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Tumoral calcinosis and hyperparathyroidism
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EDITOR
M ANNIE D. PAINE, JR, MD
GENERAL MANAGER RENE G. ABADIE
MANAGING EDITOR BONNIE L. BLUNDELL
CONTRIBUTING EDITOR FRANK J. ILARDI, MD
JOURNAL COMMITTEE
CONWAY S. MAGEE, MD Chairman
A.G. KLEINSCHMIDT, JR, MD PAUL F. LARSON, MD W. CHARLES MILLER, MD EMILE K. VENTRE, JR, MD JACK T. CAPPEL, JR, MD Ex officio
ADVERTISING SALES SISSY SULLIVAN-HANSEN
Established 1844. Owned and edited by The Journal of the Louisiana State Medical Society, Inc., 1700 Josephine Street, New Orleans, Louisiana 70113-1596.
Copyright 1987 by The Journal of the Loui- siana State Medical Society, Inc.
Subscription price is $12 per year in ad- vance postage paid for the United States; $15 per year for all foreign countries belonging to the Postal Union; $1.50 per
single issue.
Advertising: Contact Sissy Sullivan- Hansen, 1700 Josephine Street, New Orleans, LA; (504)561-1033, (800)462-9508.
Postmaster: Send address changes to 1700 Josephine Street, New Orleans, LA 70113-1596.
The Journal ISSN 0024-6921 is published monthly at 1700 Josephine Street, New Orleans, LA 70113-1596. Second-class postage paid at New Orleans and at additional mailing offices.
Articles and advertisements published in the Journal are for the interests of its readers and do not represent the official position or endorsement of The Journal of the Louisiana State Medical Society, Inc. or the Louisiana State Medical Society. The Journal reserves the right to make the final decision on all content and advertisements.
VOLUME 139 / NUMBER 1 / JANUARY
ARTICLES
Richard S. Godfrey, MD 26
David M. Faddis, MD Philip J. Daroca Jr, MD Carl M. Sutherland, MD
Yuruk Iyroboz, MD, MPH 35
Official Call for the 1987 House of Delegates
Tumoral calcinosis and hyperparathyroidism
Consumer price differentials between container and brand products of oral antibiotics in Louisiana
DEPARTMENTS
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6 |
New Members |
|
11 |
ECG of the Month |
|
15 |
Otolaryngology/Head and Neck Surgery Report |
|
21 |
Auxiliary Report |
|
24 |
Calendar |
|
46 |
Classified Advertisements |
INFORMATION FOR AUTHORS
MANUSCRIPTS should be of a reasonable length and double spaced on firm white paper 8V2 x 1 1 inches with adequate margins. This applies to all text elements: references, legends, footnotes, etc. Single spaced manuscripts and photo copies will not be considered. The original and one duplicate should be submitted. Manuscripts are received with the explicit understanding that they are not simultaneously being considered by any other pub- lication. Accepted manuscripts become property of THE JOURNAL and may not be published else- where without permission from the author and THE JOURNAL. Manuscripts are subject to copy edit- ing.
TITLE PAGE should carry (1 ) the title of the article, which should be concise but informative; (2) first name, middle initial, and last name of each author, with highest academic degree(s); (3) name and address of author to whom requests for reprints should be addressed, or statement that reprints will not be available from the author.
ABSTRACT should be the second page consisting of no more than 1 50 words. The abstract should be a factual (not descriptive) summary of the work and should contain: 1) a brief statement of the paper's purpose, 2) the approach used, 3) the material stud- ied, and 4) the results obtained. Emphasize new and important aspects of the study or observations.
KEY WORDS should follow the abstract and be identified as such. Provide three to J 0 key words or short phrases that will assist indexers in cross- indexing your article. Use terms from the Medical Subject Headings list from Index Medicus when possible.
SUBHEADS should be used to provide guidance for the reader. This format is flexible but the subheads would ordinarily include: Methods and Materials, Case Reports, and Discussion.
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Journals
(1) Authors: Use the surname followed by initials without punctuation. The names of all authors should be given unless there are more than three, in which case the names of the first three authors are used, followed by "et al." (2) Title of article. Capi- talize only the first letter of the first word. (3) Name of journal. Abbreviated according to Index Medi- cus. (4) Year of publication; (5) Volume number: (6) Inclusive page numbers.
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2
JOURNAL VOL 139 NO 1 JANUARY
OFFICIAL
CALL
For the 1987 House of Delegates March 13-15, 1987
IN ACCORDANCE WITH the constitution and bylaws of the Louisiana State Medical Society, the House of Delegates is being called into annual session at 9 am, Friday, March 1 3, 1 986 at the Clarion Hotel in New Orleans, Louisiana. The House will consider such business as presented and required of its annual session. The House will be called to order in the usual manner and remain in session until its duties are complete.
The delegation representation of the component societies in the House for the 1987 Annual Meeting is as follows:
|
Acadia |
2 |
East Baton Rouge |
26 |
Natchitoches |
1 |
St. Mary |
2 |
|
Allen |
1 |
East & West Feliciana |
1 |
North Central |
2 |
St. Tammany |
6 |
|
Ascension |
1 |
Evangeline |
2 |
Orleans |
62 |
Shreveport |
23 |
|
Assumption |
1 |
Franklin |
1 |
Ouachita |
11 |
Tangipahoa |
3 |
|
Avoyelies |
1 |
Iberia |
3 |
Pointe Coupee |
1 |
Terrebonne |
4 |
|
Beauregard |
1 |
Iberville |
1 |
Rapides |
9 |
Tri-Parish |
1 |
|
Bossier |
2 |
Jefferson |
21 |
River Parishes |
2 |
Vermillion |
2 |
|
Calcasieu |
10 |
Jefferson Davis |
1 |
Sabine |
1 |
Vernon |
1 |
|
Catahoula-Ccncordia |
1 |
Lafayette |
12 |
St. Bernard |
2 |
Washington |
2 |
|
Claiborne |
1 |
Lafourche |
3 |
St. Landry |
4 |
Webster |
1 |
|
DeSoto |
1 |
Morehouse |
1 |
St. Martin |
1 |
The current general officers, delegates to the AMA, past presidents, past speakers of the House, Journal editor, emeritus officers, district societies and one representative from each medical school are also members of the House of Delegates. The Medical Student Section is entitled to one delegate and one alternate delegate in a nonvoting capacity.
Total Delegates
|
Component societies |
230 |
Delegates and alternate delegates to the AMA |
10 |
|
Medical schools |
3 |
General officers, past presidents, past speakers of the House, |
|
|
Medical Student Section |
1 |
Journal editor and emeritus officers |
34 |
|
District societies |
10 |
Total Delegates |
288 |
REGISTRATION facilites will be maintained in the Clarion Hotel for delegates, alternate delegates, officers, executives of the com- ponent medical societies and invited guests. Registration hours will be as follows:
Thursday, March 12 1 - 5pm Saturday, March 14 8am - 5pm
Friday, March 13 8am - 5pm Sunday, March 15 8am - noon
ANNUAL
MEETING
JOURNAL VOL 139 NO 1 JANUARY
3
LOUISIANA STATE MEDICAL SOCIETY
General Officers
Jack T. Cappel, Jr, MD President
James W. Vildibill, Jr, MD President-Elect
Robert G. Miller, MD .... Immediate Past President
Paul B. Lansing, MD First Vice President
James R. Bergeron, MD .... Second Vice President
Elmo J. LaBorde, MD Third Vice President
Adolph A. Flores, Jr, MD Secretary-Treasurer
Daniel H. Johnson, Jr, MD Speaker,
House of Delegates
Samuel A. Leonard, MD Vice Speaker,
House of Delegates
Wallace H. Dunlap, MD Chairman
Council on Legislation
A.G. Kleinschmidt, Jr, MD Alternate Delegate
Robert L. diBenedetto, MD Alternate Delegate
Broox C. Garrett, MD Alternate Delegate
Conway S. Magee, MD Alternate Delegate
A. Jay Binder, MD Alternate Delegate
Ralph H. Riggs, MD Delegate Emeritus
Past Speakers, House of Delgates
Humphrey A. Hardy, Jr, MD Charles B. Odom, MD Maurice E. St. Martin, MD Eugene F. Worthen, MD
Councilors
Ronald J. French, MD District One
Frank J. George, MD District Two
Philip A. Robichaux, Jr, MD District Three
Milton C. Chapman, MD District Four
John Charles Cooksey, MD District Five
Charles D. Belleau, MD District Six
Donald R. Blocker, MD District Seven
Bernard L. Kaplan, MD District Eight
Emile K. Ventre, Jr, MD District Nine
Stanford A. Owen, MD District Ten
AMA Delegation
W. Charles Miller, MD Chairman
Gordon W. Peek, MD Delegate
Daniel H. Johnson, Jr, MD Delegate
Donald J. Palmisano, MD Delegate
Eugene F. Worthen, MD Delegate
Past Presidents, Advisory Board to House of Delegates
Cuthbert J. Brown, MD 1961-62
Ralph H. Riggs, MD 1962-63
Charles B. Odom 1965-66
Joseph A. Sabatier, Jr, MD 1966-67
Filmore P. Bordelon, Jr, MD 1968-69
W. Charles Miller, MD 1970-71
Edward M. Harrell, MD 1971-72
Eugene C. St. Martin, MD 1972-73
James H. Stewart, MD 1973-74
Humphrey H. Hardy, Jr, MD 1974-75
F. Michael Smith, Jr, MD 1975-76
Arthur G. Kleinschmidt, Jr, MD 1977-78
Broox C. Garrett, MD 1978-79
David M. Carlton, MD 1979-80
Gerald R. LaNasa, MD 1980-81
Robert L. diBenedetto, MD 1981-82
Eugene F. Worthen, MD 1982-83
Sam L. Gill, MD 1983-84
Donald J. Palmisano, MD 1984-85
Robert G. Miller, MD 1985-86
4
JOURNAL VOL 139 NO 1 JANUARY
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JOURNAL VOL 139 NO 1 JANUARY
5
NEW MEMBERS
Applications for membership have been received from the follow- ing physicians by the respective parish medical societies as of Oc- tober 6, 1986. The Louisiana State Medical Society is pleased to welcome:
■ Ascension
Isreal B. Coutin, MD, PO Box 579, Gonzales 70707. Dr. Coutin received his medical degree from George Washington University in 1985. He specializes in family medicine.
■ Jefferson
Aida L. Blasini, MD, 5248 Forest Park Lane, New Orleans 70114. Dr. Blasini received her medical degree from the University of Puerto Rico in 1983. She specializes in internal medicine.
John B. Cazale, MD, 4204 Teuton Street, Metairie 70006. Dr. Cazale received his medical degree from Lousiana State University in New Orleans in 1973. He specializes in orthopedic surgery.
Bradley T. Collins, MD, 535-A Orion Street, Metairie 70005. Dr. Collins received his medical degree from Louisiana State University in New Orleans in 1983. He specializes in internal medicine.
Owen B. Leftwich, MD, 3715 Williams Blvd., New Orleans 70121. Dr. Leftwich received his medical degree from Louisiana State Uni- versity in New Orleans in 1980. He specializes in ophthalmology.
Carlos A. Sirven, MD, 515 Westbank Expressway, Gretna 70053. Dr. Sirven received his medical degree from Louisiana State Uni- versity in New Orleans in 1981. He specializes in obstetrics and gynecology.
Joseph F. Uddo Jr, MD, 3106 Houma Blvd., Metairie 70006. Dr. Uddo received his medical degree from Louisiana State University in New Orleans in 1981. He specializes in general surgery.
■ Lafayette
Thomas E. Whigham, MD, 4212 West Congress, Lafayette 70506. Dr. Whigham received his medical degree from the University of Texas in Galveston in 1979. He specializes in internal medicine.
■ Lafourche
Andrew H. Hoffmann III, MD, 1101 Audobon Ave., Thibodaux 70301. Dr. Hoffmann received his medical degree from Louisiana State University in New Orleans in 1982. He specializes in pa- thology.
Wayne J. Pharo, MD, 1253 Canal Blvd., Thibodaux 70301. Dr. Pharo received his medical degree from Louisiana State University in New Orleans in 1981. He specializes in cardiology.
■ Orleans
Deborah A. Abernathy, MD, 1430 Tulane Ave., New Orleans 70112. Dr. Abernathy received her medical degree from Louisiana State University in New Orleans in 1978. She specializes in hematology.
Paul W. Brown, MD, 3712 McArthur Blvd., New Orleans 70114. Dr. Brown received his medical degree from Tulane in 1980. He specializes in internal medicine.
Phillip A. Cole, MD, 3700 St. Charles Ave., New Orleans 70115. Dr. Cole received his medical degree from the University of Mis- sissippi in 1967. He specializes in cardiology.
Carolyn B. Daul, MD, 1416 Marengo St., New Orleans 70115. Dr. Daul received her medical degree from Tulane in 1979. She spe- cializes in allergy.
George W. Howard, MD, 3712 MacArthur Blvd., Suite 205, New Orleans 70114. Dr. Howard received his medical degree from Tu- lane in 1981. He specializes in internal medicine.
Samuel W. Parry II, MD, 1430 Tulane Ave., New Orleans 70112. Dr. Parry received his medical degree from Tulane in 1975. He specializes in hand surgery.
Roberto E. Quintal-Aviles, MD, 1401 Foucher, New Orleans 70115. Dr. Quintal-Aviles received his medical degree from Tulane in 1974. He specializes in cardiology.
Charles Rene, MD, 2536 Tulane Ave., New Orleans 70119. Dr. Rene received his medical degree from the University of Haiti in 1975. He specializes in obstetrics and gynecology.
Richard E. Selser Jr, MD, 1514 Jefferson Highway, New Orleans 70121. Dr. Selser received his medical degree from Louisiana State University in New Orleans in 1981. He specializes in ophthalmol- ogy-
Rashid J. Tamimie, MD, 914 Union Street, New Orleans 70112. Dr. Tamimie received his medical degree from Southern Illinois University in 1979. He specializes in occupational medicine.
Judith J. Temple, MD, 1430 Tulane Ave., New Orleans 70112. Dr. Temple received her medical degree from Tulane in 1979. She spe- cializes in internal medicine.
Jose L. Zamora, MD, 1514 Jefferson Hwy., New Orleans 70121. Dr. Zamora received his medical degree from the University of Chihoahoa in Mexico in 1975. He specializes in cardiovacsular sur- gery.
Gerald M. Robertson, MD, 3418 Medical Park Drive, Monroe 71203. Dr. Robertson received his medical degree from the University of Mississippi in 1968. He specializes in psychiatry.
6
JOURNAL VOL 139 NO 1 JANUARY
Iharles C. Sledge, MD, 506 Broadway, Delhi 71232. Dr. Sledge •eceived his medical degree from the University of Mississippi in 1983. He specializes in family medicine.
Harvey C. Thrower, MD, 3421 Medical Park Drive, Monroe 71211. Dr. Thrower received his medical degree from the University of Alabama in Birmingham in 1974. He specializes in diagnostic ra- diology.
(oseph A. Wapenski, MD, 3510 Medical Park Drive, Monroe 71203. Dr. Wapenski received his medical degree from Ohio State Uni- versity in 1978. He specializes in psychiatry.
■ St. Bernard
Marcia B. Davila, MD, 800 Virtue St., Suite 111, Chalmette 70043. Dr. Davila received her medical degree from Tulane in 1980. She specializes in internal medicine.
ifl Shreveport
iLeonard V. Mastrodomenico, MD, 1910 Warrington Place, Shreve- oort 71101. Dr. Mastrodomenico received his medical degree from Mew Jersey Medical School in 1980. He specializes in diagnostic radiology.
fohn A. Mata, MD, PO Box 33932, Shreveport 71130. Dr. Mata received his medical degree from Northwestern University in 1980. He specializes in urology.
fl Vermillion
Steven A. Collins, MD, PO Box 176, Abbeville 70511. Dr. Collins received his medical degree from Louisiana State University in New Orleans in 1981. He specializes in anesthesiology.
\M Webster
Carl H. Hines, MD, 128 Homer Road, Minden 71055. Dr. Hines received his medical degree from Louisiana State University in Shreveport in 1979. He specializes in family practice.
!■ Intern/ Resident Members
Nancy L. Chiarello, DO, 1430 Tulane Ave., New Orleans 70112. Dr. Chiarello received her medical degree from Texas College of Osteopathy in 1983. She specializes in psychiatry.
Kerry P. Pulver, MD, 1514 Jefferson Hwy., New Orleans 70121. Dr. Pulver received his medical degree from Louisiana State Uni- versity in New Orleans in 1981. He specializes in internal medicine.
■ Ouachita
Michael O. Broyles, MD, PO Drawer 1339, West Monroe 71291. Dr. Broyles received his medical degree from Louisiana State Uni- versity in Shreveport in 1978. He specializes in radiology.
ERRATUM
On page 7 of the November 1986 issue of the Journal, Jean D. Ross, MD was described as specializing in pediatrics. Dr. Ross specializes in pediatric hematology and oncology. The Journal regrets the error.
JOURNAL
Nesidioblastosis: Diagnosis and treatment
JOURNAL VOL 139 NO 1 JANUARY
7
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8
JOURNAL VOL 139 NO 1 JANUARY
Norton W. Voorhies, MD, Editor
ECG OF THE MONTH
ALPHABETICAL TRILEMMA
JORGE I. MARTINEZ-LOPEZ, MD
The tracing shown below belongs to a 76-year-old black woman. The three leads — limb leads 2 and AVF, and precordial lead Vx — were recorded simultaneously in the Out-Patient Clinic. The clinical diagnosis was hypertensive cardiovascular disease, complicated by aortic regurgitation and compensated cardiac failure. Medications included antihypertensives and digitalis.
What is your diagnosis? Elucidation is on page 12.
JOURNAL VOL 139 NO 1 JANUARY
11
ECG of the Month
Case presentation is on page 11.
