarding the ellects ol other drugs on the serum digoxin concentration r/iyro/dadministration to a digilalized, hypothyroid patient may increase
the dose requirement ol digoxin Concomitant use ot digoxin and sympathomimetics increases the risk ol cardiac arrhythmias because bbth enhance ectopic pacemaker activity Succinylcholine may cause a sutJ- den extrusion of potassium trom muscle cells, and may thereby cause arrhythmias in digilalized patients Although 0 adrenergic blockers or calcium channel blockers and digoxin may be uselul in combination to control atrial tibritlalion, their additive ellects on AV node conduction can result in complete heart block. Carcinogenesis No long-term animal studies have been pertormed to evaluate carcinogenic potential Pregnancy: Pregnancy Category C Animal reproduction studies have not been conducted with digoxin Digoxin should only be given to a pregnant woman il clearly needed
Nursing Mothers Studies have shown that the digoxin concentration in the mother's milk is lar below the usual infant maintenance dose and should have no pharmacologic ellecl upon the inlant Nevertheless, cau- tion should be exercised when digoxin Is administered to a nursing woman ADVERSE REACTIONS The overall incidence ot adverse reactions has been reported as 5 to 20%, with 15 to 20% (1 to 4% ol all patients) ot them being considered serious Evidence suggests that the incidence ol toxicity has decreased since the introduction ol the serum digoxin assay and improved standardization ol digoxin tablets. Cardiac toxicity accounts lor about one-hall, gastroinlestinal disturbances lor about one- lourth, and CNS and other toxicity lor about one-lourth of Ihese adverse reactions Adults: Carrf/ac-unitocat or multilorm VPCs, ventricular tachycardia, AV dissociation, accelerated junctional (nodal) rhythm and atrial tachycardia with block, excessive slowing ol the pulse, AV block (Wenckebach) ot increasing degree may proceed to complete heart block Gastrointestinal: anorexia, nausea, vomiting, occasionally diarrhea, and very rarely hemorrhagic necro- sis ol the intestines and abdominal pain
CNS: visual disturbances, headache, weakness, dizziness, apathy and psychosis. Other gynecomastia
Inlants and Children: Anorexia, nausea, vomiting, diarrhea and CNS disturbances may be present but are rare as initial symptoms in infants Cardiac arrhythmias are more reliable signs of toxicity Digoxin In chil- dren may produce any arrhythmia fi/lost common are conduction disturbances or SVTs, such as atrial tachy- cardia with or without block, and junctional (nodal) tachycardia Ventricular arrhythmias are less common Sinus bradycardia may also be a sign ol impending digoxin toxicity, especially in intants. even in the absence of first degree heart block, September 1 991 51(2253
PLEASE CONSUL T FULL PRODUCT INFOHMA TION BEFORE PRESCRIBING
References: 1 . Packer M, Gheorghiade M, Young JB, et at. Randomized, double- blind, placebocontrolled, withdrawal study of digoxin in patients with chronic heart failure treated with converting-enzyme inhibitors, J Am Coll Cardiol. 1992;19:260A. Abstract. 2. Young JB, Uretsky BF, Shahidi FE, Yellen IG, Harrison MC, Jolly MK. MulHcenter, double-blind, placebo-controlled randomized withdrawal trial of the efficacy and safety oF digoxin in patients with mild to moderate chronic heart foilure not treated with converting enzyme inhibitors, J Am Colt Cardiol. 1992;19:259A, Abstract.
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64
NCMJ / February 1993. Volume 54 Number 2
Zantac' 150T3blels CONDENSED
(ranitidine hydrochloride) BRIEF SUMMARY
Zantac' 300 Tablets
(ranitidine hydrochloride)
Zantac ° Syrup
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The following is a brief summary only Before prescribing, see complete pre-
scfibing mfofmalion in Zantac* product labeling
INDICATIONS AND USAGE: Zantac' is indicated in
1, Stion-term treatment of active duodenal ulcer. IWost patients heal within 4 weeks. Studies available to dale hawe nol assessed the safety of ranitidine in uncomplicated duodenal ulcer for periods ol more Ihan 8 weeks,
2. IVIainlenance therapy for duodenal ulcer palienis at reduced dosage after healing of acule ulcers
3 The treatment of pathological hypersecretory conditions (eg., Zollinger- Ellison syndrome and syslemic mastocytosis)
4. Short-term treatment ol active, benign gastric ulcer. Most patients heal within 6 weeks and the usefulness of further treatment has not been demon- strated. Studies available to date have not assessed ifie safely of ranitidine m uncomplicated, benign gastric ulcer for periods of more than 6 weeks.
5. Treatment of gastroesophageal rellui disease (GERD). Symptomatic re- lief commonlv occurs within 1 or 2 weeks after starling therapy with Zantac 150mgbi.[f.'
6 Treatment of endoscopically diagnosed erosive esophagitis. Healing of endoscopicaliy diagnosed erosive esophagitis occurs at 4 weeks (47%), 8 weeks (71 ^o), and 12 weeks (84%) ol therapy with Zantac 150 mg q.i.d. Symptomatic relief of heartburn commonfy occurs within 24 hours of therapy initiation with Zantac
Concomitant antacids should be given as needed tor pain relief to patients with active duodenal ulcer; active, benign gastric ulcer; hypersecretory states; GERD: and erosive esophagitis.
CONTRAINDICATIONS: Zantac' is contramdicated tor patients known to have hypersensitivity to the drug.
PRECAUTIONS: General: 1 . Symptomatic response to Zantac" therapy does not preclude the presence of gastric malignancy. 2 Since Zantac is excreted primarily by the kidney, dosage should be adiusted m patients with impaired renal function (see DOSAGE AND ADMINISTRATION) Caution should be ob- served in patients with hepatic dysfunction since Zantac is metabolized m the liver
Laboratory Tests: False-positive tests for urine protein with Multistix" may occur during Zantac therapy, and therefore testing with sulfosalicylic acid is recommended
Drug Interactions: Although recommended doses of Zantac do not inhibit the action of cytochrome P-450 enzymes in the liver, there have been isolated re- ports of drug interactions that suggest that Zantac may affect the bioavail- ability of certain drugs by some mechanism as yet unidentified (e.g., a pH- dependent effect on absorption or a change m volume of distribution).
Increased or decreased prothrombin times have been reported during con- current use 0' ranitidine and warfarin However, m human pharmacokinetic studies with dosages of ranitidine up to 400 mg per day, no interaction oc- curred: ranitidine had no effect on warfarin clearance or prothrombin time. The possibility of an interaction with warfarin at dosages ot ranitidine higher than 400 mg per day has not been investigated
Pregnancy: Teratogenic Effects: Pregnancy Category B: Reproduction stud- ies have been performed in rats and rabbits at doses up to 160 times the hu- man dose and have revealed no evidence of impaired fertility or harm to Ihe fetus due to Zantac. There are, however, no adequate and well-controlled studies in pregnant women Because animal reproduction studies are not al- ways predictive of human response, this drug should be used during preg- nancy only if clearly needed.
Nursing Mothers: Zantac is secreted in human milk. Caution should be exer- cised when Zantac is administered to a nursing mother. Pediatric Use: Safety and effectiveness in children have not been established ADVERSE REACTIONS: Headache, sometimes severe, seems to be related to Zantac" administration. Constipation, diarrhea, nausea/vomiling, abdominal discomfort/pain, and, rarely, pancreatitis have been reported There have been rare reports of malaise, dizziness, somnolence, insomnia, vertigo, tachycar- dia, bradycardia, atrioventricular block, premature ventricular beats, and arthralgias. Rare cases of reversible mental confusion, agitation, depression, and hallucinations have been reported, predominantly in severely ill elderly patients. Rare cases of reversible blurred vision suggestive of a change in ac- commodation have been reported. Rare reports of reversible involuntary mo- tor disturbances have been received.
In normal volunteers. SGPT values were increased to at least twice the prelreatment levels in 6 of 12 subjects receiving 100 mg q i d intravenously for 7 days, and in 4 ot 24 subjects receiving 50 mg q.i.d. intravenously tor 5 days. There have been occasional reports ot hepatitis, hepatocellular or hepa- tocanalicular or mixed, with or without jaundice In such circumstances, rani- tidine should be immediately discontinued. These events are usually re- versible, but m exceedingly rare circumstances death has occurred.
Blood count changes (leukopenia, granulocytopenia, and thrombocytope- nia) have occurred in a few patients. These were usually reversible. Rare cases of agranulocytosis, pancytopenia, sometimes with marrow hypoplasia, and aplastic anemia and exceedingly rare cases of acquired immune hemolytic anemia have been reported.
Although controlled studies have shown no antiandrogenic activity, occa- sional cases of gynecomastia, impotence, and loss of libido have been re- ported in male patients receiving Zantac, but the incidence did not differ from that in the general population.