DIAGNOSIS — To be discussed
For the physician who is confronted by a tracing such as the one shown above, it is best to approach its interpretation systematically: describe the recording; state the obvious; speculate on the cause(s) respon- sible for the findings; and finalize the ECG diagnosis on the basis of deductive reasoning.
In describing the tracing shown here and stating the obvious, several preliminary statements can be made. First, QRS complexes are abnormally wide (0.12 sec.) Second, if any one R-R interval is selected as the basic interval, it will be noted that other R-R intervals are slightly shorter than, equal to, or slightly longer than the basic R-R interval. Third, no visible P waves are recorded in close proximity to the QRS complexes. Fourth, all T waves are twin-peaked, and the first peak is taller than the second. This twin-peaking is the subject of the discussion to follow. The second peak will be designated by the letter "X" until its exact origin is deduced.
One can now speculate on the possible causes for the X wave recorded on the tracing. Diagnostic possibilities can be narrowed down to three: notched T waves, U waves, or P waves. Since "dilemma" de- fines a situation involving two choices, one involving three possible choices should be referred to as a "tri- lemma." In fact, it is an alphabetical trilemma because X = T, U, or P. Let us now examine the choices and their significance.
Notching of the T waves has been reported in 4% to 13% of subjects with no recognizable heart disease, as well as in the presence of cardiac and non-cardiac disease. At best, T-wave notching is a non-specific finding; whether or not notching of the T wave should be considered an abnormal ECG finding in itself has not been resolved. The notch on the T wave may be found on either the ascending or descending limb of the T wave or at its summit, creating the twin-peaked T wave. It is more common for the notch to be re- corded in the precordial than in the limb leads. Re- gardless of the location of the notch, the peak-to-peak interval remains constant.
On the surface ECG, the U wave is a separate
deflection of relatively low amplitude, recorded in early diastole, with its apex approximately 100 msec away from the end of the T wave (T-U interval). In most cases, the T-U junction is isoelectric at the base- line and the U wave is readily identifiable as a separate deflection. However, fusion of the T and U waves can occur (short T-U interval) when the U wave occurs early or when the QT interval is prolonged, and leads to twin-peaking of the T waves. In difficult cases, use of a nomogram devised by Lepechskin or simulta- neous recording of the surface ECG and a phonocar- diogram is useful in making the distinction between notched Ts and T plus U.
The P wave of the ECG is inscribed as a result of atrial depolarization caused by the arrival of an elec- trical front originating in either the sinoatrial node or in ectopic cardiac sites.
Before finalizing the ECG diagnosis, it is impor- tant to return to the tracing and measure several in- tervals. From these measurements, the following ob- servations can be made. First, the interval between the summit of the T wave and that of the X wave is not constant. In other words, if any one single TX interval is designated as the basic interval, others pre- ceding or following it are shorter than, equal to, or longer than the basic interval. Second, the QRS-X and the X-QRS intervals are constant throughout the trac- ing. In contrast, the X-X intervals vary in length.
Based on all of the above observations, one can deduce that the X wave, in this case, represents a P wave. The variation in the P-P interval is the result of sinus arrhythmia. The P-R interval is constant and extraordinarily long (0.52 sec.) and there is 1:1 A:V conduction. The abnormally wide QRS complexes are indicative of defective intraventricular conduction of the sinus impulses due to complete left bundle branch block.
The PR interval includes the duration of the P wave and the isoelectric PR segment. It represents the interval of time elapsed between the onset of atrial and ventricular depolarization. Therefore, during sinus rhythm, the PR interval is the sum total of transmis- sion time from the time of SA nodal impulse discharge to the arrival of the impulse at the level of the Purkinje network.
Prolongation of the PR interval is termed first- degree AV block, a misnomer because there is no actual block, but merely a delay in conduction of the su-
12
JOURNAL VOL 139 NO 1 JANUARY
praventricular electrical stimulus, exceeding the nor- mal value of 0.2 sec. The delay in conduction of the supraventricular impulse can be localized to one or more areas: intraatrial region, AV node, bundle of His, and areas distal to the bundle of His. It is un- fortunate that the surface ECG is not accurate in lo- calizing the area of delayed conduction. For precise localization of the site of delay intracardiac electro- graphic studies are required.
The ECG pattern of prolonged PR interval and bundle branch block recorded in the tracing is of ad- ditional interest. Equal first-degree block in both branches of the bundles can present as a prolonged PR interval without a change in the morphology of the QRS com- plex, i.e., prolonged PR interval with narrow QRS complexes. This ECG diagnosis can only be made if during the recording the degree of block in the two branches becomes unequal. In contrast, the pattern of a long PR interval and complete left bundle branch block shown here can result from one of two situa- tions, either first-degree AV block in the AV node combined with unilateral bundle branch block or un- equal first-degree block in both bundle branches, with conduction delay being greatest on the left side.
A final, but inlikely, explanation for this tracing is that the P waves represent non-conducted atrial premature impulses in bigeminy, and the abnormally wide QRS complexes result from a ventricular escape rhythm. ■
SELECTED REFERENCES
1. Lepechskin E: The electrocardiographic diagnosis of bilateral bundle branch block in relation to heart block. Prog Cardiovasc Dis 1964;6:445-471.
2. Gould LA, Reddy CVR, Gomprecht RF; First-degree A-V block due to triple block in the A-V conduction system. Angiology 1973;24:585-588.
3. Lepechskin E: Advances in Electrocardiography , Schlant RC, Hurst JW (ed). New York, NY, Grune & Stratton, Inc., 1976, pp 353- 375.
4. Watanabe Y, Toda H, Nishimura M: Clinical electrocardi- ographic studies of bifid T waves. Br Heart J 1984;52:207-214.
5. Sherron P, Torres-Arant E, Tamer D, et al: Site of conduction delay and electrophysiologic significance of first-degree atrio- ventricular block in children with heart disease. Am ] Cardiol 1985;55:1323-132 7.
From the Cardiology Section, Department of Medicine, LSU Medical Center, and the Heart Station, Charity Hospital of Louisiana,
New Orleans, LA, 70112.
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JOURNAL VOL 139 NO 1 JANUARY
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THE ARMY RESERVE IN THE SOUTHEAST NEEDS PHYSICIANS WHO SPECIALIZE IN FAMILY PRACTICE, TO JOIN AN EXCEPTIONAL TEAM.
WE UNDERSTAND THE DEMANDS ON A BUSY PRACTITIONER. SO WE’RE FLEXIBLE ABOUT TIME, PARTICULAR- LY WHEN IT’S TIME YOU WANT TO SHARE WITH YOUR COUNTRY.
IN THE ARMY RESERVE, YOU’LL FIND OPPORTUNITIES THAT ARE CHALLENGING AND VARIED. OPPOR- TUNITIES TO PARTICIPATE IN EX- CITING TRAINING PROGRAMS AND WORK WITH OUTSTANDING PHYSI- CIANS FROM EVERY AREA OF THE COUNTRY AND TO EXTEND ASPECTS OF YOUR SPECIALITY. WE THINK A FIRST PHONE CALL COULD PROVE TO BE REWARDING.
THE ACTIVE ARMY HAS MORE SOLDIERS WITH FAMILIES THAN EVER BEFORE. SO WHEN YOU JOIN THE ARMY MEDICAL TEAM AS A FAMILY PRACTI- TIONER, EXPECT TO SPEND MOST OF YOUR TIME SERVING NOT ONLY SOLDIERS, BUT THEIR SPOUSES AND CHILDREN, TOO. WHAT’S MORE, YOU WON’T HAVE TO WORRY ABOUT THE PAPERWORK, MALPRACTICE INSURANCE PREMIUMS, OR THE COSTS INCURRED IN RUNNING A PRIVATE PRACTICE.
WORKING WITH A TEAM OF HIGHLY TRAINED PROFESSIONALS, YOU CAN RECEIVE ASSIGNMENTS ALMOST ANYWHERE IN THE U.S. AS WELL AS OVERSEAS. PLUS UP TO 30 DAYS OF PAID VACATION AND REASONABLE WORK HOURS.
ALL IN ALL, YOUR ARMY FAMILY PRACTICE WILL BE A REWARDING EXPERIENCE.
TALK TO YOUR LOCAL U.S. ARMY OR ARMY RESERVE MEDICAL DEPARTMENT COUNSELOR FOR MORE INFORMATION ON FAMILY PRACTICE IN THE ARMY.
ARMY RESERVE MEDICINE 144 ELK PLACE, SUITE 1504 NEW ORLEANS, LA 70112 CALL COLLECT: (504) 589-2373
ARMY. ARMY RESERVE. BE ALLYOU CAN BE.
14
JOURNAL VOL 139 NO 1 JANUARY
OTOLARYNGOLOGY/
HEAD AND NECK SURGERY REPORT
NEUROFIBROMATOSIS OF THE HEAD AND NECK
RICHARD M. WEIR, MD; PAUL A. BLAIR, MD
A case of Von Recklinghausen disease involving the head and neck is presented. This is an autosomal dominant disorder with variable penetrance. Incidence is 1:2500-3000 and 50% of these cases are spontaneous. The criteria for diagnosis includes six or more cafe-au-lait pigmentations of 1.5 cm or greater and family history, multiple neurofibroma. Plexiform neurofibroma are pathognomonic. There is a myriad of associated conditions including mental retardation, seizure disorders, cranial nerve involvement, acoustic neuromas, kyphoscoliosis and endocrine abnormalities. Malignant degeneration occurs in 3% to 15% of the cases. Treatment consists of early and repeated surgical excision with preservation of vital structures. Close followup, genetic counseling, and attention to associated conditions are required.
A 18-year-old black male presented with the com- plaint of progressive difficulty in swallowing. He had first noticed this eight months earlier at which time he had a biopsy of a lesion of the left tonsil. Pathology report revealed a neurofibroma. Since Jan- uary, the patient had noted increased distortion of his oral cavity and enlargement of his left neck and submaxillary area. He denied dyspnea, weight loss, hoarseness or decreased hearing. He did complain of a "muffled” voice. Physical exam revealed a well de- veloped, slim black male with multiple nodules in the subcutaneous tissue of his arms and legs. He had a 4x7 cm mass in the left neck and a 2x4 cm mass in the left submaxillary area. Intra-oral exam revealed deviation of the uvulva to the right, and a large mass in the left peritonsillar area. Cranial nerve examina- tion was normal. The larynx was not well visualized. Ophthamology consultation reported a normal exam. Audiogram, tympanometry and reflexes were nor- mal. CT scan was obtained which showed continuity between the neck and oral masses (Fig 1). Digital an- giography showed displacement laterally of the ca- rotid and jugular vessels, but no major vascular struc- tures within the mass. The patient subsequently ►
JOURNAL VOL 139 NO 1 JANUARY
15
underwent excision of the neck mass, lateral pharyn- gotomy and excision of the pharyngeal mass. Portions of the neck mass were easily separated from the sur- rounding tissues, however tumor was left attached to the carotid and jugular vessels. The vagus nerve was preserved. There was incomplete removal of the pha- ryngeal tumor. The patient had an unremarkable postoperative course. After three weeks postop, the oral cavity was well healed, he had a normal voice and indirect laryngeal exam showed normal mobility of both vocal cords. Pathology report showed mul- tiple neurofibromas as well as the presence of plexi- form neurofibroma.
DISCUSSION
In 1793, Tilesius first described the disorder. Virchow pointed out its familiar nature in 1847. 1 Robert Smith reported a case of cutaneous tumors in 1849 and in 1882, Fredrich Von Recklinghausen gave his classic presentation of the disease which now bears his name.2
Von Recklinghausen disease occurs in all races and the widely accepted incidence is one in 2500 to 3000 of all live births. It is transmitted as an autosomal dominant trait and has variable penetrance. A total of 50% of cases will have no familial history and are felt to represent spontaneous mutations. Two-thirds of patients will have clinical evidence of disease within the first year of life and 75% of cases will have come to medical attention by age 20. 3
The clinical features of Von Recklinghausen dis- ease include multiple cafe-au-lait pigmentation, gen- eralized cutaneous neurofibroma, central nervous system tumors, skeletal deformities, and various en- docine, cardiovascular and developmental abnormal- ities. The widely held criteria for diagnosis would require presence of at least six cafe-au-lait of greater than 1.5 cm.2' 4 Griffith, et al, requires the presence of at least two of three classical findings: (1) multiple neurofibroma, (2) multiple cafe-au-lait, (3) positive family history to confirm the diagnosis.5 Adkins and Ravitch include patients with more than five cafe-au- lait and multiple neurofibroma or a positive family history and skeletal abnormalities in their series.6
Neurofibromas are generally felt to arise from Schwann cells, which are derived from neural crest origins. Mesodermal tissues, however, is also af- fected. Three major types of tumors are seen: (1) neu-
Figure 1. CT scan of neck showing retromandib- ular extension of neck mass.
rolemmoma — which are usually solitary, well-en- cupsulated and thus easily removed from the underlying neural tissue and have a low malignancy potential; (2) neurofibroma — which are usually mul- tiple, nonencapsulated and thus difficult to separate from adjacent tissue, and have a 5% rate of malignant degeneration; and (3) plexiform neurofibroma — which consist of multiple tortuous cords of tissue which fol- lows peripheral nerves.2 Plexiform neurofibroma is described as “bag of worms" on clinical palpation and is considered pathognomonic of VRD, even in the absence of other findings.2 The term “molluscum fi- bromata" is applied when the patient manifests mul- tiple neurofibroma as small nodules in the subcuta- neous tissues. “Elephantiasis neuromatosis" has been used to describe the massive, disfiguring growth
16
JOURNAL VOL 139 NO 1 JANUARY
vhich may occur in untreated cases.7 Malignant de- generation is reported to occur in from 3% to 15% of all cases, though rates up to 30% have been quoted.2' 4- 7- 8
Neurofibroma may occur in any location of the body. Primary involvement in the head and neck is from 22% to 40%. 4- 6 The most common site in the head and neck is the scalp and face, followed by the orbit and peri-orbital skin. Cranial nerve involvement is common, as are intracranial tumors.1- 6 9 In the child, the most common intracranial tumor is the astrocy- toma, while in the adult it an acoustic neuroma. CN III & VIII are involved most commonly. Acoustic neu- romas are bilateral 82% of the time.2 The presence of a single intracranial tumor should initiate the search for other tumors, as multiple intracranial tumors are common in this disease. Trigeminal, facial and vagus nerves are involved frequently. Examination for their involvement should be made. Other sites in the head and neck include mandible, facial bones, sphenoid, and oral cavity. Involvement in the neck is usually a ; plexiform neurofibroma. Kyphoscoliosis is present in i the cervical vertebra in 20% of patients, and can cause difficulties with respiratory compromise, endotra- cheal intubation, and vertebral collapse.2- 6 Medias- tinal masses may present as neck masses. Other find- ings include developmental delay, mental retardation (in 10%), seizure disorders, phenochromocytoma (in 1%) and MEA III.2-7 Growth of tumors appears to be enhanced at puberty.
TREATMENT
Treatment of these tumors is largely surgical. In the past, prolonged observation of lesions was common due to the concerns of malignant degeneration if in- complete removal was attempted. This concern has been eliminated by the long term follow up of many patients following subtotal removal of a variety of lesions.5 7 Surgical removal is often difficult and time consuming. Incomplete removal of lesions is the rule rather than the exception, as in this case. Hypertro- phy of vessels supplying neurofibroma is not uncom- mon and preoperative embolization of large vessels has been advocated.1 Vital structures in the head and neck may be involved and judicious removal is re- quired. Portions of tumor may need to be left attached to vital structures. There is no indication that this is
detrimental, indeed some authors feel this may cause regression of some tumors.5- 6- 7 Adkins and Ravitch stress that these tumors will have progressive growth and hence advocate early removal.7 They feel that multiple excisions, if necessary, allow less removal and less damage to functional support structures (ie, orbit, mandible) than allowing neurofibroma to grow to large and bulky sizes. Other authors also encourage early and repeated surgical removal.5- 6- 9
It is important not to overlook the other condi- tions found with this disease. Disruption of the cer- vical spinal column due to tumor or due to kypho- scoliosis is a major problem in some children.2- 6 Stabilization may be required at an early stage. Mental development may be delayed. Seizure disorders and other neurological abnormalities need appropriate medical management and follow-up. Due to the pro- gressive nature of this disease, these patients need lifelong and close attention. Yearly physical exami- nations and audiograms should be obtained in all pa- tients. CT scans and other radiologic exams are ob- tained as indicated. Any rapid growth or pain in a neurofibroma should be suspected of malignant de- generation. Care has to be individualized. Early and often repeated surgical intervention is necessary in most of these patients. Genetic counseling should be given to all patients of childbearing age. ■
1. Kimmelamn CP: Otolaryngologic aspects of neurofibromatosis. Arch Otolaryngol 1979;105:732-736.
2. Holt GR: E.N.T. Manifestation of VRD. Laryngoscope 1978;88(10):1617-1632.
3. Batsakis JG: Tumors of the Head and Neck, ed 2. Baltimore, Wil- liams & Wilkins Co., 1980, pp 317-318.
4. Maceri DR, Saxon KG: Neurofibromas of the head and neck, Head Neck Surg 1984;6(4):842-850.
5. Griffith BH, Lewis VL, McKinney P: Neurofibromas of the head and neck, Surg Gynecol Obstet 1985;160(6):534-538.
6. Adkins JC, Ravitch MM: The operative management of VRD in children, with special reference to the head and neck. Surgery 1977;82(3):342-348.
7. Shack RB, Reilley AF, Lynch JB: Neurofibromas of the head and neck. South Med J 1985;160(6):534-538.
8. Wright BA, Jackson D: Neural tumors of the oral cavity: A review of the spectrum of benign and malignant oral cavity and jaws. Oral Surg 1980;49(6):509-522.
9. Adekeye EO, Abiose A, Ork RA: Neurofibromatosis of the head and neck: Clinical presentation and treatment. / Maxillofac Surg 1984;12(2):78-85.
Requests for reprints should be sent to Paul A. Blair, MD, Dept, of Otolaryngology — Head and Neck Surgery, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112; (504)588-5453.
JOURNAL VOL 139 NO 1 JANUARY
17
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18
JOURNAL VOL 139 NO 1 JANUARY
Shirley Bertucci, LSMSA President
AUXILIARY REPORT
ON LEADERSHIP AND THE AUXILIARY
SANCY H. McCOOL
What began in 1929 as an auxiliary created for physician spouses, with social activities in the forefront, has evolved into a most prestigious organi- zation with opportunities for growth and achievement among individual mem- bers, a united effort toward aiding phy- sician spouses wherever possible, and the continued improvement of com- munity health. Membership in the Aux- iliary makes you a part of an organiza- tion of physicians' spouses united by a common goal — to improve the quality of health and life for all people.
The federated structure of our or- ganization has enabled us to continually study and improve our community involvement in health areas such as organ donation, child abuse, seat belt safety, smoking and smokeless tobacco usage, and immu- nization. In our local communities, members often work in coalition with civic organizations. On the state level, the LSMSA offers workshops and speakers on legislation and health issues of vital concern to our local parish auxiliaries at both the Mid-Year Board Meeting and the annual convention. For the past two years, the Auxiliary has provided a Leadership Con- ference to officers and members of our 16 parish aux- iliaries, members-at-large, and resident physician/ medical student spouses. The AM A A offers two lead- ership confluences for parish and county leaders each year. Outstanding speakers from across the nation lend their expertise to these most informative meet- ings, and materials and publications are made avail- able to help in implementing vital health programs at the parish and state levels.
We realize that it is imperative that we train and
educate our Auxiliary leaders in order that they may successfully implement these health programs in the commu- nities, and that the physician spouse can be an effective, favorable representative of the medical community as a whole. We must be certain that media coverage reflects the true image of the physician and that the physician's spouse be con- cerned, informed and involved in the community of the parish, state and na- tion.
In seeking leaders for our Auxili- aries, we, like many other organiza- tions, have certain criteria. A leader must be informed, organized, open to constructive sug- gestions, able to delegate responsibility, communicate effectively with members, project a positive image to the community of the organization and spark enthu- siasm. The oft-quoted phrase "leaders are born, not made," seems fallible as we recognize the opportun- ities for training and growth offered.
We look with pride at our Auxiliary as it has grown to over 1,800 members statewide and at the outstanding record of achievements in promoting awareness of health issues vital to the well-being of all our citizens. In these days of changes and contin- uing challenges to the medical profession, we rec- ognize the need to continue to recruit physician spouse members, and to train these members to be effective leaders in the projection of a caring and concerned medical family. ■
Mrs. McCool ( wife of Dr. E. Edward McCool) is president-elect of the
Louisiana State Medical Society Auxiliary.
JOURNAL VOL 139 NO 1 JANUARY
21
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JOURNAL VOL 139 NO 1 JANUARY
23
CALENDAR
February
February 1-4
American Society for Parenteral and Enteral Nutrition 11th Clinical Congress, New Orleans, Louisiana. Contact: Kelly G. Tilton, Conventions & Exhibits, A.S.P.E.N., 8505 Cameron Street, Suite 500, Silver Spring, MD 20910; (301)587-6315.
February 2-4
Trauma Management 1987, Hotel Inter-Continental, San Diego, California. Sponsored by UC San Diego School of Medicine. Contact: UCSD School of Medicine, M-017, Con- tinuing Medical Education, La Jolla, Ca 92093; (619)534-3940.
February 2-4
South Florida Winter Hand Symposium, Bahia Mar Resort, Ft. Lauderdale, Florida. Sponsored by Florida Hand Rehabilitation and endorsed by Plastic Surgery Educational Foundation. Contact: Jane Guterman, South Florida Winter Hand Symposium, 2734 Polk Street, Suite 1, Hollywood, FL 33020; (305)921-HAND.
February 5-7
21st Annual Symposium on Cosmetic Surgery, Hyatt Regen- cy, Miami, Florida. Sponsored by The Plastic Surgery Educa- tional Foundation. Contact: Thelma Mac Gregor, Cedars Medical Center, Cosmetic Surgery Symposia, 1400 N.W. 12th Avenue, Miami, FL 33136.
February 7-14
Orthopedic Emergencies, Snowbird Resort, Snowbird, Utah. Sponsored by the American Institute of Postgraduate Educa- tion and Scripps Memorial Hospital-Encinitas. Contact: Edith S. Bookstein, Conference Management Associates, PO Box 2586, La Jolla, CA 92038; (619)454-3212.
February 10-14
Cardiopulmonary Rehabilitation Status '87, Gainesville, Florida. Sponsored by the University of Florida Center for Exercise Science. Contact: Michael L. Pollock, PhD, Direc- tor, Center for Exercise Science, University of Florida, Dept, of Medicine, Box J-277, Gainesville, FL 32610; (904)392-0584.
February 12-14
Basic Rhinoplasty, Dallas, Texas. Sponsored by Division of Plastic and Reconstructive Surgery at the University of Texas Health Science Center and The Plastic Surgery Educational Foundation. Contact: Ann Parchem, Continuing Education,
University of Texas Health Science Center, 5323 Harry Hines Blvd., Dallas, TX 75235; (214)688-2166.
February 14-17
36th Annual Symposium on Cataracts in the Nineties, Hyatt Regency, New Orleans, Louisiana. Sponsored by the New Orleans Academy of Ophthalmology. Contact: Emily Busby, New Orleans Academy of Ophthalmology, Eye, Ear, Nose & Throat Hospital, 145 Elk Place, Room 203, New Orleans, LA 70112.
February 15-21
Advances in Plastic and Reconstructive Surgery, Park City, Utah. Contact: Plastic Surgery Educational Foundation, 233 North Michigan Ave., Suite 1900, Chicago, IL 60601; (312)856-1818.
February 16-20
The Physician in Management, Seminar I, Sheraton Sand Key, Clearwater Beach, Florida. Contact: Sherry Mason, American Academy of Medical Directors, 4830 W. Kennedy Blvd., Suite 648, Tampa, FL 33609; (813)873-2000.
February 17-19
Maxillofacial Trauma, Los Angeles, California. Sponsored by the American Academy of Facial Plastic and Reconstruc- tive Surgery and the Dept, of Otolaryngology-Head & Neck Surgery of the Postgraduate Division of the University of Southern California School of Medicine. Contact: Donna Hoffman, Administrator, USC Dept, of Otolaryngology- Head & Neck Surgery, 1200 N. State Street, Box 795, Los Angeles, CA 90033; (213)226-7315.
February 20-21
Post Traumatic Stress Disorder and Other Psychiatric Se- quelae of Trauma, New Orleans, Louisiana. Sponsored by Tulane University Medical Center. Contact: J.A. D'Angelo Jr, Director, Office of Continuing Education, Tulane Medical Center, 1430 Tulane Ave., New Orleans, LA 70112-2699; (504)588-5466.
February 21-28
Radiology for Emergency & Primary Care Physicians, Royal Lahaina Resort, Maui, Hawaii. Sponsored by the American Institute of Postgraduate Education and Scripps Memorial Hosptial-Encinitas. Contact: Edith S. Bookstein, Conference Management Associates, PO Box 2586, La Jolla, CA 92038; (619)454-3212.
February 21-28
Duke at Vail: Symposium on Inflammatory Diseases, Vail, Colorado. Sponsored by Division of Dermatology and Divi-
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JOURNAL VOL 139 NO 1 JANUARY
sion of Rheumatology and Immunology. Contact: Angelika Langen, Box 3135, Duke University Medical Center, Durham, NC 27710; (919)684-2504.
February 23-26
International Symposium on Plastic Surgery in Bangkok,
Bangkok, Thailand. Contact: Plastic Surgery Educational Foundation, 233 North Michigan Ave., Suite 1900, Chicago, IL 60601; (312)856-1818.
February 24-27
Update Your Pediatrics-1987, New Orleans, Louisiana. Spon- sored by Tulane University Medical Center. Contact: J.A. D'Angelo Jr, Office of Continuing Education, Tulane Medical Center, 1430 Tulane Ave., New Orleans, LA 70112-2699; (504)588-5466.
February 26-28
Advanced Perinatal Ultrasound Seminar, Buena Vista Palace Hotel, Lake Buena Vista, Florida. Sponsored by the Depart- ment of Radiology, Orlando Regional Medical Center and the Center for Medical Ultrasound, Bowman Gray School of Medicine. Contact: Lennard D. Greenbaum, MD, Chief, Section Diagnostic Ultrasound, 1416 South Kuhl Ave., Orlan- do, FL 32806; (305)841-5229.
February 27-28
Smoking, Disease and Their Management, New Orleans, Louisiana. Contact: Ochsner Medical Foundation, Continu- ing Medical Education, 1516 Jefferson Hwy., New Orleans, LA 70121; (504)838-3702.
February 27 - March 1
Facial Plastic Surgery on the Non-Caucasian, New Orleans, Louisiana during Mardi Gras. Sponsored by the American Academy of Facial Plastic and Reconstructive Surgery. Con- tact: AAFPRS, 1101 Vermont Ave, NW, Suite 404, Washington, D.C. 20005; (202)842-4500.
February 28 - March 2
Mardi Gras Anesthesia Update, New Orleans, Louisiana. Sponsored by Tulane University Medical Center, Louisiana Society of Anesthesiologists and the New Orleans Anesthesia Society. Contact: J.A. D'Angelo Jr, Office of Continuing Education, Tulane Medical Center, 1430 Tulane Ave., New Orleans, LA 70112-2699; (504)588-5466.
February 28 - March 7
6th Annual Park City Oculoplastic Meeting, Symposium on Head, Orbital and Ocular Trauma, New Orleans, Louisiana. Contact: Darrell Wolfley, MD, LSU Eye Center, 2020 Gravier St., Suite B, New Orleans, LA 70112; (504)568-6700.
March
March 1-6
IX World Congress of Plastic & Reconstructive Surgery,
New Delhi, India. Contact: Aloke C. Bagchi, Program Coor- dinator, IX World Congress of Plastic Surgery, 6101 N. Talman Ave., PO Box 59577, Chicago, IL 60659; (312)465-8337.
March 1-7
Internal Medicine Symposium, Cancun, Mexico. Sponsored by the University of Kansas Medical Center. Contact: Eileen Buttron, Office of Continuing Education, 39th and Rainbow Blvd., Kansas City, KS 66103; (913)588-4494.
March 1-7
Update '87: Office Obstetrics and Gynecology, Shadow Ridge Resort, Park City, Utah. Presented by Scott & White. Contact: Charlene E. Lee, Communications Specialist, Scott & White, 2401 South 31st Street, Temple, TX 76508; (817)774-2821.
March 1-8
Winter Scientific Seminar, Ski Utah for Mardi Gras, Park City, Utah. Offered by the Orleans Parish Medical Services Bureau in conjunction with the Orleans Parish Medical Socie- ty. Contact: OPMS, 1800 Canal Street, New Orlenas, LA 70112; (504)523-2474.
March 2-6
Internal Fixation in Hand Surgery, Vail, Colorado. Spon- sored by the American Society for Surgery of the Hand. Con- tact: American Society for Surgery of the Hand, 3025 South Parker Road, Suite 65, Aurora, CO 80014; (303)755-4588.
March 5-7
2nd International Interdisciplinary Conference on Hyperten- sion in Blacks, Peachtree Plaza Hotel, Atlanta, Georgia. Sponsored by Emory University School of Medicine, American Heart Association, National Heart, Lung and Blood Institute and the Association of Black Cardiologists. Contact: Continuing Medical Education, Emory University School of Medicine, 110 WHSCAB, 1440 Clifton Road, NE, Atlanta, GA 30322; (404)727-5695.
JOURNAL VOL 139 NO 1 JANUARY
25
TUMORAL CALCINOSIS AND HYPERPARATHYROIDISM
RICHARD S. GODFREY, MD; DAVID M. FADDIS, MD; PHILIP J. DAROCA JR, MD; CARL M. SUTHERLAND, MD
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JOURNAL VOL 139 NO 1 JANUARY
Tumoral calcinosis is a rare disorder in which calcified masses develop predominately in the black race. The disease is associated with trauma, hyperphosphatemia and genetic predisposition;
however, it has not been associated with hypercalcemia and hyperparathyroidism. A case report of a patient with hyperparathyroidism and tumoral calcinosis is presented and a review of the
literature included.
The development of multilocular cystic structures filled with calcareous material in the hips, elbows and shoulder of a 12-year-old boy was reported by Derut in 1899. 1 In 1942, Ghormley and McCrary2 re- ported similar lesions found in three siblings, which they attributed to calcified bursae. Inclan, et al,3 in- troduced the term “tumoral calcinosis," in 1943, de- scribing calcified masses in three unrelated Cubans. They emphasized:
. . . the gigantic and progressive nature of the calcification, the spread of the growth beyond the muscular and bursal structures and the anatomic distribution in regions in which bursae and glid- ing cellular tissue are present.
Lesions of tumoral calcinosis appear character- istically near large joints and the wrists, feet and hands during childhood and adolescence. Approximately 200 cases have been described,4- 5 with a preponderant incidence of blacks (approximately 80%). A familial tendency has also been noted, with both sexes in- volved and limited to a single generation, suggesting a recessive autosomal mode of inheritance. Prince, et al4 in a review of 40 cases from the literature, divided patients into those with hyperphosphatemia and those with normal serum phosphorus levels. Incidence of positive family history, onset before age 20, black race, and multiple lesions were significantly higher in pa- tients with hyperphosphatemia. There are, in addi- tion, several reports5'9 of tumoral calcinosis in patients with renal failure. These patients had hyperphos- phatemia, tended to be older, and (with the exception of one case) hypercalcemia was not documented.6
The etiology of tumoral calcinosis is as yet un- defined. In addition to the early theories of trauma and non-specific calcification of bursae, an accumu- lation of reports in the literature point toward hy-
perphosphatemia as having an etiologic role.6- 10-13 The elevated levels of serum phosphorus and frequent occurrence of the disease in siblings point to an inborn or hereditary error of metabolism. Mechanisms of the metabolic disorder may include endogenous hy- pervitaminosis D12 and an intrinsic proximal tubular defect.13 Chronic renal disease and hyperphospha- temia have been associated with tumoral calcinosis, indicating that hereditary factors are not a prerequi- site. The role of hyperphosphatemia is emphasized in a case report by Mozafferian, et al,14 who success- fully treated tumoral calcinosis using a low-calcium and phosphorus diet, along with aluminum hydrox- ide antacid to lower serum phosphorus. The vast ma- jority of cases of tumoral calcinosis, however, have been treated by surgical excision although tumors fre- quently recur.3- 10- 14-17
CASE REPORT
A 56-year-old black woman with a 20-year history of hypertension and two-year history of chronic renal failure, was admitted for work-up of hypercalcemia (11.6 mg/dL). Her only complaints were occasional cramps of the hands and feet and a one-month history of a lump in her back, which caused discomfort when pressure was applied. She denied any trauma, and had received an epidural anesthetic 22 years earlier for a hysterectomy.
The patient's medicines included: Zyloprim® (100 mg po qd). Minipress® (50 mg po q 8 h), and Dyazide® (1 tab po qd). On physical examination she was nor- motensive, well-developed, and well-nourished, with a single abnormality of a 4 x 5 cm firm mobile mass located on her back immediately to the right of L-4 to L-5 vertebrae. The mass was slightly tender to deep palpation.
Admission laboratory studies disclosed the fol- lowing values: serum calcium, 11.6 mg/dL (normal 9.0 to 11.0); phosphorus, 5.6 mg/dL (normal 2.5 to 4.5; serum alkaline phosphatase, 90 u/L; total protein, 6.9 g/dL; serum albumin, 3.9 g/dL; parathy- roid hormone (PTH), 33,888 pg/ml (normal <2000); blood urea nitrogen, 89 mg/dL (normal 5 to 20 mg/ dL); and creatinine, 5.5 mg/dL (normal 0.8 to 1.2 mg/ dL). A KUB x-ray showed a 3x5 cm calcified soft tissue mass posterior to the fourth and fifth lumbar vertebrae (Fig 1). Computed tomography scan dem-
JOURNAL VOL 139 NO 1 JANUARY
27
Figure 1. Lateral lumbar spine film showing cal- cification posterior to L-4 and L-5.
onstrated a multiseptate, cystic, densely calcified le- sion contiguous to but not invasive into, the spine (Fig 2). Ultrasonography of the neck showed a 2-cm structure consistent with parathyroid gland in the left superior thyroid pole.
An excision of the mass was performed on March 20, 1985 through a transverse incision. The lesion was multiloculated and embedded in a dense, adhesive, fibrous capsule, which extended into the surrounding muscular sheaths (Fig 3). The tumor was also fixed to the posterior spinous process of the L-4 vertebrae and required sharp dissection for removal.
On March 28, 1985 the patient underwent a sub- total parathyroidectomy. At surgery, four hyper- plastic parathyroid glands were identified and his- topathology disclosed parathyroid hyperplasia with oxyphilic nodules. Postoperatively the patient's cal- cium and phosphorus levels dropped to 9.8 mg/dL and 2.9 mg/dL, respectively; her PTF1 value dropped to 760 pg/ml. On six months' follow-up examination, she is without complaints and has no palpable re- currence of the tumor in her back.
Figure 2. Computed tomography scan showing calcification adjacent to posterior spi- nous process of L-4.
Figure 3. Tumoral calcinosis — surgical specimen.
MATERIAL AND METHODS
All four parathyroid glands were microscopically hy- perplastic. While the glands maintained a lobular-like architecture, adipose tissue was replaced by a cellular
(Continued on page 31)
JOURNAL VOL 139 NO 1 JANUARY
(Continued from page 28)
proliferation. Multinodularity was typical of the hy- perplastic process in each of the glands. The hyper- plastic cells consisted of chief cells, nodules of oxy- philic cells, transitional water-clear and frank water- clear cells (Fig 4).