Incidents of rash, including rare cases suggestive of mild erythema multi- forme, and, rarely, alopecia, have been reported, as well as rare cases of hy- persensitivity reactions (e.g., bronchospasm, fever, rash, eosmophilia), ana- phylaxis, angioneurotic edema, and small increases in serum creatinine, OVEHDOSAGE: There has been limited experience with overdosage. Reported acule ingestions of up to 1 8 g orally have been associated with transient adverse effects similar to those encountered in normal clinical ex- perience (see ADVERSE REACTIONS) In addition, abnormalities of gait and hypotension have been reported.
When overdosage occurs. Ihe usual measures to remove unabsorbed ma- terial from the gastrointestinal tract, clinical monitoring, and supportive ther- apy should be employed.
Studies in dogs receiving dosages of Zantac" in excess of 225 mg/kg per day have shown muscular tremors, vomiting, and rapid respiration. Single oral doses of 1 .000 mg/kg in mice and rats were not lethal. Intravenous LD50 values m mice and rats were 77 and 83 mg/kg, respectively DOSAGE AND ADMINISTRATION: (See complete prescribing information in Zantac- product labeling )
Dosage Adjustment tor Patients With Impaired Renal Function: On the ba- sis of experience with a group of subjects with severely impaired renal func- tion treated with Zantac, the recommended dosage in patients with a creati- nine clearance less than 50 mL per minute is 1 50 mg or 1 0 mL (2 teaspoon- fuls equivalent 10 150 mg of ranitidine) every 24 hours. Should the patient's condition require, the frequency of dosing may be increased to every 12 hours or even further with caution. Hemodialysis reduces the level ot circu- lating ranitidme. Ideally, the dosing schedule should be adjusted so that the timing of a scheduled dose coincides with the end ot hemodialysis
May 1992
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HEALTH CARE OF ARTISTS
Dance Medicine
An Orthopaedist's View
William T. Hardaker, Jr., M.D., and Lynn M. Vander Woude, PA-C
The art form of theatrical dance includes the disciplines of classical ballet, modem dance, ethnic dance, and various mixed forms, such as Broadway and jazz. Ballet originated in the triumphal processions and royal feasts of the Italian Renais- sance, and was then brought to France, where it became a central theme of elabo- rate court presentations of King Louis XIV. Louis founded the first school of ballet — ^L' Academie Royal de la Danse — which provided the steps and sequences that, even today, constitute the artistic language of classical ballet. Pierre Bauchamps, the king's choreographer, refined the five basic foot positions and the concept of turn-out, which provides freedom of movement while preserving the aesthetic line so characteristic of this art form. Grace and ease of movement, coupled with the apparent defiance of gravity, characterize contemporary bal- let performance.'
While ballet has its roots in aristoc- racy and tradition, modem dance has its origins in change, if not rebellion. This form arose at the turn of the century in defiance of the rigid standards and tech- niques of classical ballet. It has evolved to encompass a multitude of movement styles and expressions. In contrast to the styhzed positions of ballet, modem dance emphasizes freedom of movement, often
taken to extraordinary, even bizarre, ex- tremes. If ballet choreography attempts to defy gravity, then modem dance en- hances this force, producing angular movements, rooted to the earth .This bond with natural forces allows unique oppor- tunity for creativity, individuality, and personal expression in movement.
Although the principles and charac- ter of dance disciplines have remained relatively constant, the anatomical and physical demands of dance have in- creased.^' Contemporary choreographers extend dancers to the absolute limits of their athletic and artistic skills. Classwork prepares dancers to meet the physical and artistic demands of performance. Ballet class begins with warm-up exercise at the barre — a wall-mounted wooden railing that provides external support while the student develops balance and carriage. Bending and stretching movements are f)erformed in a graduated fashion of ever-increasing speed and complexity. Following barre exercise, the dancer moves to central floor activities — com- plicated routines involving coordinated arm and leg movement as well as tums and jumps. The movements are executed slowly at first but, like barre exercises, progress from slow to fast, from simple to complex, always concentrating on bal- ance, strength, and aesthetic line.
Balletclasses vary little in basic stmc- ture, but modem dance classes offer great diversity in organization, movement, and teaching techniques. These variations can be so radically different that specialized instruction and training techniques may be required before regular participation in class.
Regardless of the discipline, classes usually last 60 to 90 minutes. Many pro- fessional and aspiring professional danc- ers attend several classes daily, five to six days per week. Ballet and modem dance students often "cross-train" in the other discipline, as well as taking technique classes in jazz, Broadway, and ethnic dance. They may extend the cross- training concept to develop strength and endur- ance through free weight and isokinetic circuit training, cycling, stair-stepping, and other contemporary fitness activi- ties.^
Pathomechanics of Dance Injury
The grace, elegance, body control, and projection of dancers are well-recognized, but only recently has the medical com- munity come to appreciate the extraordi- nary coordination, physical strength, and endurance of these remarkable athletes.
Dr. Hardaker is assistant professor and Ms. Vander Woude is senior physician associate, Division of Orthopaedics, Department of Surgery, Duke University Medical Center, Durham. Dr. Hardaker Is also attending orthopaedic surgeon for the American Dance Festival, an international festival of dance held each summer at Duke. Although modern dance Is emphasized, all disciplines, including ballet, ethnic, and mixed forms are covered In the festival curriculum.
NCMJ / February 1993. Volume 54 Number 2
67
Many exercise physiologists and kinesiologists consider that elite profes- sional dancers represent ultimate ath- letes.'"'* Few professional sports demand such time, intensity, and duration of train- ing as professional dance. And it is these athletic and physical demands that place the dancer at risk of injury. Stephens has reported that as many as 17% of profes- sional dancers in major companies are unable to dance at a given time because of injury.'
Although acute injuries do occur in dance,'" most are chronic, especially in- juries to the foot and ankle.^" In review- ing data from the American Dance Festi- val, we found that 38% of 21 1 reported injuries occurred in the foot and ankle; Quirk'^ noted a similar prevalence of foot and ankle injuries in Australian ballet dancers. Chronic injuries generally occur through a single primary mechanism: the repetitive impact loading of the lower extremities on a relatively hard, unyield- ing surface — the dance floor. Unlike the competitive athlete who uses specially designed footwear to absorb shock and stabilize the foot and ankle, the ballet dancer wears only a thin slipper or toe-shoe, and the modem dancer wears no shoes at all. All of the forces of cyclic -loading must, therefore, be ab- sorbed by the lower extremities. It is the failure to effectively and efficiently ab- sorb these forces that leads to the charac- teristic injuries of dance."
Variations in the anatomy of the leg play determine to a large extent whether absorption and dissipation of energy within the lower extremities is effective or not. Genu varus, genu valgum, exces- sive femoral anteversion, and leg length discrepancies are several of the anatomi- cal conditions that promote ineffective shock absorption. The cavus foot, with its inherently rigid mid-tarsal joints, absorbs energy poorly because "normal prona- tion" mechanics are obstructed, and cy- chc impact forces are directed to struc- tures poorly suited to absorb stress. Cavus feet are especially vulnerable to mid-foot strain, plantar fasciitis, and stress frac- tures."
The ability to externally rotate the hip and leg is fundamental to all forms of
dance, but is especially emphasized in classical ballet. Each of the five basic positions have in common maximum external rotation of the leg (Figure 1). Under ideal circumstances, turn-out is achieved primarily at the hip joint with much lesser contributions from the knee and ankle joints."'" The "ideal" 90 de- grees of turn-out involves approximately 60 to 70 degrees of external rotation at the hip with the remaining 20 to 30 degrees accruing from the natural outward incli- nation of the knee and the ankle joints (Figure 2). Several factors determine the abihty to externally rotate at the hip: the bony configuration of the acetabulum, the angleof femoral anteversion, theelas- ticity of the anterior hip capsule, and the flexibility of the muscle groups that cross the hip joint." The most common cause of limited turnout isan increased femoral neck-shaft angle or increased femoral anteversion (Figure 3). These bony con- straints of the hip joint cannot be changed in the skeletally mature dancer, but turn-out can be increased by proper stretching of the soft tissues about the hip joint, particularly in younger dancers with ligamentous laxity."
Dance students with poor "natural turn-out" may compensate by forcing outward rotation at the knee or ankle joints (Figure 4). Unfortunately, these maneuvers destroy the aesthetic line, and expose the leg to injury. Forced external rotation of the knee can strain the medial ligamentous complex, as well as injure the meniscal structures.'''"'"''" "Rol- ling-in" — a dance term for forced ever- sion and pronation at the foot and ankle complex — is another maladaptive tech- nique used to increase external rotation of the leg (Figure 5). This maneuver places excessive strain on the medial struc- tures of the foot and makes them particu- larly vulnerable to injury."'""^
Each dance discipline's characteris- tic choreography leads to "selection" of students based on aesthetic and physical characteristics. The aspiring dancer must havecertainaesthetic traits includingpro- jection, charisma, musicality, and sound technique. However, before these aes- thetic characteristics can ever be displayed at the elite level, the dancer must have the
right body type. Classical ballet has gen- erally selected dancers with long arms and legs, a moderate torso with small waist, a slender neck, and small head. All of these characteristics contribute to the classic stage silhouette recognized as the Balanchine ideal .^•'■^' Size and weight are espec ially important because lighter danc- ers are easier to partner and therefore are preferred by most ballet companies.