The back tumor measured 5 x 5 x 3.5 cm; the cut surface showed yellowish gritty areas, which ap- peared partially liquified in areas. The process was surrounded by condensation of fibrous tissue.
Microscopic findings showed a process of calci- nosis occurring in fibroadipose tissue. The process consisted of irregular basophilic-stained foci of calci- fication, bordered by fibrous tissue containing histio- cytic and multinucleated foreign body-type and oc- casional osteoclast-like giant cells. In some areas, a histiocytic cellular component was present at the in- terface with the adjacent fibrous tissue. In these, giant cells contained single and multiple rounded calcified particles within the cytoplasm. There was a mild distribution of lymphocytes in these foci and active fibroblasts. In areas, the pattern suggested that cal- cification begins with histiocytes or giant cells, fills the cytoplasm and eventually destroys the cell re- leasing the calcific particles into the central mass of calcific debris (Fig 5).
DISCUSSION
The patient reported in this study is remarkable in that she manifested the pathologic characteristics of tu- moral calcinosis, in the setting of hypercalcemia and absence of family history. She had a rapidly enlarging, multilobulated calcium deposition near a subcuta- neous, periarticular space, which spread into and through muscular tissue, but had no visceral or vas- cular involvement. Her pre-existing condition of hy- percalcemia, however, brings into question the di- agnosis of tumoral calcinosis. Tumoral calcinosis is considered to be a distinct clinicopathologic disease process, which does not result from hypercalcemia. 4' 1214 There are, however, a few reports of hypercal- cemia in patients with tumoral calcinosis.6' 10 Our pa- tient is the first reported case known to us to have hypercalcemia, hyperparathyroidism, and tumoral calcinosis. Although some authors18 might classify her calcific tumor into a different category, it is histo- pathologically identical with tumoral calcinosis. This
Figure 4. Parathyroid-hyperplasia (x 110) chief cells and portion of module of transitional oxy- philic cells.
Figures. Calcinosis (x 275) interface with calcium deposits, histiocytes, and giant cells.
case report underscores the possible importance of treating the chemical as well as anatomic manifesta- tion of the disease. In this case a parathyroidectomy was performed to control hypercalcemia.
CONCLUSIONS
If tumoral calcinosis is a disease of calcification with multiple causes, the case in presentation may not be ►
JOURNAL VOL 139 NO 1 JANUARY
31
unique. The etiology of our patient's hyperparathy- roidism is not definite. A 20-year history of hyper- tension may have led to chronic renal failure and sec- ondary hyperparathyroidism. The presence of oxyphilic nodules in glands with parathyroid hyper- plasia is consistent with a preceding history of renal disease. Without a documented period of hypocal- cemia, however, it is possible she had primary hy- perparathyroidism with subsequent hypercalcemia leading to chronic renal failure. Whatever the cause of her hypercalcemia, it is also possible her lesion was related to another factor, such as trauma or hyper- phosphatemia.
The pathogenic mechanism of tumoral calcinosis remains to be clarified. The Prince, et al,4 study, in which two thirds of patients had normal phosphorus levels, indicates that hyperphosphatemia is not a pre- requisite. A history of trauma is also not always pres- ent.5' 10' 12-18 This patient, with a history of hyperpar- athyroidism and hypercalcemia, adds another dimension to a yet unexplained process. By present- ing this case, it is hoped that physicians will be as- sisted in recognizing an unusual disorder and con- tinue to work toward a better understanding thereof.
REFERENCES
1. Duret MH: Tumeurs multiples et singulieres des bourses ser- evses. Bull Soc Anat Paris 1899;74:725-728.
2. Ghormley R, McCrary W: Multiple calcified bursae and calcific cysts in soft tissues. Tr West SA 1942;51:292-296.
3. Inclan A, Leon P, Camjo MG: Tumoral calcinosis. JAMA 1943;121:490-495.
4. Prince M, Schaefer P, Goldsmith R: Hyperphosphatemic tu- moral calcinosis. Ann Intern Med 1982;96:586-591.
5. Knowles S, Declerck G, Anthony P: Tumoral calcinosis. Br J Surg 1983;70:105-107.
6. Barton DL, Reeves RJ: Tumoral calcinosis: report of three cases and review of the literature. AJR 1961;86:351-358.
7. Vasuder KS, Tapp E, Harris M: Tumoral calcinosis in Britain. Br Med] 1973;1:676.
8. Burkholder T, Braund R: Massive calcinosis with chronic renal insufficiency due to polycystic kidneys: case report. J Urol 1947;57:1001-1009.
9. Sommer F, Treas E: Britray zom Kronkhirtsbilde der Lipokal- zimo granulomatose (ime besondere feorm der calcinosis univ- ersalis). Fortschr Gob Rontgenstr Nuklearmed Erganzungsband 1941;63:205-214.
10. Lafferty FW, Reynolds ES, Pearson OH: Tumoral calcinosis: A metabolic disease of obscure etiology. Am J Med 1965;38:105- 118.
11. Wilber JF, Slatopolsky E: Hyperphosphatemia and tumoral cal- cinosis. Ann Intern Med 1968;68:1044-1049.
12. Clark E, Swischule L, Hayden C: Tumoral calcinosis, diaphys- itis, and hyperphosphatemia. Radiology 1984;151:643-646.
13. Mitnick P, Goldfarb S, Slatopolsky E: Calcium and phosphate metabolism in tumoral calcinosis. Ann Intern Med 1980;92:482- 487.
14. Mozafferian G, Rafferty F, Pearson O: Treatment of tumoral calcinosis with phosphorus deprivation. Ann Intern Med 1972;77:741-745.
15. Berg D: Tumoral calcinosis. Br J Surg 1972;59:570-571.
16. Gan K: Tumoral calcinosis: A case report and review of the literature. Br J Plast Surg 1982;35:177-180.
17. Amamonthedo H: Calcinosis. Am J Surg 1960;99:955-956.
18. Enzinger FM: Soft-tissue Tumors. New York, Mosby, 1983.
ACKNOWLEDGMENTS
The authors would like to express their appreciation to Gae O.
Decker-Garrad for editorial assistance and Jeannette Saunders for
manuscript typing.
From the Departments of Surgery and Pathology at Tulane University
School of Medicine in New Orleans, LA.
Requests for reprints should be sent to Carl M. Sutherland, MD, Tulane University School of Medicine, Department of Surgery, 1430 Tulane Avenue, New Orleans, LA 70112 ; (504) 588-5355.
Supported in part by the Meredith H. Knipe Memorial Fund.
32
JOURNAL VOL 139 NO 1
JANUARY
CONSUMER PRICE DIFFERENTIALS BETWEEN CONTAINERS AND BRAND PRODUCTS OF ORAL ANTIBIOTICS
IN LOUISIANA
YURUK IYRIBOZ, MD, MPH
Retail prices of 91 brand products consisting of 27 standard oral forms (ie, capsules, tablets) in 57 different containers (ie, bottles containing 100, 200 capsules) was provided by the manufacturers. A list of 35 items representing the least expensive oral products for ampicillin, amoxicillin, erythromycin, tetracycline and chlorampenicol was prepared. Prices significantly varied between different containers and brand products for the same amount of the same antibiotic (20% to 60%). Average prices for the least expensive products of each antibiotic were 52% lower than average prices of other products. A survey showed that only 2.5% of the least expensive products were available at the pharmacies. The findings suggest that potential cost-savings by drug product selection largely depends on the purchasing practices of pharmacies (inventory) rather than the physicians' permissive attitudes. Research on these practices is underlined. Pharmacy retail price of certain products were found to be as much as 331% higher than the price given by the manufacturers.
Drug product selection, the act of dispensing a lower cost equivalent product to that prescribed, is considered to be an important approach to cost containment in health care. It has been advocated by both consumer groups and governments.
Since 1961, 49 state legislatures and the District of Columbia have enacted laws which permit drug product selection.
The majority of studies related to cost-savings in drug product selection compare prices of generic products with those of brand names. However, find- ings of these studies are not always consistent with cost-savings. Although some studies have found po- tential savings in generically written prescriptions,1-4 others have shown that actual savings to the patients are minimal.5 According to Brennan, the price differ- ences between generic and brand names are often smaller than predicted from wholesale prices, because prices of the brand name products are usually over- stated; whereas least expensive generic equivalents usually are not available at the list price.6 On the other hand, prescription of generic drugs does not neces- sarily mean that substitution will take place.7 Phar- macists cannot substitute less expensive drugs unless ►
JOURNAL VOL 139 NO 1 JANUARY
35
they have them in inventory.8 A study has shown that for less than 2% of generic prescriptions were generic products actually dispensed.9
Prices of drugs do not only differ between generic and brand names. They also differ among various brands and different containers/packages of the same drug under the same brand name. Can research on these differentials besides those between generic and brand names lead to a significant cost-containment approach? Apparently, there are few studies focusing on these differentials alone, to the best of our knowl- edge.
As opponents and proponents of generic pre- scribing continue to debate their views, it is tempting to direct attention to other possible and practical ap- proaches to cost-saving drug product selection. An- tibiotics are among the most commonly prescribed medications in this country.10'12 The purpose of this paper is to present the results of an investigation into consumer price differentials between different con- tainers/packages of the most commonly used oral an- tibiotics under the same and different brand names.
METHODOLOGY
Selection of Oral Antibiotics
Oral forms of the following antibiotics were studied; amoxicillin, ampicillin, erythromycin, tetracycline and chloramphenicol. They were selected considering their frequent use in the most commonly occurring infec- tions such as of the upper respiratory, urinary, and gastrointestinal tracts, skin and sexually transmitted disease.13'31
Inventory of Commercial Forms and Least Expensive Products
An inventory of commercial forms and containers and retail price for each of the oral antibiotics studied has been prepared. The information necessary for this inventory has been obtained from published sources and written communications with the pharmaceutical companies.32 Price of each form/container for each of the antibiotics was standardized to price per each mg. of the active ingredient. These prices were cross tab- ulated for each form and container under each phar- maceutical company manufacturing the same anti-
TABLE1
AVERAGE PERCENTAGE OF COSTS-SAVED BY SELECTION OF PRODUCTS IN LARGER CONTAINERS OF THE SAME ORAL ANTIBIOTIC FORM AND BRAND NAMES; SIGNIFICANCE OF DIFFERENCE BETWEEN AVERAGE PRICES
|
Significance of Difference |
Average % |
|
|
Antibiotic |
p< . . . |
Cost-Saving |
|
Erythromycin |
.005 |
13 |
|
Amoxicillin |
.001 |
18 |
|
Ampicillin |
.001 |
18 |
|
Tetracycline |
.01 |
29 |
|
Chloramphenicol |
.01 |
22 |
|
Average % of Cost-Saving in all products: 20% |
biotic. This tabulation made it possible to recognize both the most and least expensive forms/containers both under the same and different brand names. A list of 35 items representing the least expensive prod- ucts of the antibiotics studied was thus prepared. The list consisted of seven columns tabulated across each commercial form of the antibiotics; 1) antibiotic's name and the commercial form (i.e., capsules/liquid), 2) dose in mg.s per unit (i.e., 250 mg.s per capsule/125 mg.s per 5 ml.s), 3) quantity of units per container (i.e., 100 capsules or 200 ml.s per bottle), 4) manufacturer's name, 5) availability of the product at the pharmacy, 6) retail price of the product if it is available, 7) retail price of a less expensive corresponding product in the same dose per unit and quantity per container if it is available at the pharmacy. This list was used during interviewing the pharmacies for the availability of the least expensive products listed by the study.
The statistical significance of average differences in prices between the least and most expensive and all other products have been computed for each of the antibiotics.
Availability of the Least Expensive Products
Availability of the least expensive products, retail prices of which were obtained by the manufacturers, was tested in two metropolitan areas of Louisiana. A list of pharmacies for both areas has been prepared
36
JOURNAL VOL 139 NO 1 JANUARY
TABLE 2
AVERAGE PERCENT OF COSTS-SAVED BY SELECTION OF THE LEAST EXPENSIVE PRODUCT; SIGNIFICANCE OF DIFFERENCE BETWEEN THE AVERAGE PRICES FOR THE MOST AND LEAST EXPENSIVE PRODUCTS FOR THE SAME ORAL ANTIBIOTIC FORMS
|
Antibiotic |
Significance of Difference p< . . . |
Average % Cost- Saving |
|
Eyrthromycin |
.001 |
44 |
|
Amoxicillin |
.001 |
69 |
|
Ampicillin |
.001 |
58 |
|
Tetracycline |
.05 |
70 |
|
Chloramphenicol |
.05 |
59 |
|
Average % of Cost-Saving in all products = 60% |
from the lists supplied by the Louisiana Board of Phar- macy and the most recent phone listings (1984). A random sample representing one half of the phar- macies was selected. The 54 pharmacies in the sample were visited and pharmacists interviewed for the availability of the 35 least expensive products listed by the study. They were also asked whether they had less expensive products than the ones listed including the generic drugs.
RESULTS
Responses of the Pharmaceutical Companies
Twelve out of 20 pharmaceutical companies produc- ing the oral antibiotics under study promptly re- sponded to our written communication.32 One com- pany was liquidated and one had merged with another. The response rate was 12/18, 67%. From this information, we were able to study the prices of 91 brand products including generics consisting of 27 standard oral forms in 57 different containers con- taining different amounts.
Price Differentials
Price per mg. of the active ingredient decreased sig- nificantly by an average of 20% for all the products as the number of antibiotic units increased in con- tainers of the same commercial form and brand name
TABLE 3
AVERAGE PERCENTAGE OF COSTS-SAVED BY SELECTING THE LEAST EXPENSIVE PRODUCT FOR A GIVEN COMMERCIAL FORM AMONG ALL PRODUCTS EXCLUDING THE MOST EXPENSIVE ONES; SIGNIFICANCE OF DIFFERENCES
|
Significance of Difference |
Average % |
|
|
Antibiotic |
p< . . . |
Cost- Saving |
|
Erythromycin |
.005 |
39 |
|
Amoxicillin |
.001 |
56 |
|
Ampicillin |
.001 |
53 |
|
Tetracycline |
.05 |
59 |
|
Chloramphenicol |
.05 |
53 |
|
Average % of Cost-Saving in all products = 52% |
(Table 1).
Regardless of brand names, the average price of the most expensive products for a given commercial form was significantly higher by an average of 60% more than the average for the least expensive prod- ucts (Table 2).
The average price for the least expensive prod- ucts for a given commercial form when compared with the average price of all products excluding the most expensive ones was significantly lower by an average of 52% (Table 3).
One unexpected finding was that generic prod- ucts manufactured by some companies were more expensive than the least expensive brand products revealed by the study. These were capsules of 250 mg.s in containers of 100 both for amoxicillin and erythromycin. This finding does not support the views which assume that generic products are less expen- sive than brand products.7
Availability of Least Expensive Products in Pharmacies
Of the 54 pharmacies sampled in both areas, seven (13%) did not wish to participate in the study. There- fore, interviews were undertaken with the remaining 47 (87%) pharmacies. Twelve pharmacies (26%) did ►
JOURNAL VOL 139 NO 1 JANUARY
37
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JOURNAL VOL 139 NO 1 JANUARY
not have any of the products in our list of the least expensive oral antibiotics. The remaining 35 (74%) pharmacies had an average of 3.4 (9.7%) of the prod- ucts listed. Overall availability of the least expensive products in all of the pharmacies studied was 2.5%.
Three pharmacies (6.4%) declined to give the re- tail prices of the products listed, although, they said that they had some of them in stock. None of the pharmacies had products less expensive than the ones listed by the study. The prices of products listed under the least expensive varied greatly among pharmacies. A total of 30% of the pharmacies which had some of the products listed under least expensive gave the same retail price given by the manufacturers. The remaining 70% gave retail prices as much as 331% (average 173%) more than the retail prices of the man- ufacturers.
DISCUSSION
Results of the study show that both dispensing from larger containers without practicing drug-product se- lection and brand interchange excluding generic products can lead to significant cost-savings. How- ever, both of these approaches can be practiced pro- vided that pharmacies have larger containers and less expensive products in stock and the pharmacists are willing to dispense less expensive products. Survey of the pharmacists yielded that only a few of the least expensive products listed in the study were available. These findings raise the question “What factors in- fluence the decision to purchase products in phar- macies?" Some surveys suggest that reputation of the manufacturer, preserver's influence as well as the quality and availability of the product and availability of information on the product play the leading roles.8 One of these factors, "quality of the product" poses challenging questions such as "are there products of low quality in this country in spite of all the controls and regulations enforced by Federal agencies such as FDA?," "do they (pharmacists) have a formal source of scientific information or are they basing their as- sumptions about quality on a few observations or con- sumer complaints?" These questions are in need of answers before the present drug product selection practices can be objectively evaluated.
Survey of the pharmacies showed that price var-
iation among the pharmacies for the same amount of the same drug was as much as 331%. This surprising variation has also been observed in other stud- ies.3' 7, 33 According to Gumbhir and Rodowskas, "these differences are not dependent upon the operational characteristics of pharmacies, but probably are a func- tion of the difference in drug cost to pharmacy."4 Results of the study show that dispensing from larger containers leads to significant cost savings since wholesale prices are apt to decrease as the amounts purchased by the pharmacy increase. This is justifi- able by decreasing costs of manufacturing and in ac- cordance with the general rules of market economy. However, for a given product the amounts purchased by a pharmacy is likely to be dependent on the fre- quency of dispensing that drug. Therefore, a drug which is dispensed only several times a year is not expected to be bought in large quantities and con- tainers. Yet, is this a general practice? Even if this is general practice, it does not necessarily mean that pharmacies purchase those drugs which they dis- pense most in large containers. They may purchase large quantities but in many small containers. As this study has shown price differentials are significant be- tween a variety of containers. These questions under- line the importance of research on the purchasing practices of pharmacies.