While the dancer's physical traits determine the aesthetic line that leads to selection, anatomical variation and the vulnerability to injury provides another kind of natural selection process. Elite dancers, like other world-class athletes, form the pinnacle of a broad pyramid of competitive students, most of whom are removed from participation through se- lective attrition or injury based on ana- tomic factors. Indeed, at the elite level of dance, a kind of "Darwinism" ensures that the successful dancer has no signifi- cant anatomical variation."
Dance Training for Children
Theatrical dance is popular among chil- dren and adolescents. While the physical demands of dance are well-established, the effects of such training on the imma- ture musculoskeletal system are unclear. Despite this uncertainty, we feel a well-qualified, experienced dance teacher is essential to the health of the developing dancer. As in athletics, quality instruc- tion provides the foundation for success and minimizes the chances of injury. Qualified dance teachers understand ba- sic anatomy, especially its variations and applications to dance techniques. A good instructor recognizes the physical limita- tions of each dancer and encourages sound technique.
The proper age for beginning dance training depends on the child's attention span and general physical maturity. Girls often begin dance class at age seven or eight, or earlier. Usually three to four years of dance class are required before the young female dancer develops the strength and coordination to begin pointe dancing. Prerequisites for dancing en
68
NCMJ / February 1993. Volume 54 Number 2
Third
Fifth
Neutral
Turnout
Acetabulum y
^20-30'
f
\
Femoral head
;'' '>.->>. 60-70°
4
^^
'
N-^ O
1 lf^^^\~^\
(v /^X^"^.«r^\
'^Kzy^J
Increased
Anteversion
Hip in Neutral Rotation
Hip in Turnout
Figure 1 : (above left) The five basic positions of classical ballet have in comnnon maximum external rotation of the leg. Figure 2: (above top) The dancer's hip in turn-out. Under ideal circumstances, the desired 90 degrees of turn-out is achieved by acombination of external rotation of the hip, knee, and ankle joint. Most of the external rotation occurs at the hip joint (60 to 70 degrees) with the remaining 20 to 30 degrees occurring in combination from the foot, ankle, and knee joints. Figure 3: (above bottom) Multiple factors are responsible for the ability to maximally externally rotate the hip. Probably the most common cause of decreased turn-out is an increase in the femoral neck-shaft angle, a condition known as increased femoral anteversion.
Forced external rotation of the
c:^
Rolling-in
Figure 4: (left) The dancer with poor "natural turn-out" may compensate for lack of external rotation at the hip by forcing external rotation at the knee or at the foot and ankle complex. Figure 5: (right) "Rolling-in" refers to forced eversion and pronation at the foot and ankle complex and represents a maladaptive technique to increase external rotation of the leg.
NCMJ / February 1993, Volume 54 Number 2
69
pointe include development of the intrin- sic muscles of the foot and ankle suffi- cient to allow execution of all the basic steps at the barre in demi-pointe and without breaks in technique.^
Adaptive and Maladaptive Responses to Dance
Dance training has definite effects on the musculoskeletal structures of the lower extremities and low back. Radiographs of the legs and feet of experienced danc- ers show changes not routinely seen even in high-performance athletes." Cortical thickening due to stress hypertrophy is found in the metatarsal bones, tibias, fibu- las, and femurs of exf)erienced dancers."
Long distance runners and joggers wear shoes constructed of high technol- ogy materials to provide maximum cush- ioning and stability. In contrast, ballet dancers wear thin slippers and modem dancers, no shoes. Dancers routinely de- velop adaptive bony and soft tissue changes (corns, callouses, blisters, bun- ions, and ingrown nails) that reflect the stress of impact and functional forces on the fooL''^"
The extreme dorsiflexion required by dcmi-plie can lead to impingement of the anterior lip of the tibia on the talar neck (Figure 6). Repeated contact may lead to formation of exostoses that can be readily seen on lateral radiographs (Fig- ure 7), and symptoms of anterior ankle pain and restricted motion may de- velop.^""'"'^ Conversely, posterior talar impingement or "dancer's heel" may oc- cur because of compression of posterior capsular structures when the dancer is in the relev6 positions of demi- and full pointe. This is particularly apparent in dancers with an enlarged posterior tu- bercle or OS trigonum. With the extreme plantar flexion of the ankle, an enlarged OS trigonum or posterior tubercle com- presses adjacent synovial and capsular structures (Figure 8). After repeated im- pingement, secondary inflammatory
changes cause thickening and fibrosis of the capsule and painful decrease in plan- tar flexion motion at the ankle joinL^""-^'^'
Female dancers, especially those at- tending professional schools, are often preoccupied with thinness and may se- verely restrict their dietary intake.^''^'^' These eating habits can lead to medical problems, menstrual irregularities, and, in some cases, anorexia nervosa. In such cases, referral to an internist, gynecolo- gist, or psychiatrist specialized in eating disorders is appropriate.
The Dance Medicine Team
Proper medical care of the dancer is best achieved by a team that includes the artis- tic director, the dance teacher, the dance therapist, and the physician. Together, this diverse group can play a prominent and effective role in the medical care of dancers. Formerly the diagnosis of dance injuries was usually made by fellow danc- ers, dance teachers, or physical thera- pists. Injuries were treated by self-medication and professional referral made only as a last resort after all other attempts at care were exhausted or had proved ineffective. During the past de- cade the concept of the dance medicine team has reversed this trend. Many dance teachers now seek early referral to an orthopaedist with a background in dance medicine. Dancers recognize that early, accurate diagnosis and an aggressive treat- ment protocol based on an understanding of the basic mechanisms of dance injury provide optimal recovery, prompt return to dance, and minimal risk for re-injury. An accurate diagnosis followed by prompt, appropriate treatment is only the first step in complete care of dance inju- ries. A highly structured rehabilitation program, supervised by a physical thera- pist, is fundamental to a successful out- come. Failure to rehabilitate the injured extremity can lead to further injury and additional time lost from dance. The goals
of rehabilitation include the sequential restoration of motion, strength, and en- durance, followed by proprioception, coordination, and timing. Water-barre exercises are helpful in accelerating reha- bilitation of many lower extremity inju- ries. The injured dancer takes advantage of the buoyant effect of water to relieve stress on the injured extremity. The exer- cises are performed with the uninjured leg as the leg of support and the injured leg as the working leg (Figure 9). These roles can be reversed later in the rehabili- tation."'^
The dance teacher must tactfully, yet convincingly, create an awareness in each dancer of his or her physical limitations, often counseling and guiding dancers to dance disciplines that best accommodate their physical attributes. The teacher in- structs the pupils in proper nutrition, muscle strengthening, and conditioning to support a lifetime of strenuous physi- cal challenge. Above all , the dance teacher must be ever cognizant of dance tech- nique, realizing that improper technique not only detracts from the aesthetic ideal, but makes the dancer vulnerable to in- jury-
The artistic director plays a signifi- cant role in the prevention of dance inju- ries. Proper planning of tour and rehearsal schedules allows time for sufficient rest and avoids the fatigue that leads to im- proper technique and overuse, both com- mon precursors to dance injury."" The artistic director should insist on a proper floor surface for rehearsal and perfor- mance. The dance floor not only affects performance but can cause injury. The ideal dance floor is neither too hard nor too soft, it absorbs some impact energy yet provides an appropriate counterforce to return energy to the extremity."'"'^' Floors that are too hard cause excessive muscle fatigue and stress fractures. Fi- nally, the artistic director should appro- priately match choreographic require- ments to a given dancer's physical capa- bilities so as not to extend dancers be- yond their physical limitations. □
70
NCMJ / February 1993, Volume 54 Number 2
Figure 6: The demi-plie position in ballet is characterized by extreme dorsiflexion at the ankle joint and can lead to impinge- ment of the anterior lip of the tibia on the talar neck.
Large posterior i tubercle
Figure 8: The releve positions of demi- and full pointe can lead to compression of posterior synovial and capsular structures from an enlarged os trigonum or posterior tubercle.
"Dancers recognize that early,
accurate diagnosis and on
aggressive treatment protocol
based on an understanding of
the basic mechanisms of dance
Injury provide optimal recovery,
prompt return to dance, and
minimal risk for re-injury."
Figure 7: Repeated contact of the anterior lip of the tibia on the talar neck can lead to the formation of exostoses that may be readily demonstrated on lateral radiographs.
Figure 9: Water-barre exercises, taking advantage of the buoyant effect of water, are an effective technique for reha- bilitating dance injuries of the lower extremity.
NCMJ / February 1993, Volume 54 Number 2
71
References
1 Sachs C. World History of the Dance. New York: WW Norton, 1937.
2 Hardaker, WT Jr. Foot and anide injuries in classical ballet dancers. Orthopaedic Clin N A 1989;20:621-7.
3 Kirkendall D. Calabrese LH. Physiologic as- pects of dance. Clin Sports Med 1983;2:525.
4 MicheUU, Gillespie WJ.WalaszekA. Physi- ologic profiles of female professional balleri- nas. Clin Sports Med 1984;3:199-209.