Some reports blame the physicians and expect them to prescribe lower priced drugs.7' 34 It will be very unrealistic to expect the physicians to keep an inventory of prices for drugs in this turmoil of a fluc- tuating pharmaceutical market. There are hundreds of brand and generic products and many new ones are being introduced to the market every day. Even if we assume that the physicians can play a role, the actual drug-product selection and the cost-saving process take places at the pharmacies at the discretion of the pharmacists. While at the pharmacies, many factors yet to be uncovered are influential. In short, effective drug product selection leading to potential cost-savings does not seem to be the responsibility of the prescribers and pharmacists only. Both profes- sionals are bound by factors inherent to their practices and do not readily have access to a thorough and updated price listing of the drugs in the market. At the present state of affairs, they neither have a need nor an apparent incentive to maintain such a list of the least expensive products.
JOURNAL VOL 139 NO 1 JANUARY
39
Platt suggests that, governments can play a much more active role in containing health care costs, since no party is willing to do it voluntarily. He does not think that consumer education will play a major role in cost-containment in this environment where ad- vances in diagnosis and treatment are aggressively promoted which in turn significantly increases public interest in these advances.35 Hirsch advocates pro- motion of competition by facilitating informed con- sumer choice.36
The findings of the study as well as these sug- gestions for cost-containment confront us with the following questions in drug product selection: 1) is the information on drug prices and the magnitude of their variation for the same amount of the same drug which can lead to potential cost-saving readily avail- able to all concerned parties, including the con- sumers? 2) can systematically updated provision of such information bring about effective drug-product selection? 3) if so, whose responsibility will it be to provide this information?
The majority of the drug product selection laws were enacted during the last decade. Accumulating experience and pressures both from consumers and third parties as well as the soaring costs of heatlh care are expected to enhance research which will answer the majority of these questions posed in this study. However, one ethical issue remains to be challenged as soon as possible and that is “How long are we going to let the consumers pay for these incredible price differences?" ■
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36. Hirsch BD: Antitrust and medical ethics. JAMA
1983;250(20):2759-2760.
Dr. lyriboz is a fellow in the Department of Pediatrics at Ochsner Medical Institution in Neio Orleans, LA and also with the Department of Health Sciences, School of Health, Physical Education and Recreation at Louisiana State University in Baton Rouge, LA.
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42
JOURNAL VOL 139 NO 1 JANUARY
WEALTH SCIENCE* LIBRARY
ft) JRNAL
OF THE LOUISIANA STATE MEDICAL SOCIETY February 1987
STACKS
Nesidioblastosis: Diagnosis and treatment
WHILE YOU'RE BUSY TAKING CARE OF PATIENTS, WHO TAKES CARE OF YOU?
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(LAMMICO)
is proud to announce the formation of
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A wholly owned subsidiary of LAMMICO
to more fully address the insurance needs of Louisiana physicians.
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EDITOR
M ANNIE D. PAINE, JR, MD
GENERAL MANAGER RENE G. ABADIE
MANAGING EDITOR
BONNIE L. BLUNDELL
CONTRIBUTING EDITOR FRANK J. ILARDI, MD
JOURNAL COMMITTEE
CONWAY S. MAGEE, MD Chairman
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ADVERTISING SALES SISSY SULLIVAN-HANSEN
TOURNAL
OF THE LOUISIANA STATE MEDICAL SOCIETY 1987
VOLUME 139 / NUMBER 2 / FEBRUARY
ARTICLES
Established 1844. Owned and edited by The Journal of the Louisiana State Medical Society, Inc., 1700 Josephine Street, New Orleans, Louisiana 70113-1596.
Copyright 1987 by The Journal of the Loui- siana State Medical Society, Inc.
Subscription price is $12 per year in ad- vance postage paid for the United States; $15 per year for all foreign countries belonging to the Postal Union; $1.50 per
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Advertising: Contact Sissy Sullivan- Hansen, 1700 Josephine Street, New Orleans, LA; (504)561-1033, (800)462-9508.
Postmaster: Send address changes to 1700 Josephine Street, New Orleans, LA 70113-1596.
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David E. Schenk |
22 |
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Patricia C. Moynihan, MD |
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Jerome S. Blackman, MD |
31 |
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40 |
Nesidioblastosis: Diagnosis and treatment
Character traits underlying self-neglect and their connection with heart disease
Advisory opinion of the Medicolegal
Interprofessional Committee
The Journal ISSN 0024-6921 is published monthly at 1700 Josephine Street, New Orleans, LA 70113-1596. Second-class postage paid at New Orleans and at additional mailing offices.
Articles and advertisements published in the Journal are for the interests of its readers and do not represent the official position or endorsement of The Journal of the Louisiana State Medical Society, Inc. or the Louisiana State Medical Society. The Journal reserves the right to make the final decision on all content and advertisements.
DEPARTMENTS
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New Members |
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9 |
ECG of the Month |
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Otolaryngology/Head and Neck Surgery Report |
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Bookshelf |
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2
JOURNAL VOL 139 NO 2 FEBRUARY
NEW MEMBERS
Applications for membership have been received from the follow- ing physicians by the respective parish medical societies as of No- vember 24, 1986. The Louisiana State Medical Society is pleased to welcome:
■ Jefferson
Richard C. Kline, MD, 1514 Jefferson Hwy., New Orleans 70121. Dr. Kline received his medical degree from Louisiana State Uni- versity in New Orleans in 1980. He specializes in gynecologic on- cology.
Carl R. Martino, MD, 4200 Houma Blvd., Metairie 70011. Dr. Mar- tino received his medical degree from Case Western Reserve in 1980. He specializes in diagnostic radiology.
<■ Lafayette
Wilson H. Luy-Tan, MD, 4212 West Congress Street, Lafayette 70506. Dr. Luy-Tan received his medical degree from the University of Philippines in 1979. He specializes in neurology.
Debra R. Zimmerman, MD, 4550 Ambassador Caffery, Lafayette 70505. Dr. Zimmerman received her medical degree from the Uni- versity of Illinois in 1974. She specializes in internal medicine.
Richard W. Zimmerman, MD, 4550 Ambassador Caffery, Lafayette 70505. Dr. Zimmerman received his medical degree from the Uni- versity of Illinois in 1974. He specializes in internal medicine.
■ Natchitoches
Otis R. Barnum, DO, 215 Highway 1 South, Natchitoches 71457. Dr. Barnum received his degree from Kansas City College of Os- teopathy in 1977. He specializes in internal medicine.
■ Orleans
Dennis Kay, MD, 1514 Jefferson Hwy., New Orleans 70121. Dr. Kay received his medical degree from Tulane University in 1981. He specializes in diagnostic radiology.
William M. Swartz, MD, 1430 Tulane Ave., New Orleans 70112. Dr. Swartz received his medical degree from the University of Colorado in 1972. He specializes in plastic surgery.
■ Rapides
Julio E. Iglesias, MD, 431 West Lafayette St., Winnfield 71483. Dr. Iglesias received his medical degree from the National University of Cordoba in 1973. He specializes in general surgery.
Joe H. Rankin, MD, 3330 Masonic Drive, Alexandria 71301. Dr. Rankin received his medical degree from the University of Texas in Houston in 1981. He specializes in radiology.
Fielding C. Sauls, MD, 201 Fourth Street, Alexandria 71301. Dr. Sauls received his medical degree from Louisiana State University in New Orleans in 1977. He specializes in cardiothoracic surgery.
■ St. Tammany
Dorothy H. Banish, MD, Route 1, Box 10-B, Hwy. 21, Covington 70433. Dr. Banish received her medical degree from New York Medical College in 1980. She specializes in internal medicine.
Thomas H. Hall, MD, 1922 Corporate Square, Suite D, Slidell 70458. Dr. Hall received his medical degree from Louisiana State University in New Orleans in 1983. He specializes in internal med- icine.
Michael J. Haas, MD, 2615 N. Causeway Approach, 1-177, Mande- ville 70448. Dr. Haas received his medical degree from Louisiana State University in New Orleans in 1983. He specializes in family practice.
Deborah L. Pickens, MD, 1001 Gause Blvd., Slidell 70458. Dr. Pickens received her medical degree from the University of Ar- kansas in 1981. She specializes in pediatrics.
Ronald D. Sylvest, MD, 1270 North Hwy. 190, Covington 70433. Dr. Sylvest received his medical degree from Louisiana State Uni- versity in New Orleans in 1980. He specializes in orthopaedics.
■ Shreveport
Carol S. Clemons, MD, 2515 Line Avenue, Shreveport 70114. Dr. Clemons received her medical degree from Louisiana State Uni- versity in New Orleans in 1981. She specializes in ophthalmology.
Juanita G. McBeath, MD, 1800 Irving Place, Shreveport 71101. Dr. McBeath received her medical degree from the University of Texas Southwestern Medical School in Dallas in 1983. She specializes in neurology.
■ Terrebonne
Rodney J. Landreneau, MD, 301 Williams Avenue, Houma 70360. Dr. Landreneau received his medical degree from Louisiana State University in New Orleans in 1978. He specializes in general sur- gery.
■ Intern/ Resident Members
EAST BATON ROUGE
Robert L. Crosby III, MD, 711 Concordia, Baton Rouge 70806. Dr. Crosby received his medical degree from the University of Missis- sippi in 1972. He specializes in internal medicine.
Karl G. Haydel, MD, 5825 Airline Hwy., Baton Rouge 70805. Dr. Haydel received his medical degree from Louisiana State University in New Orleans in 1986. He specializes in family practice.
SHREVEPORT
Robert J. Bashaw, MD, 1520 Kings Hwy., Shreveport 71130. Dr. Bashaw received his medical degree from the University of Texas in Galveston inl983. He specializes in ophthalmology.
JOURNAL VOL 139 NO 2 FEBRUARY
7
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JOURNAL VOL 139 NO 2 FEBRUARY
Norton W. Voorhies, MD, Editor
ECG OF THE MONTH
MASQUERADERS
JORGE I. MARTINEZ-LOPEZ, MD
The rhythm strip shown below, precordial lead Vlr belongs to a 63-year-old black woman. It was recorded a few hours after surgery. No other information accompanied the tracing.
What is your diagnosis? Elucidation is on page 11.
JOURNAL VOL 139 NO 2 FEBRUARY
9
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JOURNAL VOL 139 NO 2 FEBRUARY
ECG of the Month
Case presentation is on page 9.
DIAGNOSIS: Sinus tachycardia; intermittent, wide QRS complexes, cause to be established.
Sinus tachycardia, at 107 times a minute, is associated with normal PR, QRS and QT intervals. The QS pat- tern observed in the narrow QRS complexes repre- sents a normal variant and not an old myocardial infarction.
Prominent throughout the rhythm strip are the abnormally wide QRS complexes of identical config- uration, which recur primarily in a trigeminal pattern. Each of the wide QRS complexes is preceded by a P wave — with a very short PR interval — and followed by secondary ST-T wave changes.
The genesis of these wide QRS complexes is the subject of the discussion to follow.
DISCUSSION
It is often difficult to decide whether abnormally wide QRS complexes occur as a result of ventricular ectopic activity or in response to a supraventricular electrical impulse. To make this distinction, it is customary to record long rhythm strips and, in most instances, pre- cordial lead Vj is selected because of its established value in differentiating between complete RBBB, aber- rant ventricular conduction, and ventricular ectopy. Examination of rhythm strips includes a search for atrial activity and analysis of the configuration of the wide QRS complexes. A preceding P wave, if present, is said to be “the most helpful criterion" for distin- guishing between wide QRS complexes of supra- ventricular origin and those caused by ventricular ec- topic activity. However, the presence of a P wave in front of a wide QRS complex does not imply auto- matically that a supraventricular impulse is respon- sible for the wide QRS complex. With respect to the wide QRS itself, it has been shown that certain con- figurations are more likely to be associated with su- praventricular impulses, while others are more likely to indicate a ventricular ectopic origin.
Further examination of the tracing shown above discloses that each of the wide QRS complexes: (a) measures 0.12 sec; (b) has an “atypical" RBBB pattern; (c) is preceded by a P wave — with a very short PR
interval of inconstant length; and (d) has a fixed cou- pling interval with the preceding narrow QRS. Of particular importance, as will be seen later, is the first PR interval that follows the wide QRS complex: it is always longer than all other PR intervals.
In view of the above, the diagnostic possibilities that must be considered to explain the wide QRS com- plexes are three: atrial premature impulses with aber- rant ventricular conduction, intermittent ventricular pre-excitation, and ventricular ectopic activity.
Aberrant ventricular conduction (AVC) is a benign electrophysiological phenomenon that may occur with any supraventricular rhythm in either normal or ab- normal hearts. AVC is dependent upon unequal re- fractory periods of the bundle branches, early impulse formation, or length of the preceding R-R interval. AVC occurs whenever one or more supraventricular impulses arrive early at the intraventricular conduct- ing system, finds one of the bundle branches in a refractory state, and have to propagate to the ventri- cles by way of the intact branch, and then from muscle fiber to muscle fiber. The resulting abnormal propa- gation of the impulse causes a wide, distorted QRS, usually with a classic RBBB pattern.
That the wide QRS complexes present in the trac- ing are not due to AVC caused by atrial premature impulses (API) is supported by the following find- ings. First, measurement of P-P intervals shows that P waves that precede the wide QRS complexes fall at the expected time. Therefore, they are not premature, but sinus P waves. Second, PR intervals for the wide QRS complexes are too short. APIs that find refrac- toriness downgrade are associated with lengthened PR intervals. Third, the configuration of the wide QRS complexes is not consistent with that recorded during AVC. Fourth, no incomplete compensatory pause fol- lows wide QRS complexes. APIs usually have the capacity to enter the sinus node, discharging and re- setting it, resulting in incomplete compensatory pauses.
Ventricular pre-excitation (VP), the second diag- nostic possibility, implies that, in relation to atrial events, some or all of the ventricular muscle is de- polarized earlier by supraventricular impulses than would be expected had the impulse depolarized the ventricles by way of the normal atrioventricular con- ducting system. VP can occur when one or more ac- cessory pathways, which bypass the normal con- ducting system at some point, are present. Typically,
JOURNAL VOL 139 NO 2 FEBRUARY
11
VP causes characteristic changes in the ECG: a short PR interval (p.12 sec or less), a broad QRS complex (0.12 sec or longer), an initial delta wave, and sec- ondary ST-T wave changes. VP can occur intermit- tently and has been reported in 25% to 76% of pa- tients.
The wide QRS complexes in this tracing do not represent intermittent VP. In the first place, the wide QRS complexes do not display a delta wave; nor were any recorded in the other 11 leads. Lastly, the sinus P waves preceding the wide QRS complexes move into and out of the QRS without having any effect in either the configuration or the duration of the QRS. Movement of the sinus P wave is caused by sinus arrhythmia, which also causes the variation in length of the short PR interval.
Ventricular ectopy, therefore, remains as the only viable mechanism responsible for the wide QRS com- plexes. Although ventricular premature impulses (VPI) most often occur in either early or mid-diastole, VPIs can occur late in diastole (end-diastolic). Because end- diastolic VPIs occur so late, they may either intersect the P wave or follow it causing an illusory short PR interval. Observations gleaned from the rhythm strip lend strong support for a ventricular ectopic origin for the wide QRS complexes. The first is the config- uration of the wide QRS complexes: although a so- called RBBB pattern is present, it is significantly dif- ferent from the "classic” appearance of RBBB, and indicates left ventricular ectopic activity. A second finding supporting ventricular ectopy is the length- ening of the first PR interval after each wide QRS. This first interval is always longer than that of sub- sequent PR intervals of narrow QRS complexes. This finding is indirect, but conclusive, evidence in favor of ventricular ectopy and represents concealed retro- grade ventriculo-atrial conduction. Simply stated, this means that the end-diastolic VPI depolarized the ven- tricular musculature anterogradely and, at the same time, was conducted retrogradely causing depolari- zation of the bundle of His and AV node. Therefore, when the next sinus impulse descended toward the ventricles, it encountered partial refractoriness as it traversed the AV node and bundle of His. Because the end-diastolic VPI occurs so late in diastole, it is not capable of totally blocking the subsequent sinus impulse and no compensatory pause — complete or incomplete — occurs.
Masqueraders are relatively common in electro-
cardiography, but the astute interpreter can usually recognize their true identity. Wide QRS complexes preceded by a P wave may masquerade as either AVC or VP, when they really are end-diastolic VPIs. Ac- curate identification is not of intellectual importance, but rather of clinical and therapeutic importance. ■
SELECTED REFERENCES
1 . Schamroth L, Chesler E: Phasic aberrant ventricular conduction. Br Heart J 1963;219-226.
2. Sandler IA, Marriot HJ: The differential morphology of anom- alous ventricular complexes of RBBB-type in Lead Vp Ventricular ectopy versus aberration. Circulation 1965;31:551-556.
3. Gozensky C, Thorne D: Rabbit ears: an aid in distinguishing ventricular ectopy from aberration. Heart Lung 1974;3:634-636.
4. Sabetti K: Distinguishing between ectopic ventricular activity and aberrant ventricular conduction of supraventricular im- pulses. Heart Lung 1979;5:949-952.
5. Klein GJ, Gulamhusein SS: Intermittent pre-excitation in the Wolff-Parkinson-White syndrome. Am J Cardiol 1983;52:292-296.
6. Prystowsky EN, Miles WM, Heger JJ, et al: Pre-excitation syn- dromes: Mechanisms and management. Med Clin North Am 1984;68:831-893.
From the Cardiology Service, Department of Medicine, William Beaumont Army Center, El Paso, TX 79920-5001.
The opinions or assertions contained herein are the private views of the author and are not to be construed as official or as reflecting the views of the Department of the Army or Department of Defense.
12
JOURNAL VOL 139 NO 2 FEBRUARY
OTOLARYNGOLOGY/
HEAD AND NECK SURGERY REPORT
RHINOPHYMA: A SURGICAL MANAGEMENT
MACK L. CHENEY, MD; THOMAS A. GRAVES, MD;
PAUL A. BLAIR, MD
Rhinophyma is a disease of the nose characterized by chronic inflammation and hypertrophy of the skin. The process represents a significant cosmetic deformity and it has been generally considered to be the final stage of acne rosacea. A brief review of the etiology of rhinophyma and our method of surgical management is presented.