5 Teitz C. Sports medicine concerns in dance and gymnastics. Clin Sports Med 1983; 2:571-93.
6 McLain.D.Artisticdevelopmentofthedancer. Clin Sports Med 1983;2:563-70.
7 Thomasen E. Diseases and injuries of ballet dancers. Universitetsforlaget 1 . Artius, Den- mark, 1982.
8 Nicholas JA. Risk factors, sports medicine and the orthopaedic system: an overview. J Sports Med 1975;3:243-59.
9 Stephens RE. The epidemiology of dance injuries. In: Ryan AJ. Dance Medicine: A Comprehensive Guide. Chicago, Pluribus Press, 1987.
10 Hardaker WT Jr, Colosimo AJ, Malone TR,
Myers M. Ankle sprains in theatrical dancers. Med Prob Perform Aits 1988;3:146.
11 HardakerWTJr,MorgelloS,GoldnerJL.Foot
and ankle injuries in theatrical dancers. Foot and Ankle 1985;6:59-69.
12 Quirk R. Ballet injuries: the Australian expe-
rience. Clin Sports Med 1983;2:507-14.
13 Hardaker WT Jr, Erickson L, Myers M. The
pathogenesis of dance injury. In: Shell CG, ed. The Dancer as an Athlete. Champaign, IL. Human Kinetics Press, 1 984; 1 1-29.
14 Gelabert R. Tuming-oul. Dance Magazine,
Febniary 1977;86.
15 CUppinger K. Biomechanical considerations
in turnout. In: Solomon R. Preventing Dance Injuries: An Interdisciplinary Perspective. Reston, VA. National Dance Association. 1990.
16 MiUerEH,SchneiderHJ,BronsonJL,McLain
DA. A new consideration in athletic injuries: the classical ballet dancer. Clin Orthopaed 1975;111:181-96.
17 Howse AJG. Orthopaedist aids ballet. Clinical
OrthoRelRes. 1972;89:52.
1 8 Hamilton WG. Foot and ankle injuries in danc-
ers. CUn Sports Med 1988;7:143.
19 SammarcoGJ, Miller EH. Forefoot conditions
in dancers: part I and part 11. Foot and Ankle. 1982;3:85-98.
20 Myers M. Talking technique: is the grand pli^
obsolete? Dance Magazine. June, 1982.
21 Vincent, LM. Competing with the sylph: danc-
ers in pursuit of the ideal body form. Kansas City, MO. Andres and McNeil, 1979.
22 Hardaker WT Jr, Erickson LC. Medical con-
siderations in dance training for children. Am Fam Physic 1987;35:93-9.
23 Sammarco GJ: Diagnosis and treatment of
dancers. Clin Orthopaed 1984;187:176-87.
24 ParksJCn, Hamilton WG.PalteisonAH,etaI.
The anterior impingement syndrome of the ankle. J Trauma 1980;20:895.
25 Kleiger B. Anterior tibial talar impingement
syndrome in dancers. Foot and Ankle 1982;3:69-73.
26 Hamilton WG. Tendinitis about the ankle joint
in classical ballet dancers. Am J Sports Med 1977;2:84-8.
27 Howse AJG. Posterior block at the ankle joint
in dancers. Foot and Ankle 1982;3:81-4.
28 Frisch RE, Wyshak G, Vincent L. Delayed
menarche and amenorrhea in ballet dancers. N Engl J Med 1980;303:17-1.
29 Maloney MJ, Klykylo WM. An overview of
anorexia nervosa, bulemia, and obesity in children and adolescents. J Am Acad Child Psychiatry 1983;22:99-107.
30 Malone TR, Hardaker WT Jr Rehabilitation
of foot and ankle injuries in ballet dancers. J Ortho Sports Phy Ther 1990;41:335-61.
31 Seals, JG. A study of dance surfaces. Qin
Sports Med 1983;2:557-61.
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HEALTH CARE OF ARTISTS
The Role of Somatic Education in Dance i\/ledicine and Rehabilitation
Glenna Batson, M.A., PT
Dance science is a dynamic field that meshes the distinct knowledge bases of arts and medicine. The problems of trans- lating scientific fact into useful dance technique and dance art into concrete approaches in rehabilitation have sparked a flurry of research, philosophical de- bate, and interest from many disciplines outside the realm of art and medicine. In the integration of theoretical and experi- ential knowledge, dance science draws ideas from orthopedics and sports medi- cine, neurophysiology, endocrinology, physics, cybernetics, biomechanics, ex- ercise science, motor learning and motor control, psychology, nutrition, commu- nications, art, philosophy, and somatics. Somalics, although still on the frontiers of research and exploration, offers a po- tential link in understanding and apply- ing the principles of dance and medicine.
Somatics Defined
Somatics is an eclectic field of study and practice that has sensorimotor education at its core. It is based on the underlying, unifying principle that human beings are neurally organized, cybernetic systems thatare self-adjusting, self-correcting, and self-improving as long as they are senso- rially aware that movement options ex- ist' Humans have the ability to activate neurologic mechanisms to produce im- proved coordination and function. In so- matic learning, becoming aware of what
is felt — kinesthetically and propriocep- tively — is of major importance.^ This awareness of the "what" and the "how" of action facilitates learning.
The late Thomas Hanna popularized the term "somatics."' He used the word "soma" to mean "the living body in its wholeness," not simply a "body," but as a living process, at once an objective phenomenon perceived from the outside and simultaneously a subjective experi- ence perceived from the inside.' More than seeing the body as an isolated entity within the environment, the somatics ap- proach sees the body as sensing and mov- ing within the environment,' striving to achieve stability and balance through adaptation and change. In essence, the soma is purposive.'
Somatics weds body, mind, psyche, and spirit into a creative process* of neu- romuscular change and growth expressed through movement and through the con- scious awareness of movement. Con- scious sensory awareness is the vehicle for neuromuscular change.
Juhan states in Job's Body, "As the mind organizes the rest of the body's tissues into a life process, sensations to a large degree organize the m ind. . .the mind does not need ideas about the body that can be read or told. It needs physical movement, and concrete sensations, the raw data that directly informs, that acti- vates the reflexes, and that organizes pat- terns."^
Somatics and Dance
Somatics is considered education, not therapy, although its results may indeed be therapeutic. The somatic educator fa- cilitates the process of healing, but is not the "fixer" of symptoms or pathology. Somatics is also known as "bodywork," "body therapy," "mind-body integration," "movement therapy," "movement reedu- cation,"* and "integrative movement sys- tems."' There are two components to somatics: active and receptive. In the "active" mode, the educator recruits the client's conscious awareness of and co- operation with movement. Examples in- clude the Alexander Technique, Feldenkrais Awareness Through Move- ment, Aston Patterning, Body-Mind Cen- tering, Ideokinesis, and Bartenieff'sFun- damentals. Receptive therapies renderthe client more "passive" and include mas- sage, craniosacral therapy, and Felden- krais Functional Integration. For many years, traditional medicine considered these techniques "alternatives," but danc- ers often sought them first for help be- cause of their fears of, and frustrations with, conventional treatment.'
Somatics has found a comfortable audience among dancers perhaps because of its emphasis on sensing. It literally and figuratively makes sense. Rare is the in- dividual, especially in Western culture, who senses himself or herself moving, who pays attention to the quality of the
Ms. Batson is the physicial therapist for the North Carolina School of the Arts, Winston-Salem 271 1 7-21 89.
74
NCMJ / February 1993, Volume 54 Number 2
movement during mundane or skilled activity, who uses perceptual intent and the conscious direction of sensory im- pulses to achieve movement goals. Yet, this is the hallmark of dance training. Dancers use their perceptual intent, their directed kinesthetic, proprioceptive, and visual awareness, to leam and perfect movement. They use images and meta- phors to keep an ongoing, directed sen- sory awareness that helps organize their neuromuscular system. The dancer is constantly sensing and guiding the inter- nal and external spatial pathways of trunk and limbs, cultivating specific movement qualities and timing in an effort to unify the physical reality with the aesthetic ideal. Many terms exist in the somatics lexicon for this kinesthetic ability; prac- titioners of the Alexander Technique re- fer to it simply as "good use," implying both a characteristic and an action.
Although the philosophy and prin- ciples of dance and somatics overiap, somatics is not a substitute for dance technique. In dance, the nervous system is concerned with the facihtation of mo- tor activity; movement is the primary focus. In somatics, the nervous system is concerned with the inhibition of motor activity; sensing is predominant'
Somatics and Rehabilitation
Nor is somatics a substitute for medicine, but it can provide an adjunct to standard diagnosis and treatment, because it en- ables the perceptual shift from a cause- and-effect paradigm to a systems one. Somatics can help medicine interpret the importance and manner in which dancers sense themselves while moving, and the way dancers use their sensory awareness to leam and perfect movement. This en- hances our ability to assist dancers fully and effectively in rehabilitation.
Somatic learning improves align- ment, flexibility, and strength.' Somatics can accelerate and enrich rehabilitation by ensuring a safe, full, and effective return to performance. The dancer's past — his or her personal history and train- ing— and the ciurent presenting anatomi-
cal problems gain clarity when the kines- thetic grammar of somatics is added.