Although there is no consensus as to the etiology of rhinophyma, the disease has been associated with excessive alcohol consumption, gastric disor- ders, and the intake of spicy foods.1 However, neither clinical investigation nor past history elicited from pa- tients has substantiated a definite relationship to al- cohol addication. One theory regarding the etiology of acne rosacea has been that in many instances the disease is caused by the organism, Demodex folliculo- rum, which invades the sebaceous glands and folli- cles. Some have reported cures of the disease with the use of parasiticidal ointments alone.2
PATHOLOGY AND PATHOGENESIS
The first stage of acne rosacea is one of erythema which affects the central areas of the face. In the initial stages it is transient, but as the disease progresses it becomes more permanent. Telangiectasia appear on the nose and the medial portions of the cheek. After a variable period of time, the second stage of the disease begins and the face becomes oily and acnei- form lesions of the nose and face appear.
In some instances the third stage of the acne ro- sacea will develop varing in time from a few months ►
JOURNAL VOL 139
NO 2
FEBRUARY
13
Fig 1. Anterior view of rhinophymatous nose.
Fig 2. Posterior view of rhinophymatous nose.
to years. The nasal tip and alae become enlarged dur- ing this stage owing to progressive, benign, but marked hypertrophy of the sebaceous glands, the blood vessels, and connective tissues of the nose. It is at this point in the clinical evolution of this disease that the patient can be diagnosed as having rhino- phyma. Characteristically the nose appears red, rough, and nodular in character with associated telangiec- tasia of the face and nasal region.2
This condition typically develops very slowly over a period ranging from five to 20 years. The course of the disease is chronic and presents no symptoms other than the characteristic cosmetic deformity, however, nasal breathing can be impaired in the advanced stages of this disease.
DIAGNOSIS
Rhinophyma is easily diagnosed in most cases as the patient will have the dull, red, purplish color of the nose with associated multinodular involutions of the alae and nasal tip. Hypertrophy of the tissue of the nose produce lobulated masses varing in size from 3mm to several centimeters. When the disease has become highly developed the nost appears prodigious and is markedly disfigured (Figs l, 2). Microscopi- cally, there is a squamous epithelium with slight hy- perkeratosis, hypertrophy and hyperplasia of the se- baceous glands distended with keratin. There is also squamous cell metaplasia and fibrosis with chronic
(continued to page 17)
14
JOURNAL VOL 139 NO 2 FEBRUARY
Fig 3. Method of loop cauterization of nasal dermis.
Fig 4. Method of nasal dermabrasion.
Fig 5. Nasal contour at completion of dermabra- sion.
(continued from page 14)
inflammation of the dermis.2- 3
SURGICAL TREATMENT
In the treatment of rhinophyma, both surgical and non-surgical measures have been employed. Radia- tion has been used by some but has been of limited effectiveness in treatment.4 It is our feeling that sur- gical management of rhinophyma in early and ad- vanced stages is optimal. Our method of correction will be discussed. Once the diagnosis of rhinophyma is made, the patient is educated as to the disease process and is offered surgical management for cor- rection of the cosmetic deformity. The combination ►
JOURNAL VOL 139 NO 2 FEBRUARY
17
of electrocuatery excision and dermabrasion has proven effective in a series of five cases performed in the last four years at Charity Hospital in New Orleans and the Veterans Administration Hospital in Biloxi.
The loop cautery is used to debulk the lobulated tissue of the dermis and to sculpture the tissue over- lying the nasal cartilages (Fig 3). The dermabrater is used to fine-tune the resection and provide good cos- metic contour of the alae and nasal tip (Figs 4, 5). The nose is then covered with vaseline gauze dressing for a period of approximately two weeks. A light dressing can be employed for the remaining recovery period which will last from three to four weeks. In our hands, this has proved to be an effective method of managing rhinophyma and, although we lack a long term fol- low-up in our five patients, we have had no recur- rence of this cosmetic problem. ■
REFERENCES
1. Pastorek NJ: The Management of Rhinophyma. Otolaryngol Clin North Am 1972;5(October):639-646.
2. Lewis K: Rhinophyma. Plast Reconstr Surg 1959;24(19):190-200.
3. Fisher W: Rhinophyma: Its surgical treatment. Plast Reconstr Surg 1970;45(5):466-470.
4. Elliott R, Hoehn J, Stayman W: Rhinophyma: Surgical refine- ments. Ann Plast Surg 1978;1:298-301.
From the Department of Otolaryngology — Head and Neck Surgery, Tulane University School of Medicine, New Orleans, LA.
Requests for reprints should be sent to Paul A. Blair, MD, Dept, of Otolaryngology — Head and Neck Surgery, 1430 Tulane Avenue, Neiv
Orleans, LA 70112; (504)588-5453.
EAST
f'ST-
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The journal seeks reviews of the following books. Interested physicians should contact Frank J. Ilardi, MD, Book Review Editor, Journal of the LSMS, 5000 Highway 190, Suite D-3, Covington, Louisiana 70433.
BOOKSHELF
CURRENT EMERGENCY THERAPY
Richard Edlich, MD; Daniel Spyker, MD (eds), Aspen Publishers, Inc., Rockville, MD, 1986, 314 pages.
DIMENSIONS OF GRIEF
Steven Shuchter, MD, Jossey-Bass, Inc. Publishers, San Francisco, CA, 1986, 360 pages.
FAMILY PRACTITIONER S GUIDE TO TREATING DEPRESSIVE ILLNESS
Joseph H. Talley, MD, Precept Press, Inc., Chicago, IL, 1986, 303 pages.
MEDICAL ASSESSMENT OF THE ELDERLY SURGICAL PATIENT
Gwen Seymour, MD, Aspen Publishers, Inc., Rock- ville, MD, 1986, 314 pages.
OB/GYN EMERGENCIES: THE FIRST SIXTY MINUTES
Roy Farrell, MD (ed). Aspen Publishers, Inc., Rock- ville, MD 1986, 340 pages.
“DO YOU KNOW A PSYCHIATRIC HOSPITAL WHERE MY CHILD CAN RE TREATED?”
Referring a family to a psychiatric hospital for their child’s treatment can be a difficult decision for any physician. At River Oaks, our staff understands the special needs of both the patient and the family in coping with mental illness, behavior problems, and emotional disorders. River Oaks — a private, 126-bed facility, offers a broad range of programs for the individual.
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For more information on clinical services, admission or referral, contact the Admissions Department, call us collect at (504) 734-1740; Crisis Center, call 733-CARE; Outpatient Clinic 733-5591.
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Gregory P. Roth William R. Sorum, M.D.
Managing Director Clinical Director
THE NEW ORLEANS CENTER FOR PSYCHOTHERAPEUTIC MEDICINE
A Universal Health Services Hospital
JOURNAL VOL 139 NO 2 FEBRUARY
19
ALENDAR
March
March 1-6
IX World Congress of Plastic & Reconstructive Surgery,
New Delhi, India. Contact: Aloke C. Bagchi, Program Coor- dinator, IX World Congress of Plastic Surgery, 6101 N. Talman Ave., PO Box 59577, Chicago, IL 60659; (312)465-8337.
March 1-6
Internal Fixation in Hand Surgery, Vail, Colorado. Contact: American Society for Surgery of the Hand, 3025 South Parker Road, Suite 65, Aurora, CO 80014; (303)755-4588.
March 1-7
Internal Medicine Symposium, Cancun, Mexico. Sponsored by the University of Kansas Medical Center. Contact: Eileen Buttron, Office of Continuing Education, 39th and Rainbow Blvd., Kansas City, KS 66103; (913)588-4494.
March 1-7
Update '87: Office Obstetrics and Gynecology, Shadow Ridge Resort, Park City, Utah. Presented by Scott & White. Contact: Charlene E. Lee, Communications Specialist, Scott & White, 2401 South 31st Street, Temple, TX 76508; (817)774-2821.
March 1-8
Winter Scientific Seminar, Ski Utah for Mardi Gras, Park City, Utah. Offered by the Orleans Parish Medical Services Bureau in conjunction with the Orleans Parish Medical Socie- ty. Contact: OPMS, 1800 Canal Street, New Orlenas, LA 70112; (504)523-2474.
March 2-6
Internal Fixation in Hand Surgery, Vail, Colorado. Spon- sored by the American Society for Surgery of the Hand. Con- tact: American Society for Surgery of the Hand, 3025 South Parker Road, Suite 65, Aurora, CO 80014; (303)755-4588.
March 5-7
2nd International Interdisciplinary Conference on Hyperten- sion in Blacks, Peachtree Plaza Hotel, Atlanta, Georgia. Sponsored by Emory University School of Medicine, American Heart Association, National Heart, Lung and Blood Institute and the Association of Black Cardiologists. Contact: Continuing Medical Education, Emory University School of Medicine, 110 WHSCAB, 1440 Clifton Road, NE, Atlanta, GA 30322; (404)727-5695.
March 8-13
U.S. - Canadian Division of the International Academy of Pathology Annual Meeting, Chicago, Illinois. Contact: Dr. Nathan Kaufman, U.S. - Canadian Division of the Interna- tional Academy of Pathology, Building C, Suite B, 3515 Wheeler Road, Augusta, GA 30909; (404)733-7550.
March 8-13
8th Annual Mammoth Mountain Emergency Medicine Ski Conference, Mammoth Lakes, California. Contact: Medical Conferences, Inc., PO Box 52-B, Newport Beach, CA 92662; (714)650-4156.
March 9-13
Hawaii 87: Critical Issues in Primary Care, Waiohai Hotel, Poipu Beach, Kauai, Hawaii. Sponsored by the Pacific In- stitute of Continuing Medical Education and the Hawaii Medical Association. Contact: Valerie Murray, Pacific In- stitute of Continuing Medical Education, PO Box 1059, Koloa, Kauai, HI 96756; (808)742-7471.
March 12-14
2nd International Conference on Monoclonal Antibody Im- munoconjugates for Cancer, Hotel Inter-Continental, San Diego, California. Contact: UCSD School of Medicine, M-017, Continuing Medical Education, La Jolla, CA 92093; (619)534-3940.
1987 Annual Meeting Louisiana State Medical Society March 12-15, New Orleans
March 14
The Aging Nervous System: Dementia and Behavioral Changes in the Elderly, Fargo, North Dakota. Sponsored by the Neuropsychiatric Institute. Contact: Harry A. Whitaker, PhD, The Neuropsychiatric Institute, 700 First Ave. S, Fargo, ND 58107; (701)235-5354.
March 16-20
The Physician in Management, Seminar I and II, Sheraton Sand Key, Clearwater Beach, Florida. Contact: Sherry Mason, American Academy of Medical Directors, 4830 W. Kennedy Blvd., Suite 648, Tampa, FL 33609; (813)873-2000.
20
JOURNAL VOL 139 NO 2 FEBRUARY
March 18-21
3rd National Leukemia Society of America Symposium,
Town & Country Hotel, San Diego, California. Contact: Medical Programs Dept., Leukemia Society of America, 733 Third Ave., New York, NY 10017; (212)573-8484.
March 19-27
Specialty Series in Primary Care: Cardiology, Infectious Diseases & Endocrinology, Palm Springs Spa Hotel, Palm Springs, California. Contact: UCSD School of Medicine, Con- tinuing Medical Education, M-017, La Jolla, CA 92093; (619)534-3940.
March 20-21
Motor Speech Disorders: Apraxia and Dysarthria, New
Orleans, Louisiana. Sponsored by Alton Ochsner Medical Foundation. Contact: CME Office, Ochsner Foundation, 1516 Jefferson Hwy., New Orleans, LA 70121; (504)838-3702.
March 26-28
Advanced Course on Body Contouring, Los Angeles, Califor- nia. Sponsored by Plastic Surgery Educational Foundation. Contact: PSEF, 233 North Michigan Ave., Suite 1900, Chicago, IL 60601.
March 30 - April 2
Perspectives in Family Practice, King Kamehameah Hotel, Kona, Hawaii. Sponsored by the University of California at Los Angeles. Contact: Dept, of Continuing Education in Health Sciences, UCLA Extension, 10995 LeConte Ave., Los Angeles, CA 90024; (213)825-7186.
March 30 - April 10
Family Practice Review - A Comprehensive Update, Omaha, Nebraska. Sponsored by the University of Nebraska College of Medicine. Contact: Marge Adey, University of Nebraska Medical Center, Center for Continuing Education, 42nd and Dewey Ave., Omaha, NE 68105; (402)559-4152.
April
April 1
What's New in Diabetes, Kansas City, Kansas. Sponsored by the University of Kansas Medical Center. Contact: Eileen Buttron, Office of Continuing Education, University of Kan- sas Medical Center, 39th & Rainbow Blvd., Kansas City, KS 66013; (913)588-4494.
April 1-5
Approaches to Common Hand Problems, Grand Cayman Islands, British West Indies. Sponsored by Plastic Surgery Educational Foundation. Contact: PSEF, 233 North Michigan Ave., Suite 1900, Chicago, IL 60601; (312)856-1818.
April 2-3
Pediatrics, Kansas City, Kansas. Sponsored by the Univer- sity of Kansas Medical Center. Contact: Eileen Buttron, Of- fice of Continuing Education, University of Kansas Medical Center, 39th & Rainbow Blvd., Kansas City, KS 66103; (913)588-4484.
April 2-5
Rhinoplasty: Nasal Aesthetic and Reconstructive Surgery,
Indianapolis, Indiana. Sponsored by the American Academy of Facial Plastic and Reconstructive Surgery, Indiana Univer- sity School of Medicine. Contact: AAFPRS Foundation, 1101 Vermont Ave. NW, Suite 404, Washington, DC 20005; (202)842-4500.
April 6-8
Newborn Screening for Sickle Cell Disease and Other Hemoglobinopathies, Bethesda, Maryland. Sponsored by the National Heart, Lung, and Blood Institute; the National Institute of Child Health and Human Development; Genetic Diseases Branch of the Health Resources and Services Ad- ministration; and the NIH Office of Medical Applications of Research. Contact: Ms. Nancy Cowan, Prospect Associates, 1801 Rockville Pike, Suite 500, Rockville, MD 20852; (301)486-6555.
April 10-11
Hypertension: New Directions, Lexington, Kentucky. Con- tact: Joy Greene, Continuing Medical Education, 132 College of Medicine Office Building, University of Kentucky, Lex- ington, KY 50536-0086; (606)233-5161.
April 22-25
Update on Surgery of the Hand and Wrist, Sea Pines, Hilton Head, South Carolina. Contact: American Society for Surgery of the Hand, 3025 South Parker Road, Suite 65, Aurora, CO 80014; (303)755-4588.
April 24-25
Contemporary Pediatrics for the Practicing Physician, Lex- ington, Kentucky. Contact: Joy Greene, Continuing Medical Education, 132 College of Medicine Office Building, Univer- sity of Kentucky, Lexington, KY 50536-0086; (606)233-5161.
JOURNAL VOL 139 NO 2 FEBRUARY
21
NESIDIOBLASTOSIS: DIAGNOSIS AND TREATMENT
22
JOURNAL VOL 139 NO 2 FEBRUARY
Nesidioblastosis, a congenital pancreatic beta-cell hyperplasia, is a condition which results in severe central nervous system damage if not diagnosed early. A review of the current literature on the diagnosis and treatment of nesidioblastosis was conducted and four recent cases were reviewed.
Long term medical management was found to be ineffective and a near total pancreatectomy is
recommended.
Nesidioblastosis is a congenital diffuse hyperpla- sia of the pancreatic beta cells. Clinical symp- tomology results from severe hypoglycemia second- ary to hyperinsulinemia and can lead to permanent mental retardation. If nesidioblastosis is detected earlv enough, this retardation can be prevented through rapid and aggressive treatment. However, the large degree of variation in clinical presentation often leads to a delay of treatment or misdiagnosis. Four cases of this condition are reviewed as well as recent literature on its differential diagnosis. Preferred treatment, which is now considered to be by surgical rather than medical means is also discussed.
DIFFERENTIAL DIAGNOSIS
Typically the nesidioblastic child will present during the first six months of life, often within the first week. Signs and symptoms may be less obvious, and even absent, in newborns and infants.1 Svmptoms will be the same as those for hypoglycemia and can include, in order of frequency of clinical presentation, jitteri- ness, tremors, cyanotic episodes, apathy, convul- sions, intermittant apneic spells, weakness, high- pitched cries, headache, limpness, lethargy, difficulty feeding, eye rolling, twitching, mental confusion, sweating, pallor, hypothermia, and cardiac arrest.2
Samples of blood should be drawn during the initial hypoglycemic episode and evaluated for glu- cose. The definition of hypoglycemia is a determi- nation in at least two separate instances of plasma glucose (PG) levels to be <35 mg% in term infants during the first 72 hours after birth and <45 mg% subsequently. Premature infants and children past infancy are hypoglycemic with PG levels <25 mg% and <50 mg% respectively.3
Upon diagnosis of hypoglvcemia, medical man- agement should be initiated immediately for main-
tenance of normal plasma glucose, as even repeated subclinical episodes may cause brain damage.4 Med- ical management may be accomplished by frequent oral feedings, dextrose IV, or subcutaneous injections of epinephrine. Epinephrine is preferable to gluco- corticoids, glucan, ACTH, or GH because, though its effects mav be transient, it inhibits insulin secretion rather than antagonizing the action of insulin.3
Nesidioblastic infants have inappropriately high levels of insulin and low levels of ketones. Clinically, a single finding of all of the following plasma values in the presence of PG levels of <40 mg% will be di- agnostic for the condition: insulin >12.1 uU/ml, B- Hvdroxybutyrate <1.1 mM, and FFAs <0.46 mM.5 Additional findings can include a requirement for high levels of IV glucose to keep plasma levels normal (up to 20 mg/kg/min), a similar physical appearance to infants of diabetic mothers, and an increased depo- sition of fat placing these infants in the upper per- centile ranks of birth weight.6 It must be stressed, however, that these infants do not present a unified or specific svmptomology. Tremendous variation may be seen between affected individuals, with insulin values varying enormously in individual patients.