When a dancer comes for physical therapy treatment in the acute phase of injury , the kinesthetic and proprioceptive senses have been altered by pain, swell- ing, inflammation, atrophy, joint subluxation, etc. Psychologically, there are feelings of panic and loss. There also are structural mal-alignments, compen- satory movement patterns, technical faults, poor training, and the Uke. These sometimes seem illusive and insidious if the injury is chronic. Usually, physical therapists progress the dancer quickly from the acute phase with conventional rehabilitation goals, (pain relief, protect- ing the joints and muscles, maintaining or regaining range of motion, strength and endurance, and maintaining the body's level of fitness) while supporting the psychophysical effects of "down" time.'
Of course, returning to dance perfor- mance means much more than just restor- ing strength, flexibility, and endurance to the injured area. Maladaptive, inefficient movement habits must be re-pattemed to fully restore skilled function and to avoid future injury. Treatment of only the in- jured tissue leaves the most important and complex aspect of rehabilitation — movement reeducation — up to the tech- nique teacher and the dancer's innate, but flawed, sensory wisdom as he or she returns to class and performance. The dancer may quickly be back to the clinic. Moreover, general exercise and conven- tional approaches to postural reeducation will not permanently change a dancer's maladaptive posture and may, in fact, lead to additional postural tensions and movement inefficiencies' such as when the dancer learns to "tuck" his or her pelvis (to tighten the abdominals and glutteals and oppose tight lumbar exten- sors to correct an excessive lordosis).
The Reeducation Process
From the outset we recruit the dancer's sensory abilities to reeducate movement by creating a therapeutic environment of ongoing somatic (re)education. The
dancer begins the process by "unravel- ing"' (bringing to conscious awareness) the undesirable neuromuscular habits, gains conscious control of movement through experiencing greater ease and support throughout his or her movement range, and mitigates against the return of old habits to prevent permanent neuro- muscular change.
Somatic "exercises" enable dancers to move quickly out of the acute phase into active conditioning because they perform them in a pain-free range with little muscular effort. By working below the level of muscular resistance and pain, the dancer's nervous system responds more readily and appropriately, finding more efficient ways of supporting and moving.' Somatics lets the dancer work on his or her body 24 hours a day — well beyond clinic time — without pain or fa- tigue, an excellent rehabilitation strategy for the dancer to whom "rest" is elusive.
I describe here an eclectic approach that combines principles of somatic edu- cation with specific techniques from ideokinesis and physical therapy. There are five overlapping steps:
Step 1: Creating a therapeutic environ- ment in which to recognize and undo compensatory, habitual, and maladaptive movements.
Step 2: Utilizing ideokinesis to program new neuromuscular patterns.
Slep3: Gaining conscious control through initiating movements of limited range.
Step 4: Reinforcing new neuromuscular patterns by performing physical conditioning exercises with ki- nesthetic and visual specificity.
Step 5: Accelerating, refining, and inte- grating the new pattern by apply- ing it to dance movements.
Step 1: Creating a therapeutic envi- ronment. We provide an environment quiet and safe enough to heighten the dancer's sensory awareness — a percep- tual background in which to facilitate neuromuscular change. All somatic edu- cation techniques first remove the person from the field of gravity in which they habitually act (have the person lie down
NCMJ / February 1993, Volume 54 Number 2
75
so that the support for the whole body comes from the floor or table). Effortless support helps the dancer overcome the compensation for pain and dysfunction. In the acute phase of injury, this environ- ment is one of meditative rest, where the dancer can begin to heighten diminished sensory impulses — ^kinesthetic, proprio- ceptive, and visual — and can contact an even deeper somatic sensation, the "felt sense," a non-movement based sense, at the root of the healing dialogue.'"
With increased awareness comes the experience of difference or contrast be- tween feelings and movements, and thus the possibility of choice.' Awareness of how the tension feels enables the dancer to release it more easily.' Awareness is, in and of itself, corrective. To simply be awareofsomething alters the physiologic course, as one discovers by paying atten- tion to their breathing.
Dr. Lulu Sweigard, who developed the visualization technique of ideokinesis, coined the phrase. Constructive Rest Po- sition (CRP) to describe this creative en- vironment. It is in CRP that the dancer can more easily discover his or her own reflex patterns of response,^ identify the tension patterns that actively interfere
with movement, and ultimately distin- guish such tension from more appropri- ate impulses of weight and movement Sweigard used CRP mainly to practice ideokinesis in which mentally visualized imagery facilitates improved neuromus- cular coordination (see Step 2). The value of CRP lies in minimizing all mechanical (skeletal) and neuromuscular forces on the body, so that the mind, by sensing and visualizing, can accelerate the reprogram- ming of the nervous system. Keener ob- servation and sensitivity to the body's internal cues and responses follow the dampening of neural stimuli and me- chanical forces.
Sweigard believed that rest alone does not erase an inefficient movement pattern. It may be relaxing, but it does not create tonus." In CRP, neuromuscular reprogramming occurs because the abil- ity to sense tonus, to differentiate be- tween the smallest degrees of sensation and movement, is an essential prelude to greater movement efficiency.
Step 2: Ideokinesis — Programming new neuromuscular patterns of move- ment. In the first stage, the dancer fo- cuses on his or her awareness of internal
\
Figure 1: Using ideokinesis in the constructive rest position: visualizing lines of movement to center the hip joint.
impulses to set the background in which he or she can gain more conscious control over sensorimotor processes. But, just as rest alone is not enough to accomplish permanentneuromuscularchange.aware- ness of sensory impulses, by itself, will not replace the old pattern. A new image, or mental picture of a more appropriate movement, m ust replace the old. By men- tally directing this image (the movement goal) internally through the body, ideokinesis provides the dancer with the precise subcortical patterning that pre- cedes more efficient action.
In this stage ideokinesis provides the means of visualizing clear, accurate mo- tor goals. As early as 1877 it was shown that the thought of muscle contraction sends a flow of impulses from the brain to the respective muscles.'^ Sweigard ad- vanced this concept by developing spe- cial images that, when mentally visual- ized, result in more effective and efficient movement. Why only mentally at first? Sweigard believed that postural habits exert a perpetual influence on the manner and ease of any movement. To change them, it is better not to move at first, but simply to visualize a new goal of move- ment"
Distinct from mental rehearsal and mental practice techniques used in sports training (where players visualize them- selves performing as if watching a movie), ideokinesis emphasizes visualizing im- ages or lines of movement — vectorial, rotatory, and planar — through specific anatomical sites within the body. These moving images result in better biome- chanical and muscular balance, estab- lishing a more appropriate motor plan.
If, for example, the dancer has sus- tained a hamstring strain, he or she might visualize one of Sweigard's classical lines — a line moving from the center of the knee joint to the center of the hip joint (Figure 1). Visualizing this line releases the excess muscle tension developed in the dysfunctional pattern of movement and injury, balances the muscle effort around the femoral joint by restoring the muscles to their resting lengths, and cen- ters the femoral joint for improved con- gruency.'" The line follows the vector
76
NCMJ / February 1993, Volume 54 Number 2
made by the mechanical axis in the direc- tion of gravity in CRP. A concrete image of this is to imagine the femoral shaft dropping through the pelvis into the floor to enhance the sense of weight and re- lease of muscle tension. Practicing ideokinesis in the CRP prepares the dancer to initiate thigh movement with a more centered femoral joint."
Popular with dancers for more than 25 years, ideokinesis is especially useful in integrating dance medicine and somatics. Ideokinesis "releases" the old maladaptive movement pattern, replaces it with a more optimal one, and mitigates against the return of the old — all in one image and in accordance with the skel- etal, muscular, and biomechanical design of the body. With ideokinesis, visualiza- tion facilitates knowledge of the body and enhances kinesthetic awareness."
Step 3: Gaining conscious control through initiating small-range move- ments. Still in CRP, it is now time to move. Studies show that the brain is highly active well before movement actually occurs, those moments between the point of the (un)conscious intention and the initiation of movement. The dancer ini- tiates small-range movements of the in- volved joints and muscles, paying atten- tion to the tension patterns and responses that develop throughout the body. Now, with clarity of the visual image and height- ened kinesthetic awareness, the dancer can perceive differences, detect errors, experience subtle weight shifts and re- verberations, and can match the intended image of the movement with the actual movement. In our dancer with the ham- string strain, for example, small move- ments of the thigh, in flexion, in exten- sion, and internal and external rotation, bring awareness to the locus of initiation of the femoral head, the convex-concave relationship of the joint, the differentia- tion of hip joint from lumbar spine and pelvic movement, the sequencing, tim- ing, and quality of muscle action, and the internal and external spatial pathways of the limb. The dancer can discover new options for movement and the interconnectedness of the whole body in its support for hip joint movement.
Step 4: Reinforcing the new neuromuscular pat- tern. Moving from small- range to larger move- ments, the dancer rein- forces the neuromuscular changes by continuing to use imagery during tradi- tional conditioning exer- cises in non-weight-bear- ing and weight-bearing po- sitions (Figure 2, right). Therapists facilitate touch and add verbal cues to en- sure that the specific im- age triggers accurate neu- romuscular responses. Dancers must practice a wide variety of condition- ing exercises to "streng- then" the new pattern within the field of gravity.
Step 5: Acceleration, re- finement, and integra- tion of the new pattern into dance technique.
The last step ensures that dancers integrate the new pattern of movement into their dance technique (Fig- ure 3, right). Performing arts medicine clinics, aware of this, incorporate somatics into rehabilita- tion. By applying the same ideokinetic principles to dance technique for ex- ample, the dancer ensures that new neuromuscular patterns supplant the old. ' ' Integrating somatics into rehabilitation lets dance medicine specialists re- spond more fully to danc- ers' needs. □
Figure 2: (top) Applying lines of movement to im- prove efficiency : centering tfie femur in a hamstring stretch. Figure 3: (bottom) Integrating the new pat- terns intodance technique.
NCMJ / February 1993, Volume 54 Number 2
rr
References
1 Haiina, T. The Body of Life. New York: Knopf, 1979.
2 Juhan, D. Job's Body. Barrytown, NY: Station Hill Press, 1987.
3 Goldfarb.LW. Articulating Changes: Pre- liminary Notes to a Theory for Feldenkrais. Berkeley: Feldenkrais Re- sources, 1990.
4 Eddy, M . An overv iew of the science and somatics of dance. Kinesiology and Medi- cine for Dance 1991,14:1, Fall/Winter.
5 Myers M. Perceptual awareness in inte- grative movement systems (body thera- pies) in motor performance and expressivity. The 1984 Olympic Scien- tific Congress Proceedings, Vol. 8: The Dancer as Athlete. Champaign, IL: Hu- man Kinetics Publishers, Inc., 1986.
6 Myers, M. What dance medicine and sci- ence mean to the dancer. Science of Dance
Training, Clarkson, PM, and Skrinar M, eds. Champaign, IL: Human Kinetics Books, 1988.
7 Batson, G. Dancing fully, safely, and ex- pressively— the role of the body thera- pies in dance training. JOPERD 1990; November/December:28-3 1 .
8 Myers, M. Dance science and somatics: a perspective. Kinesiology and Medicine for Dance 1991;14:1, Fall/Winter.
9 Teitz, CC. First aid, immediate care, and rehabilitation of knee and ankle injuries in dancers and athletes. The 1984 Olym- pic Scientific Congress Proceedings, Vol. 8: The Dancer as Athlete. Champaign, IL: Human Kinetics Publishers, Inc., 1986.
10 GendlLn, ET. The wider role of bodily sense in thought and language. Giving the Body Its Due. Albany: State University of New York Press, 1992.
1 1 Minton, S . Exploring the mindAxxly con- nection with imagery. Kinesiol and Medi- cine for Dance 1986;14:1, Fall/Winter.
12 Pickenhain, L. Psychophysiology of sports, exercise, and fitness: developmen- tal aspects. Mind-Body Maturity, ed., Diamant, L. New York, Hemisphere Publishing Corp., 1988.
13 Matt, PH. Ideokinesis: integrating the sci- ence and somatics of dance. Kinesiology and Medicine for Dance 1991;14:l,Fall/ Winter.
14 Dowd, I. Ideokinesis: the 9 lines of move- ment. Taking Root to Fly. Hadley, MA: Common Wealth Printing, 1981.
15 Meglin, J. Ideokinesis as it applies to injury prevention. Tlie 1984 Olympic Sci- entific Congress Proceedings, Vol. 8: The Dancer as Athlete. Champaign, IL: Hu- man Kinetics Publishers, Inc., 1988.
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78 NCMJ / February 1993, Volume 54 Number 2
HEALTH CARE OF ARTISTS
Medicine in the Vocal Arts
James A. Koufman, M.D.
The voice is not an organ. It is the external phonatory output of the vocal tract. The vocal tract consists of four component systems:
The "Generator" — The regulated breath stream provided by the lungs that is the principal force driving vibration of the vocal folds. Unless air flows through the larynx , the vocal folds can make no sound. The condition of the lungs, and how effi- ciently the breath stream is utilized, greatly influences vocal function.
The "Vibrator" — The larynx and, spe- cifically, the vocal folds themselves, which act as a vibrator. Problems in pro- ducing vibration arise in the larynx and its supporting structures, but these com- ponents do not contribute to richness of sound or subtleties of articulation. Those come from structures ("resonator" and "articulator") above the larynx.
The "Resonator" — The space above the larynx, including most of the pharynx. This resonating cavity gives the voice its harmonic overtones, its richness. Trained opera singers can manipulate the resona- tor to produce resonance at 2,500 Hz, allowing the singer's voice to be heard above an entire orchestra. Problems with
Dr. Koufman is director, Center for Voice Disorders of Wake Forest University, and associate professor, Department of Otolaryngology, Bowman Gray School of Medicine, Medical Center Boulevard, Winston-Salem 27157-1034.
the resonator are uncommon, but tonsil- lectomy, for example, may temporarily affect the resonator.
The "Articulator" — The tongue, lips, cheeks, teeth, and palate. These struc- tures shape sound into words and other vocal gestures. Medical problems involv- ing the articulator are uncommon; for the singer, most problems of the articulator can be corrected by the voice coach or teacher.
The term voice disorder implies that a problem has a laryngeal origin (within the vibrator), but it is important to re- member that the four component systems of the vocal tract interact in complex ways. For example, poor breath support may give rise to muscle tension dysphonia (abnormal muscle tension in the larynx that alters the voice). It is also important to remember that the neural regulation of these systems is complex and involves many sensory, motor, and integrating pathways within the brain. In actuality, the vocal tract is the entire person, since any abnormality of psyche or soma can give rise to an abnormahty of the voice. The voice is therefore a measure of a person's overall well-being.
Voice disorders are ubiquitous and may have a profound influence on a person's ability to communicate effec- tively. And just as professional athletes are prone to certain athletic (orthopedic) injuries, so too, professional vocalists are prone to specific problems. Tennis play- ers get tennis elbow; football players get
knee injurier, vocalists get voice disor- ders. Moreover, the scheduling demands of successful vocalists (travel, rehearsal, promotion, performance) make it more likely that they will suffer serious voice problems than the average person. In professional vocalists, voice problems may cause social, emotional, andprofes- sional hardship including public scorn, loss of reputation, and loss of income. It is therefore not surprising that profes- sional vocalists with voice problems usu- ally arrive at the doctor's office in a state of panic.
Who gets a voice disorder? And why? How are voice disorders treated? And, if possible, how can they be pre- vented? My purpose in this paper is three-fold:
• to outline an approach to management of these patients;
• to review the common voice problems of vocalists;
•to present some preliminary results from a recent study of the "laryngeal biome- chanics of the singing voice."
Approach to the Vocalist with a Voice Problem
There are three categories of "profes- sional vocalist," and each develops a somewhat different set of problems and demands. I call these three groups elite vocal performers, vocalists, and vocal professionals. The opera singer is an ex-
NCMJ / February 1993, Volume 54 Number 2
79
Table 1. Co.mmon problems of professional vocalists
Upper respiratory infection (URI, "cold," laryngitis) Gastroesopha.geal reflux-related voice abnormalities Overuse syndrc>mes ("decompensation") Problems related to misuse of the speaking voice Problems related to environmental factors Problems relatevd to singing out of range Problems related to substance abuse Problems related to medications Vocal abuse syndromes
, ample of an elite vocal perfomn'r in whom e yen the slightest aberration of v oice may ha\ '6 dire consequences. Most other pro- fessi onal singers fall into the vocalist group. ■ Actors, clergy, and radio anvd tele- vision ^oersonalities fall into the vocal professional group. Individuals in all tihree groups eariT tfieir living with their voices, but the degree of "incapacity" produced by a given voice disorder varies withi tb.e occupational vocal demands of each group. Elite \ocal performers seek mei'li- cal attention for any and every acute condition that they think might affect their voice (common colds, allergy, etc). Less-demanding patiients usually seek medical attention onlj' when the problem is more severe or chro nic. Consequently, the voice clinician mu:st take into account the vocal demands and needs of each patient. Table 1 lists (in decreasing order of frequency of occurrence) the com- monly encountered problems of vocal professionals. The management of these conditions will be addressed subse- quently.
The Spectrum of Vocal Dysfunction
Traditional medical thinking has created adicholomous model of disease: organic vs. functional. The term organic (liter- ally, "related to an organ") is usually associated with congenital, inflammatory.
or other visible struc- tural alleration(s) in the tissues of an or- gan. On the other hand, the term func- tional ("related to function") applies to conditions that result from abuse or mis- use of an anatomi- cally intact organ or organ system. A functional abnor- mality is not prima- rily the result of a structural abnormal- ity, although histo- pathological alter- ations secondary to misuse may occur. Of course, organic conditions may have a functional component in addition to any disorder of structure.