It is often more effective to diagnose nesidio- blastosis by the elimination of other possible path- ologies. The following should be considered in the diagnosis of nesidioblastosis:
A) The patient history should eliminate the pos- sibility of erythroblastosis fetalis, diabetes, ges- tational diabetes,2 or oral hypoglycemic agents.1
B) Adrenal insufficiency or hypopituitarism may be ruled out if normal levels of GH, cortisol, ACTH, and thyroxine are present.6-7
C) Disorders of glycogen breakdown and syn- thesis may be differentiated from nesidioblas- tosis in that nesidioblastic children will show a rise in glucose of 20-25 mg% in response to glu- cagon 1 mg IM even when hypoglycemic.8
D) Inborn errors as in amino acid or glucose metabolism, types I, III, IV glycogen storage dis- ease, glactosemia, gluconeogenesis, fructose 1-6 diphosphatase deficiency, and fructose in- tolerance all may be eliminated from consider- ation if persistent hypoglycemia does not exhibit hepatomegaly. The urine should show no ke- tones, reducing substances, or amino acids, nor should there be high levels of lactic acid or am-
JOURNAL VOL 139 NO 2 FEBRUARY
23
monia in the blood.4- 7 The pH should be normal with no metabolic ketosis or acidosis.1 E) Severe tolerance testing has not been found to be necessary for diagnosis. Leucine and tol- butamide testing can cause severe hypoglycemic episodes. If a newborn requires IV glucose levels higher than 10 mg/kg/min for stabilization, hy- perinsulinemia should be expected.3- 8- 9
TREATMENT
Nesidioblastosis should be treated as aggressively and rapidly as possible.9 The intensity of treatment ap- pears to be a large factor in the prevention of brain damage10 and a positive correlation has been observed between the delay of surgical treatment and conse- quent mental retardation.3 Initial medical manage- ment in most cases entails IV dextrose and diazoxide. However, long-term medical management with hy- drocortisone, diazoxide, chlorothiazide, phenytoin, propranolol, and glucagon have all been found to be ineffective.8
Current literature expresses a general agreement on the necessity of surgical intervention.1 Pancrea- tectomy should be performed in all cases in which an adenoma is not palpable. Angiography has not been found useful in the localization of adenomas in very young children, and since it increases their risk of complications, it is not recommended.1- 7 The pan- createctomy should be of sufficient degree to avoid repeated operations.9 Hamilton evaluated 45 cases given sub-total pancreatectomy and found that 12 of these were ineffective.10 Schiller reported similar find- ings with two of seven patients needing further sur- gery. Current research indicates that a near-total (95%) pancreatectomy should be performed for best re- sults.3- 8- 10- 11 A few studies indicate that a total pan- createctomy may be necessary1- 4- 11 and that patients may be easily managed post-operatively by insulin and pancreatic enzyme supplements.11
CASE STUDIES
Casel: K.S. initially presented within the first 24 hours post partum. Blood glucose levels were <45 mg%. D12 5 was given to stabilize the infant's blood glucose and the patient was released after three days. That evening the patient was hospitalized with signs of jitteriness and lethargy in conjunction with BPG of 20 mg%. D15 and decadron 1 mg q 6 hours were started
and continued for the next three days. In order to stabilize blood glucose, IV levels were increased to D20 and on to a peripheral hyperalimentation solution. Insulin levels on two separate days were 70 and 55. All other lab tests were normal. Diazoxide was given initially at a dose of 12 mk/kg/day. This was increased to 18 mg/kg/day with IV D12 5 to keep glucose levels constant. A 98% pancreatectomy was performed and post operative hypoglycemia was still present as in- dicated by the high levels of diazoxide and IV glucose still necessary. A total pancreatectomy was then per- formed with .5 u insulin being necessary post oper- atively. The child was discharged nine days later with a blood glucose of 94 mg% and no medications.
Case 2: D.S. The first day post partum this infant had a seizure, became limp and had a blood glucose level of 5 mg%. IV glucose and decadron Vi mg qid were given and then tapered off. The infant was dis- charged at 28 days but was admitted two days later with a dextrostix of 25 mg% . A leucine challenge test showed a large increase in insulin with a correspond- ing drop in glucose. Leucine intolerance was sus- pected and the child was released on a low leucine diet. The patient was readmitted two months later after having repeated seizures and blood glucose lev- els under 45 mg%. Diazoxide treatment was initiated at 10 mg/kg/day and was raised to 20 mg/kg/day but remained ineffective. A 90% to 95% pancreatectomy was then performed. Post operatively IV glucose and doses of diazoxide up to 25 mg/kg/day were still nec- essary and consequently a 98% pancreatectomy was performed. There were no complications and the child was released with only a pancreatic enzyme supple- ment to be given after feedings.
Case 3: This infant, H.M., was delivered having a blood glucose level under 10 mg%. The serum in- sulin was found to be 74 u/ml. Diazoxide treatment was unsuccessful at maintaining a satisfactory blood glucose level and consequently a 98% pancreatectomy was performed. The child was discharged three days later. Three months post operatively the child again presented hypoglycemic symptoms. Medical man- agement was unable to stabilize the blood glucose and a 99% pancreatectomy was performed. The child was discharged with controlled insulin dependent dia- betes secondary to 99% pancreatectomy.
Case 4: H.K. was brought in at the age of four
(continued to page 29)
24
JOURNAL VOL 139 NO 2 FEBRUARY
REFERENCES
(continued from page 24)
with no referring physician. A detailed history re- vealed that he had been diagnosed as hypoglycemic since the age of one year. The hypoglycemia had man- ifested itself since infancy as brief episodes before breakfast in which he would become clammy, grey, and sleepy. If fed he would wake up, otherwise he would sleep for up to three hours. These episodes occurred approximately every two weeks and in- creased to multiple apneic periods per day. This was treated with phenobarbital. An extensive endocrine evaluation failed to identify the etiology and a diag- nosis was made of idiopathic hypoglycemia. Doses of diazoxide were initiated with a later change to ephed- rine. This only partially controlled the seizure activity.
The child was later readmitted and a sleep-dep- rivation EEG conducted. The patient was diagnosed as having minor motor seizures secondary to CNS damage from years of untreated hypoglycemia. En- docrine tests again revealed no etiology for the hy- poglycemia but they indicated that the plasma insulin levels exhibited during hypoglycemia episodes varied enormously. This suggested inappropriate pancreatic responses that could possibly be due to an adenoma. Tests indicated that cortisol, ACTH, and thyroxine were normal as were the abdominal CAT scan, ultra- sound, and the pancreatic arteriogram. The hypo- glycemia showed poor responsiveness to medical management and consequently a near total 95% pan- createctomy was performed. The child was then re- leased on diazoxide, pen vee-k and depakene. The diazoxide maintenance was later stopped, with de- pakene continued for the control of minor motor sei- zures.
DISCUSSION
The cases reviewed for this paper all confirmed the information presented previously. Delayed diagnosis and treatment of nesidioblastosis may cause irrever- sible CNS damage. Long-term medical management has not been found to be effective and should only be used to maintain the patient until a confirmation of the diagnosis may be made and a near-total pan- createctomy performed. It should be noted that Case 1 and Case 2 were cousins. ■
1. Tsalikian E, Haymond M: Hypoglycemic Disorders, Service FJ (ed). Boston, G.K. Hall Medical Publications, 1983, pp 35-71.
2. Behrman R, Vaugh: Nelson Textbook of Pediatrics. Philadelphia, W. B. Saunders Co., 1983, pp 397-398, 1421-1431.
3. Thomas C, Underwood L, Carney C, et al: Neonatal and in- fantile hypoglycemia due to insulin excess. Ann Surg 1977, 185:505-516.
4. Schiller M, Krausz M, Meyer S, et al: Neonatal hyperinsulin- ism, surgical and pathologic considerations. J Pediatr Surg 1980; 15:16-20.
5. Stanley C, Baker L: Hyperinsulinism in infancy: Diagnosis by demonstration of abnormal response to fasting hypoglycemia. Pediatrics 1975;57:702-711.
6. Aynsley-Green A: Nesidioblastosis of the pancreas in infancy. Dev Med Child Neurol 1981;23:372-379.
7. Scully R, Galdabini ], McNeely B: Case reports of the Massa- chusetts General Hospital. N Engl J Med 1978;299:241-248.
8. Aynsley-Green A, Polak J, Bloom S, et al: Nesidioblastosis of the pancreas: Definition of the syndrome and the management of severe neonatal hyperinsulinic hypoglycemia. Arch Dis Child 1981;56:496-508.
9. Carcassone M, Delarue A, Letourneau J: Surgical treatment of organic pancreatic hypoglycemia in the pediatric age. J Pediatr Surg 1983;18:75-79.
10. Hamilton J, Baker L, Kaye R, Koop E: Subtotal pancreatectomy in the management of severe persistant idiopathic hypogly- cemia in children. Pediatrics 1967;39-49-58.
11. Harkin A, Filler R, AuRuskin T, et al: The role of total pan- createctomy in the treatment of unremitting hypoglycemia of infancy. J Pediatr Surg 1971;6:284-289.
Requests for reprints should be sent to Dr. Moynihan, Dept, of Surgery, Tulane University School of Medicine, 1430 Tulane Ave.,
New Orleans, LA 70112.
JOURNAL VOL 139 NO 2 FEBRUARY
29
A MARKETING STRATEGY THAT WILL COST YOU ONLY $50 A YEAR.
MARKETING and practice management experts agree that communication with patients is the key to a successful practice. One of the best tools in patient com- munication is the patient newsletter. Yet, most physicians don't have the time or staff to publish a newsletter of their own.
PH YSICIA NS' FOOTNOTES is an easy, inexpensive way to personally communicate with your patients. Physicians' Footnotes is a bimonthly newsletter providing a number of health tips about a variety of topics and is presented in a short, easy-to- read format. Its design is eye-catching and its content is interesting and relevant. Space is also provided for you to personalize the newsletter with your name or group's name.
AS A SUBSCRIBER to Physicians' Footnotes, you will receive a designated supply of the newsletter bimonthly for one set fee.
IF YOU ARE INTERESTED in subscribing to Physicians' Footnotes for 1987, return the order form below. If you have any questions concerning Physicians' Footnotes, or would like a sample copy, please contact Bonnie Blundell in the LSMS Depart- ment of Public Affairs, (504)561-1 033, (800)288-971 1 wait for dial tone, then dial 576.
IL/lLCLCini
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CHARACTER TRAITS UNDERLYING SELF-NEGLECT AND THEIR CONNECTION WITH HEART DISEASE
JEROME S. BLACKMAN, MD
Many of the so-called risk factors for coronary artery disease result from self-neglect: smoking, overeating, overdrinking, underexercising. Although internists and cardiologists attempt to educate their patients and the general public to these factors, some people continue to ignore the advice. A variety of character problems cause the identical self-neglectful behavior. Omnipotence refers to a fixed defect. Grandiosity describes compensation for feelings of inadequacy. Counterphobic defines “gamblers” who defy danger. The prognosis for treatment of the character pathology varies with the etiology.
Omnipotence is often untreatable. Grandiosity and counterphobic conditions, however, have responded to a psychoanalytic approach that elucidates the individual's need for such unsafe
personality traits.
Since the Type A personality was first described by Friedman and Rosenman,1 personality struc- ture has been viewed statistically in relation to cor- onary artery disease. Remarkably, this subject has been of little interest in the psychoanalytic literature. The general psychiatry literature deals primarily with the cardiotoxic effects of antidepressant drugs pre- scribed after myocardial infarction.
Aside from heredity, nutrition and predisposing illnesses, the risk factors for coronary artery disease — smoking, drinking, overeating and underexercis- ing — are evidence of self-neglect in terms of health. Although there are many reasons such self-destruc- tive habits may develop, in this preliminary com- munication I will discuss three areas in character func- tioning that contribute: omnipotence, grandiosity, and counterphobic traits.
THE BEHAVIOR
Omnipotence, grandiosity and counterphobic traits may all present with exactly the same behavior. The person either does not perceive dangers or denies the consequences of his actions. For example, a patient may deny the risks of smoking, or admit to the danger but feel heart disease will not ensue; regardless, the smoking persists.
Social attitudes may contribute to such notions. Many American children are raised with an encour- agement that sounds something like, "You can be
JOURNAL VOL 139
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FEBRUARY
31
anything you want if you put your mind to it." If this suggestion is not tempered, children can grow up with overestimations of their capacities and under- estimations of their vulnerabilities. On occasion, such feelings can interfere with success. But in other in- stances, success may reinforce self-aggrandizement, and lead to further success.
There are patients, who, after having a coronary occlusion, will not stop overeating, oversmoking, or underexercising. They listen to the doctor, but pay no attention. Due to pathological character traits, they will not heed the AMA's Guide to Heart Care: "A men- tal tug in the form of a conscious reminder to relax, is not only good advice, but good medicine."2
OMNIPOTENCE
Omnipotence occurs due to developmental delay. It is first normally noticed in toddlers around the age of one year, when the world becomes available to them through upright locomotion. The child this age will "get into" anything, requiring the house to be "childproofed." Only slowly does the child learn fall- ing on the floor hurts or that touching certain things will annoy the parents. Hopefully, the child's contact with reality, after a while, should convince him of his vulnerability.
Under certain circumstances, however, well- meaning parents unwittingly encourage retention of omnipotence by idealizing their child, by blaming the environment (and not clumsiness) for any pain or by not setting limits. As the child develops, residual feel- ings of invulnerability can be reinforced if the child is successful in various endeavors. For example, those who excel in sports may begin to feel that they are extremely powerful and untouchable. Various boxers and football players who felt they were "the greatest" got severely hurt because their omnipotence outlived their abilities.
Social success may likewise enhance magical thoughts of power to control others and the environ- ment. Omnipotent people react to any rejection or limitation as though it were an attack, and blame the outside world. Those who excel in intellectual spheres may condescend.
Omnipotence needs to be modulated before the grade school years. If not, there may be uneven de- velopment of conscience. Rigid expectations may de- velop of self and others in work situations, and blam-
ing others for failures is a common sequela. In intimate relationships, a sense of fairness, flexibility or re- sponsibility may be lacking. These patients refuse ad- vice, are very hard to manage after a coronary, and have a poor psychiatric prognosis.
GRANDIOSITY
Grandiosity is somewhat different from omnipotence in that it is a reparative mechanism. During childhood and adolescence, different phases of development cause children to develop feelings of inadequacy, de- riving from, for example: 1) actual limitations in ability that are perceived by the child realistically; 2) the child incorporating criticisms from parents; 3) ideals and goals that are too exalted as compared with abilities; or 4) a sense of heightened expectation and self-crit- icism due to the omission of any modulating influence from the parents.
The notion of invulnerability develops, here, as a way of not having to face one's perceived inade- quacies. Such a defensive posture may then be uti- lized to manage a variety of emotions generated by traumata later in life.
Case 1
A 55-year-old, successful, self-made man had con- quered self-esteem problems through development of exaggerated ideas of power and invulnerability. He, therefore, maintained habits of heavy drinking and smoking. Chest pain brought him to the cardiologist. Angiography indicated only a slight narrowing in one branch of a major artery, and surgery was considered unnecessary. However, he was admonished to stop smoking and drinking, to start eating less, to decrease weight, decrease his cholesterol level, and to begin exercise.
The patient's reaction to finding out about the "defect" in his heart, albeit a slight one, was to go into a severe depression and be found by his wife sitting in the living room, staring into space, for the better part of a week. He did quit smoking and drink- ing, but he had difficulty tolerating the notion that he now had any sort of bodily damage whatsoever. Old feelings of inadequacy were unearthed by the confrontation with his heart disease.
Case 2
A 29-year-old man had no evidence of heart disease whatsoever. He did have chest pain, but angiogra-
32
JOURNAL VOL 139 NO 2 FEBRUARY
phy, echocardiography, and ECG were negative.
During psychoanalytic treatment, he insisted for some time that he had heart disease the internist and radiologist were simply missing. When I confronted him with his apparent belief that he knew more than these doctors, he at first objected. As therapy pro- gressed, however, the patient drew attention to spe- cific subject areas where he considered himself an expert. He would attempt to demonstrate my inept- itude in these areas, and then kid me about having gaps in my "supposedly" superior education.
I was then able to interpret to him that his ap- parent trust in the intelligence of doctors, including me, was a reversal (projection) of his own exalted self- appraisal. Therefore, when doctors told him some- thing, he did not believe them because he uncon- sciously considered himself smarter. In response to my interpretation, he recalled that after his grand- mother, with whom he had lived for long stretches of time, took him to the doctor, she would look in her own home-remedy books or an almanac, and treat the boy accordingly. He had used this history to ra- tionalize not finishing his education, but still harbored inadequate feelings from not finishing graduate school. The identification with his grandiose grandmother had contributed to his lack of motivation to complete his studies: he had felt he did not have to study to get through, due to his "superior" intellect.
COUNTERPHOBIC PHENOMENA
Counterphobics harbor a series of intense fears, usu- ally including a fear of death. They manage these through what can best be described as dare-devil or gambling behaviors. Each time they risk their lives and live through it, they feel more confident.
An interesting example of this was a pilot who admitted he had a life-long fear of heights. He was not afraid to get on airplanes, but he could not walk near the railing on the roof of a tall building. His interest in flying was a late-developing counterpho- bic defense against chronic acrophobia.
In relation to heart disease, the counterphobic person is terrified of death, but dares death to take him by smoking and overeating. Such people often joke that their lungs are stronger than others, that they will last longer, or that their drinking is just "a risk I'm willing to take." Their fear of losing control
may cause a counterphobic defense regarding time: if they can control the advent of their own death through giving themselves a physical illness, they may feel relieved of the anxiety of dying without warning.