Many voice disorders are multifac- torial— simultaneously both organic and functional — because compensatory alter- ations of vocal function occur in virtually every case. Furthermore, the compensa- tory component may obscure the under- lying condition. Thus, the dichotomy between organic and functional appears to have little relevance to the understand- ing and management of voice disorders. The clinician must assess the degree of impairment caused by any compensatory or functional component, as well as by the organic problem. For example, a vo- caJist with viral laryngitis may complain of "no voice" prior to a performance. The degree of vocal fold edema and inflam- mation may be mild, and abnormal laryn- g(ial muscle tension (maladaptive com- pensation) may account for "most" of the loss of voice. It may not be possible to restore the voice to normal but, through the combined efforts of an otolaryn- gologist, speech ("voice") pathologist, voice coach, and manager, it is often possible to restore enough voice to per- mit f)erformanceofa"modiried program." Successful treatment of chronic voice disorders, though somewhat different from the management of acute disorders, also requires such a multidisciplinary team.
The Multidisciplinary Voice Center: Medicine in the Vocal Arts
In the U.S., anumber of multidisciplinary voice centers have been established dur- ing the past decade. Using new technol- ogy, these centers focus the collaborative efforts of voice specialists on diagnosis, treatment, and prevention of voice disor- ders. Today, most patients with voice disorders can be treated effectively, "arts medicine" has become a new subspe- cialty, and a national network of voice centers has been established.
The otolaryngologist and the sj)eech-language pathologist comprise the clinical core of the voice center; virtually every voice patient should be seen by both. The laryngologist is primarily re- sponsible for the patient's overall care, but the speech pathologist is responsible for the diagnostic voice laboratory and for most of the speech and voice therapy, and a voice teacher will be involved in the "rehabilitation" of many singers. Videostroboscopy (performed by the laryngologist) and acoustical voice analy- sis (by the speech pathologist) are used in the diagnosis and treatment of voice pa- tients. When appropriate, patients are re- ferred for ambulatory 24-hour, double-probe pH monitoring to test for gastroesophageal reflux (see below). In addition, patients sometimes need refer- ral to specialists in neurology, psychol- ogy, psychiatry, gastroenterology, gyne- cology, or internal medicine.
Clinical Assessment of Voice Patients
With new voice patients, the laryngologist usually sees the patient first, followed by the speech pathologist on the same day if possible. With return patients, the se- quence is usually reversed. The laryngologist takes a medical history and a "vocal history" (Table 2). The specific vocal complaint(s) must be elicited care- fully (Table 3). Next, an otolaryngologic examination is performed followed by videoendoscopy, including transnasal
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NCMJ / February 1993, Volume 54 Number 2
Table 2. Elements of the vocal history
What are the patient's symptoms?
What is (are) the vocal complaints?
Is there a history of vocal misuse or abuse?
Does the patient have any respiratory symptoms?
Does the patient have any gastroesophageal reflux symptoms?
Is the patient under the care
of a physician? For what reason?
Is the patient taking any medications?
Is there a history of substance abuse?
What are the vocal needs of the patient?
What is the practice and performance schedule?
Are there any environmental factors that may be important?
Has the patient had vocal training? If so, how much, when, and with whom?
fiberoptic laryngoscopy, and stroboscopy with a telescopic or optical rod. Ideally, the speech pathologist should be present during this phase of the examination but, if not, the videotaped examination may be reviewed subsequently. At the very least, the otolaryngologist should com- municate the findings and presumed di- agnosis to the speech pathologist.
While the laryngologist is usually primarily responsible for the patient's overall medical management, the speech pathologist is responsible for baseline voice documentation, acoustical voice analysis, therapeutic manipulation (so-called "unloading"), independent di- agnosis, performance of speech and voice therapy, and determining dismissal crite- ria. At times the speech pathologist as- sumes some of the functions of the laryngologist, and vice versa.
Description of the types of equip- ment employed by these specialists is beyond the scope of this paper; however,
Table 3. Common vocal complaints and their definitions
Aphonia
loss of voice
Dysphonia
abnormal voice; hoarseness
Odynophonia
discomfort or pain associated with speakinci or singing; also usually associated with abnormal laryngeal muscle tension
Vocal fatigue
dysphonia specifically associated with prolonged vocal usage
Voice break
a "momentary" pitch-specific dysphonia; a voice "crack"
Loss of range
a reduction in the pitch-range, usually a loss of a portion of the high range
Dysresonance
an abnormality of resonance
the component laboratories of a mod- ern voice center include: 1) a videoendoscopy laboratory for fiberoptic and telescopic laryngeal im- aging and videostroboscopy; 2) an (acoustical) voice laboratory equipped to perform analysis of frequen- cy-related vocal parameters (funda- mental frequency, frequency range, perturbation, signal-lo-noise ratio, and waveform analysis), aerodynamic measurement, and spectrographic analy- sis; 3) an electromyography laboratory (used in selected cases) and capable of multichannel laryngeal electromyogra- phy; and 4) a gastroenterology laboratory for ambulatory 24-hour, double-probe pH monitoring (in selected cases). Because such state-of-the-art equipment is expen- sive, most well-equipped voice centers are located at university medical centers. Two specific aspects of clinical voice assessment must be emphasized:
1) The laryngologist's examination should include both fiberoptic and tele- scopic laryngeal examination. The former allows assessment of laryngeal function during connected speech and singing and across the dynamic and pitch ranges of the voice. This is important in assessing laryngeal biomechanics and in identify- ing abnormal patterns of laryngeal muscle tension. Telescopic examination involves placing a large-bore instrument in the mouth so that during this examination the
patient can phonate only vowels. Even though telescopic examination signifi- cantly alters laryngeal biomechanics, the superior magnification and optics allow optimal examination of the Tree edges of the vocal folds for lesions such as nod- ules, polyps, cysts, and hematomas. The two techniques are complementary, and both should be employed in evaluating the professional vocalist.
2) The speech pathologist's role in "unloading" the patient may be crucial to diagnosis and effective treatment. "Un- loading" means voice therapy designed to temporarily remove compensatory vocal behaviors. Details of unloading are beyond the scope of this paper, but thera- peutic techniques include obtaining opti- mal use of the breath so^eam, softening the hardness of glottal attack (reducing the effort of initiating phonation), reduc- ing the rate of speaking, and reducing laryngeal and neck muscle tension through massage and relaxation methods.
As mentioned earlier, almost all pa- tients with voice disorders have a func- tional or compensatory component that can be reversed by voice therapy. Be- cause the voice must be unloaded during evaluation, the processes of diagnosis and U"eatment become intertwined, for it is only when compensatory behaviors are removed that the voice clinician can fully appreciate the uue underlying glottal con- dition.
NCMJ / February 1 993. Volume 54 Number 2 81
Common Problems of Vocalists
Professional vocalists have some unique risk factors for the development of voice difficulties. As a group, they are often subjected to smoke, dryness, dust, a high level of ambient noise, and inadequate amphfication in the working environ- ment. These problems may contribute to "poor vocal hygiene," poor diet and, in some cases, substance abuse. Successful vocalists may also suffer from stressful schedules, anxiety, and fragmented (even inappropriate) medical care. Table 4 lists some of the common problems of vocal professionals.
Laryngeal inflammation. Infectious and non-infectious causes of laryngeal in- flammation are among the most common reasons that professional vocalists seek medical attention. Often the patient com- plains simply of "laryngitis," without any specific cause. Indeed, to the layman, the term "laryngitis" is mistakenly used as a synonym for hoarseness (dysphonia). From the voice clinician's point of view, laryngitis implies inflammation of the larynx, and is distinct from the dysphonia that follows vocal abuse, misuse, or over- use. Tonsillitis, sinusitis, and allergy may occasionally involve the larynx and cause secondary laryngeal inflammation, but by far the most common causes of true laryngitis are viral infection and gastroe- sophageal (laryngopharyngeal) reflux.
Upper respiratory infection (viral lar- yngitis). Upper respiratory infection (URI) is usually of viral origin. It may or may not directly involve the larynx de- pending on the virulence of the invading organism and its site of predilection. Some viruses cause primary laryngeal inflam- mation with marked laryngeal edema and hoarseness, while others ("colds") cause only minor, secondary inflammation due to drainage of the by-products of the inflammatory process from above.
Treatment consists of modi fied voice rest(no non-essential talking), hydration, and use of a vaporizer (and steamy show- ers). Antibiotics (because of the possibil- ity of secondary bacterial infection), de-
Table 4. Unique problerr
s of professional vocalists
Vocal overuse
heroic schedule, inappropriate time management
Vocal misuse/abuse
Bogart-Bacall syndrome, singing out of range, inappropriate role selection, use of certain character voices, vocal fold hemorrhage, yelling/screaming, vocal nodules
Anxiety/panic
bulimia/anorexia, substance abuse
Reflux laryngitis
Environmental risk factors
"noise pollution," ambient dryness, inadequate amplification, dehydration, air travel, poor diet
Substance abuse
tobacco, alcohol, drugs (cocaine, marijuana, stimulants, depressants, beta-blockers)
Medications
antihistamines, corticosteroids, anti-inflammatory medicines, throat sprays
Suboptlmal medical care
inappropriate surgery, inappropriate medicine, inappropriate advice
congestants (usually not in combination with antihistamines), and expectorants should be prescribed. On occasion, a single large intramuscular dose of a glu- cocorticoid such as 20 mg of beta- methasone may be given to counteract the effects of the acute laryngeal swell- ing. Betamethasone has a half-life of 36 hours, so that a single dose exerts its effects for days and no "tapering" is re- quired. As an alternative, an oral regimen of betamethasone or prednisone may be used. When prescribing corticosteroids, it is important to inquire whether the patient has received such treatment pre- viously, since these drugs have adverse side effects. Some patients become de- pendent on them and may see physicians in several states to get corticosteroids; the patient who repeatedly uses steroids in order to perform may develop Gushing 's syndrome. Finally, the use of inhaled steroids and or anesthetic sprays is contraindicated because they seldom help, and they may harm the patient.
Upper respiratory infections are self-limited, and symptoms usually re- solve within several days. During the acute phase of infection, it is important that the patient avoid voice strain or over- use because this may result in prolonged difficulties. The severity of laryngeal in-
flammation, the degree of vocal impair- ment, and the short-term "performance" schedule of the vocalist are important factors in the approach to treatment. If, for example, a performer has severe lar- yngitis and a heavy performance sched- ule, then the upcoming performances should be drastically modified or can- celed. On the other hand, if a performer has mild to moderate inflammation and only a few imminent but important per- formances, medical treatment and voice therapy and modification of the perfor- mance program may be satisfactory.
Gastroesophageal reflux ("reflux lar- yngitis"). Gastroesophageal refiux, spe- cifically laryngopharyngeal reflux, is the cause of, or an important co-factor in, voice disorders in approximately half of all professional voice patients who seek medical attention. Vocalists appear to be extraordinarily prone to develop reflux, but why this occurs is unknown. These patients often have "occult reflux," with- out symptoms of heartburn or regurgita- Uon. Voice patients who complain of chronic or intermittent hoarseness, a feel- ing of a lump in the throat (globus pharyngeus), difficulty swallowing (cer- vical dysphagia), excessive throat mucus or post-nasal drip, chronic throat clear-
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ing, or cough may have clinically signifi- cant laryngeal reflux. Since reflux can cause muscle tension dysphonias and vocal nodules, and since it is a factor in the development of vocal fold granulo- mas, Reinke's edema (polypoid degen- eration), and vocal fold carcinoma, the diagnosis of reflux should be entertained in patients with any of the above symp- toms as well as those with findings of unexplained laryngeal swelling, particu- larly diffuse swelling.
The most sensitive diagnostic test for reflux laryngitis is ambulatory, 24-hour, double-probe esophageal pH monitoring. Laboratory diagnosis is im- portant because, unlike patients with "typical" reflux esophagitis commonly encountered by gastroenterologists, those with laryngopharyngeal reflux and reflux laryngitis have a high incidence of up- right (daytime) reflux, a low incidence of esophagitis, and a high rate of treatment failure using traditional anti-reflux therapy such as dietary and lifestyle modi- fication and H2 receptor-blocking drugs. Omeprazole 20 mg twice daily appears to be effective.
Vocal Abuse, Misuse, and Overuse: The Muscle Tension Dysphonias
Disorders of voice use are very common in professional vocalists. They may be lumped together under the heading of muscle tension dysphonias (MTDs). MTDs may occur in isolation, after an upper respiratory infection, or, as men- tioned above, in association with reflux. The voice clinician must evaluate each patient for each of these possible causes since every underlying cause must be identified and corrected if treatment is to be effective.
Vocal abuse. Yelling or screaming, sing- ing too loudly or "out of range," and using certain character voices may result in traumatic laryngeal damage, including the development of contact ulcers of the vocal processes, vocal fold hemorrhages, nodules (localized vocal fold swellings).
or diffuse vocal fold swelling. These le- sions are the consequences of traumatic vocal behavior and they result in vocal impairment. The best treatment for these dysphonias is prevention.
Vocalists should strictly avoid screaming (to the point of hoarseness) at athletic events and at other times, includ- ing when performing. Professional vo- calists who demonstrate findings of vo- cal abuse should be offered a program of vocal education designed to modify the abusive vocal behavior(s). Vocal fold hematomas are best treated by voice rest, occasionally by surgical drainage.
Contact ulcers on the vocal processes may be due to use of a loud speaking voice alone, but also often are associated with poor breath support, very low pitch- ing of the voice, and chronic throat clear-
"Vocal abuse in a vocal professional
is tantamount to a musician's leaving his or her instrument out in the rain; it is inappropriate and neglectful."
ing. Such ulcers may produce pain re- ferred to the ipsilateral ear (often during performance), and yet only minimally alter the vocal quality. Patients with con- tact ulcers and granulomas usually need treatment for reflux as well as for vocal abuse or misuse.
Vocal nodules, small discrete swell- ings at the junction of the anterior and middle thirds of the vocal folds, are com- mon in vocalists, and are always the re- sult of vocal trauma. These swellings may simply represent discrete areas of mucosal thickening, or they may be kera- tinized (like a callus), or angioma-like (vascular). Most patients do not need to have vocal nodules removed since, in many cases, the nodules do not signifi- cantly alter vocal quality. However, when the nodules are associated with an under-
lying submucosal cyst or have a red, "angioma-like" appearance, surgical treatment should be considered (after voice therapy has been instituted). Re- member, these are functional lesions and, with the exception of cysts and "red nod- ules," they may resolve completely when vocally abusive behavior is eradicated. Relatively few patients with vocal nod- ules ever require surgery.
All patients with traumatic vocal fold injuries should be subjected to intense scrutiny by the voice team. Abusive vo- cal behaviors, including chronic traumatic throat clearing, should be elim inated, and therapy provided to optimize vocal effi- ciency. Vocal abuse in a vocal profes- sional is tantamount to a musician ' s leav- ing his or her instrument out in the rain; it is inappropriate and neglectful. For most such patients vocal education (or reedu- cation) is effective remedial therapy.
Vocal misuse. Vocal misuse differs from abuse, in that misuse tends to be less acute, more habitual, and more insidious in its effects. Speaking or singing out of range and the use of certain character voices are the most common forms of misuse.
Many singers , both men and women, who seek medical attention for a voice problem, habitually use a very low-pitched speaking voice, which causes problems. To produce a low-pitched voice requires considerable muscular tension leading to a muscle tension dysphonia termed Bogari-Bacall syndrome (so named not because these two great actors had anything wrong with their voices, but because people with this disorder have voices that are similar in pitch to Bogart's or Bacall's). Patients with this condition almost always use the lowest note of the pitch range for speaking, and also usually demonstrate poor breath support. Why this condition occurs is conjectural; how- ever, in contemporary society, a low-pitched speaking voice is considered desirable. In men, a low-pitched voice confers authority and masculinity; in women, sophistication, worldliness, and confidence. Diagnosis of the Bogart-Ba- call syndrome requires a high index of suspicion, and correction of the syndrome
NCM J / February 1 993 , Volume 54 Number 2 83
Table 5. Suggestions for the professional vocalist: How to save your voice
1. Avoid abusing your voice.
• Do nothing to your voice that results in hoarseness and/or throat pain.
• Avoid yelling or screaming to the point of causing hoarseness.
• Avoid singing so loudly that you develop hoarseness, and avoid singing in situations that are so noisy that you cannot hear yourself singing.
• When you have a cold or laryngitis, do not try to talk or sing "over" the problem. This can lead to vocal fold damage; see your doctor.
2. Avoid misusing your voice.
• Be careful w/hen using "character voices" not to strain, and use especially good breath support.
• Don't attempt to alter your "normal" speaking voice to create an effect; particularly avoid pitching your voice too low. (If you are using the lowest note of your pitch range for everyday conversation, this is too low.)
• Avoid taking on roles that you cannot do, that is, don't attempt roles that are out of your range.
• Avoid use of long run-on sentences and a rapid speaking rate that stress the vocal apparatus; good breath support for conversational speech is every bit as important as good breath support for singing. (If you don't know what this means, you should consider taking voice lessons, and/or seeing a voice therapist.)
3. Avoid overusing your voice
• In very noisy environments such as airplanes, minimize conversation.
• Examine your "vocal schedule" carefully. Remember that all of your vocal demands are not of equal importance. Avoid making a schedule that leaves no room for rest and recovery.
• Use amplification when available and appropriate, especially for rehearsals.
• Use "marking" techniques when appropriate, especially for rehearsals.
4. Monitor your work and home envlroments for possible problems.
• Avoid, if possible, performing in smoky, dusty, and noisy places.
• Humidify your bedroom, especially during the winter when when it is dry.
5. Monitor your diet and lifestyle.
• Eat regularly, and eat a healthy diet.
• Avoid fried and other fatty foods.
• Avoid dehydration, since this adversely affects the vocal folds; drink plenty of water.
• Avoid eating or drinking, particularly alcoholic beverages, within three hours of bedtime.
• Minimize consumption of caffeine-containing foods and b