Case 3
A 66-year-old man, who had had a myocardial in- farction, suddenly started taking long walks through- out his neighborhood in the middle of the night. He was referred after his wife awakened one night, found him gone and called his doctor.
Mental status examination indicated no organ- icity. Rather, the patient explained that walking out made him feel safer. Because of the counterphobic diagnosis, brief psychoanalytic psychotherapy was instituted.
The first task was to explore what this man felt safe from. He became highly anxious while in bed, thinking "the walls are closing in." This claustopho- bia developed just after his coronary. He also revealed he was afraid of sitting still, because when he stood up he got dizzy. I interpreted that his running out protected him from facing some special fears about things closing in and about getting dizzy. He re- sponded, "I'm afraid I'm going to die."
He associated the walls closing in with his heart caving in, and the dizziness made him feel he would die imminently. He cried as he admitted he had been too ashamed to allow himself to express his fear of dying previously. I then determined, through con- sultation with his internist, that the dizziness was due to orthostatic hypotension, and advised him to stand up more slowly. His internist reassured him that the heart would not collapse and that death was not im- mediately upon him.
Brief psychoanalytically-oriented therapy, con- sisting of 12 sessions, unearthed the acute meanings of his counterphobic and phobic symptoms. The walking allowed him to face his fears more directly and obtain appropriate management. He lived peace- fully for another two years, according to follow-up from his internist.
SUMMARY
Clinical data suggest that people with certain types of personalities tend to ignore the well-known, con- trollable risk factors for coronary artery disease: over- weight, excess alcohol intake, smoking, and lack of ►
JOURNAL VOL 139 NO 2 FEBRUARY
33
SPECIFY
exercise. Such self-destructive habit patterns are at times the result of pathological character traits: om- nipotence brought about by developmental delay; grandiosity defending against feelings of inadequacy; and counterphobic traits operating to master fears of death. Psychoanalytic techniques have proven useful in helping some patients both to overcome such prob- lems and to better cooperate with cardiologic man- agement. ■
REFERENCES
1. Friedman M, Rosenman: Type A Behavior and Your Heart. New York, Fawcett, Columbine Inc., 1981.
2. American Medical Association, Guide to Heart Care, New York, Random blouse, 1984.
Mills
ADDRESS
%u*Trk-s-
Z&
Z>a»
Dr. Blackman, formerly clinical assistant professor of psychiatry at Tulane Medical School in New Orleans, LA, is now affiliated with Psychiatric Associates of Tidewater in Virginia Beach, VA.
Requests for reprints should be sent to Dr. Blackman, do P.A.T., 1020 Tirst Colonial Road, Virginia Beach, VA 23454.
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34
Each capsule contains 5 mg chlordiazepoxide HC1 and 2.5 mg didinium bromide
Please consult complete prescribing information, a summary of which follows:
Indications: Based on a review of this drug by the National Acad- emy of Sciences— National Research Council and/or other informa- tion, FDA has classified the indications as follows:
“Possibly” effective: as adjunctive therapy in the treatment of peptic ulcer and in the treatment of the irritable bowel syndrome (irritable colon, spastic colon, mucous colitis) and acute enterocolitis.
Final classification of the less-than-effective indications requires fur- ther investigation.
Contraindications: Glaucoma; prostatic hypertrophy, benign bladder neck obstruction; hypersensitivity to chlordiazepoxide HC1 and/or clidinium Br.
Warnings: Caution patients about possible combined effects with alco- hol and other CNS depressants, and against hazardous occupations requiring complete mental alertness (e.g., operating machinery, driving). Physical and psychological dependence rarely reported on recommended doses, but use caution in administering Librium® (chlordiazepoxide HC1/ Roche) to known addiction-prone individuals or those who might increase dosage; withdrawal symptoms (including convulsions) reported following discontinuation of tne drug.
Usage in Pregnancy: Use of minor tranquilizers during first trimester should almost always be avoided because of increased risk of congenital malformations as suggested in several studies. Consider possibility of pregnancy when instituting therapy.
Advise patients to discuss therapy if they intend to or do become pregnant.
As with all anticholinergics, inhibition of lactation may occur.
Precautions: In elderly and debilitated, limit dosage to smallest effective amount to preclude ataxia, oversedation, confusion (no more than 2 capsules/day initially; increase gradually as needed and tolerated). Though generally not recommended, if combination therapy with other psychotropics seems indicated, carefully consider pharmacology of agents, particularly potentiating drugs such as MAO inhibitors, pheno- thiazines. Observe usual precautions in presence of impaired renal or hepatic function. Paradoxical reactions reported in psychiatric patients. Employ usual precautions in treating anxiety states with evidence of impending depression; suicidal tendencies may be present and protective measures necessary. Variable effects on blood coagulation reported very rarely in patients receiving the drug and oral anticoagulants; causal rela- tionship not established.
Adverse Reactions: No side effects or manifestations not seen with either compound alone reported with Librax. When chlordiazepoxide HC1 is used alone, drowsiness, ataxia, confusion may occur, especially in elderly and debilitated; avoidable in most cases by proper dosage adjustment, but also occasionally observed at lower dosage ranges. Syn- cope reported in a few instances. Also encountered: isolated instances of skin eruptions, edema, minor menstrual irregularities, nausea and con- stipation, extrapyramidal symptoms, increased and decreased libido — all infrequent, generally controlled with dosage reduction; changes in EEG patterns may appear during and after treatment; blood dyscrasias (including agranulocytosis), jaundice, hepatic dysfunction reported occasionally with chlordiazepoxide HCI, making periodic blood counts and liver function tests advisable during protracted therapy. Adverse effects reported with Librax typical of anticholinergic agents, i.e., dry- ness of mouth, blurring of vision, urinary hesitancy, constipation. Con- stipation has occurred most often when Librax therapy is combined with other spasmolytics and/or low residue diets.
Roche Products Inc. Manati, Puerto Rico 00701
Prevent recurrences month after month
ZOVIRAX
(acydovir)
CAPSULES
Brief Summary
INDICATIONS AND USAGE: Zovirax Cap sules are indicated for the treatment of initial episodes and the management of recurrent epi- sodes of genital herpes in certain patients.
The severity of disease is variable depending upon the immune status of the patient, the fre- quency and duration of episodes, and the degree of cutaneous or systemic involvement. These factors should determine patient management, which may include symptomatic support and counseling only, or the institution of specific therapy. The physical, emotional and psycho- social difficulties posed by herpes infections as well as the degree of debilitation, particularly in immunocompromised patients, are unique for each patient, and the physician should deter- mine therapeutic alternatives based on his or her understanding of the individual patient’s needs. Thus Zovirax Capsules are not appropri- ate in treating all genital herpes infections. The following guidelines may be useful in weighing the benefit/risk considerations in specific disease categories:
First Episodes (primary and nonprimary infec- tions — commonly known as initial genital herpes):
Double-blind, placebo-controlled studies have demonstrated that orally administered Zovirax significantly reduced the duration of acute infec- tion (detection of virus in lesions by tissue cul- ture) and lesion healing. The duration of pain and new lesion formation was decreased in some patient groups. The promptness of initiation of therapy and/or the patient’s prior exposure to Herpes simplex virus may influence the degree of benefit from therapy. Patients with mild disease may derive less benefit than those with more severe episodes. In patients with ex- tremely severe episodes, in which prostration, central nervous system involvement, urinary retention or inability to take oral medication re- quire hospitalization and more aggressive man- agement, therapy may be best initiated with intravenous Zovirax.
Recurrent Episodes:
Double-blind, placebo-controlled studies in patients with frequent recurrences (6 or more episodes per year) have shown that Zovirax Capsules given for 4 to 6 months prevented or reduced the frequency and/or severity of recur- rences in greater than 95% of patients. Clinical recurrences were prevented in 40 to 75% of pa- tients. Some patients experienced increased severity of the first episode following cessation of therapy; the severity of subsequent episodes and the effect on the natural history of the disease are still under study.
The safety and efficacy of orally administered acyclovir in the suppression of frequent episodes of genital herpes have been established only for up to 6 months. Chronic suppressive therapy is most appropriate when, in the judgement of the physician, the benefits of such a regimen out- weigh known or potential adverse effects. In general, Zovirax Capsules should not be used for the suppression of recurrent disease in mildly affected patients. Unanswered questions con- cerning the human relevance of in vitro muta- genicity studies and reproductive toxicity studies in animals given very high doses of acy- clovir for short periods (see Carcinogenesis, Mutagenesis, Impairment of Fertility) should be borne in mind when designing long-term man- agement for individual patients. Discussion of these issues with patients will provide them the opportunity to weigh the potential for toxicity against the severity of their disease. Thus, this regimen should be considered only for appropri- ate patients and only for six months until the results of ongoing studies allow a more precise evaluation of the benefit/risk assessment of prolonged therapy.
Limited studies have shown that there are cer- tain patients for whom intermittent short-term treatment of recurrent episodes is effective. This
approach may be more appropriate than a sup- pressive regimen in patients with infrequent recurrences.
Immunocompromised patients with recurrent herpes infections can be treated with either intermittent or chronic suppressive therapy. Clinically significant resistance, although rare, is more likely to be seen with prolonged or re- peated therapy in severely immunocompromised patients with active lesions. CONTRAINDICATIONS: Zovirax Capsules are contraindicated for patients who develop hypersensitivity or intolerance to the compo- nents of the formulation.
WARNINGS: Zovirax Capsules are intended for oral ingestion only.
PRECAUTIONS: General: Zovirax has caused decreased spermatogenesis at high doses in some animals and mutagenesis in some acute studies at high concentrations of drug (see PRECAU- TIONS — Carcinogenesis, Mutagenesis, Impairment of Fertility). The recommended dos- age and length of treatment should not be ex- ceeded (see DOSAGE AND ADMINISTRATION).
Exposure of Herpes simplex isolates to acy- clovir in vitro can lead to the emergence of less sensitive viruses. The possibility of the appear- ance of less sensitive viruses in man must be borne in mind when treating patients. The rela- tionship between the in vitro sensitivity of Herpes simplex virus to acyclovir and clinical response to therapy has yet to be established.
Because of the possibility that less sensitive virus may be selected in patients who are receiv- ing acyclovir, all patients should be advised to take particular care to avoid potential transmis- sion of virus if active lesions are present while they are on therapy. In severely immunocompro- mised patients, the physician should be aware that prolonged or repeated courses of acyclovir may result in selection of resistant viruses which may not fully respond to continued acy- clovir therapy.
Drug Interactions: Co-administration of pro- benecid with intravenous acyclovir has been shown to increase the mean half-life and the area under the concentration-time curve. Urinary excretion and renal clearance were correspondingly reduced.
Carcinogenesis, Mutagenesis, Impairment of Fertility: Acyclovir was tested in lifetime bioassays in rats and mice at single daily doses of 50, 150 and 450 mg/kg given by gavage. There was no statistically significant difference in the incidence of tumors between treated and control animals, nor did acyclovir shorten the latency of tumors. In 2 in vitro cell transformation assays, used to provide preliminary assessment of poten- tial oncogenicity in advance of these more defini- tive life-time bioassays in rodents, conflicting results were obtained. Acyclovir was positive at the highest dose used in one system and the resulting morphologically transformed cells formed tumors when inoculated into immuno- suppressed, syngeneic, weanling mice. Acyclovir was negative in another transformation system considered less sensitive.
In acute studies, there was an increase, not statistically significant, in the incidence of chromosomal damage at maximum tolerated parenteral doses of 100 mg/kg acyclovir in rats but not Chinese hamsters; higher doses of 500 and 1000 mg/kg were clastogenic in Chinese hamsters. In addition, no activity was found after 5 days dosing in a dominant lethal study in mice. In 6 of 11 microbial and mammalian cell assays, no evidence of mutagenicity was ob- served. At 3 loci in a Chinese hamster ovary cell line, the results were inconclusive. In 2 mam- malian cell assays (human lymphocytes and L5178Y mouse lymphoma cells in vitro), positive responses for mutagenicity and chromosomal damage occurred, but only at concentrations at least 400 times the acyclovir plasma levels achieved in man.
Acyclovir has not been shown to impair fertil- ity or reproduction in mice (450 mg/kg/day, p.o.) or in rats (25 mg/kg/day, s.c.). At 50 mg/kg/day s.c. in the rat, there was a statistically sig- nificant increase in post-implantation loss, but no concomitant decrease in litter size. In female rabbits treated subcutaneously with acyclovir subsequent to mating, there was a statistically significant decrease in implantation efficiency but no concomitant decrease in litter size at a dose of 50 mg/kg/day. No effect upon implanta- tion efficiency was observed when the same dose was administered intravenously. In a rat peri- and postnatal study at 50 mg/kg/day s.c., there was a statistically significant decrease in the group mean numbers of corpora lutea, total implantation sites and live fetuses in the F i generation. Although not statistically signifi-
cant, there was also a dose related decrease in group mean numbers of live fetuses and implan- tation sites at 12.5 mg/kg/day and 25 mg/kg/day, s.c. The intravenous administration of 100 mg/kg/day, a dose known to cause obstruc- tive nephropathy in rabbits, caused a significant increase in fetal resorptions and a corresponding decrease in litter size. However, at a maximum tolerated intravenous dose of 50 mg/kg/day in rabbits, there were no drug-related reproductive effects.
Intraperitoneal doses of 320 or 80 mg/kg/day acyclovir given to rats for 1 and 6 months, re- spectively, caused testicular atrophy. Testicular atrophy was persistent through the 4-week post- dose recovery phase after 320 mg/kg/day; some evidence of recovery of sperm production was evident 30 days postdose. Intravenous doses of 100 and 200 mg/kg/day acyclovir given to dogs for 31 days caused aspermatogenesis. Testicles were normal in dogs given 50 mg/kg/day, i.v. for one month.
Pregnancy: Teratogenic Effects: Pregnancy Category C.^Acyclovir was not teratogenic in the mouse (450 mg/kg/day, p.o.), rat (50 mg/kg/day, s.c.) or rabbit (50 mg/kg/day, s.c. and i.v.). There are no adequate and well-controlled studies in pregnant women. Acyclovir should not be used during pregnancy unless the potential benefit justifies the potential risk to the fetus. Although acyclovir was not teratogenic in animal studies,, the drug’s potential for causing chromosome breaks at high concentration should be taken into consideration in making this determination. Nursing Mothers: It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when Zovirax is adminis- tered to a nursing woman. In nursing mothers, consideration should be given to not using acy- clovir treatment or discontinuing breastfeeding. Pediatric Use: Safety and effectiveness in children have not been established.
ADVERSE REACTIONS — Short-Tferm Administration: The most frequent adverse reactions reported during clinical trials were nausea and/or vomiting in 8 of 298 patient treat- ments (2.7%) and headache in 2 of 298 (0.6%). Less frequent adverse reactions, each of which occurred in 1 of 298 patient treatments (0.3%), included diarrhea, dizziness, anorexia, fatigue, edema, skin rash, leg pain, inguinal adenopathy, medication taste and sore throat.
Long-Term Administration: The most frequent adverse reactions reported in studies of daily therapy for 3 to 6 months were headache in 33 of 251 patients (13.1%), diarrhea in 22 of 251 (8.8%), nausea and/or vomiting in 20 of 251 (8.0%), vertigo in 9 of 251 (3.6%), and arthralgia in 9 of 251 (3.6%). Less frequent adverse reac- tions, each of which occurred in less than 3% of the 251 patients (see number of patients in parentheses), included skin rash (7), insomnia. (4), fatigue (7), fever (4), palpitations (1), sore throat (2), superficial thrombophlebitis (1), muscle cramps (2), pars planitis (1), menstrual abnormality (4), acne (3), lymphadenopathy (2), irritability (1), accelerated hair loss (1), and depression (1).
DOSAGE AND ADMINISTRATION: Treat- ment of initial genital herpes: One 200 mg cap- sule every 4 hours, while awake, for a total of 5 capsules daily for 10 days (total 50 capsules).
Cnronic suppressive therapy for recur- rent disease: One 200 mg capsule 3 times daily for up to 6 months. Some patients may require more drug, up to one 200 mg capsule 5 times daily for up to 6 months.
Intermittent Therapy: One 200 mg capsule every 4 hours, while awake, for a total of 5 capsules daily for 5 days (total 25 capsules). Therapy should be initiated at the earliest sign or symptom (prodrome) of recurrence.
Patients With Acute or Chronic Renal Im- pairment: One 200 mg capsule every 12 hours is recommended for patients with creatinine clear- ance <10 ml/min/1.73/m2.
HOW SUPPLIED: Zovirax Capsules (blue, opaque) containing 200 mg acyclovir and printed with “Wellcome ZOVIRAX 200”- Bottles of 100 (NDC-0081-0991-55) and unit dose pack of 100 (NDC-0081-0991-56).
Store at 15°-30°C (59°-86°F) and protect from light.
*In controlled studies , recurrences were totally prevented for 4 to 6 months in up to 75% of patients.
ft
Wtlleomi
Burroughs Wellcome Co. Research Triangle Park North Carolina 27709
Copr. © 1986 Burroughs Wellcome Co. All rights reserved. 86-ZOV-5
ADVISORY OPINION OF THE MEDICOLEGAL INTERPROFESSIONAL
COMMITTEE
More and more frequently , a substantial part of the practice of law and medicine is concerned with the problems of persons needing the services of both profes- sions. Appropriate cooperation between the members of these professions is important for the overall benefit of the individual patient. Unfortunately, conflicts arise between physicians and attorneys regarding their re- lationship in legal issues involving their patient/client. The Medicolegal Interprofessional Committee of the Louisiana State Bar Association and the Louisiana State Medical Society acts to informally resolve these conflicts between individuals of these two professions. In so doing, it became apparent that the Interprofes- sional Code of Physicians and Attorneys adopted in 1961 and amended in 1984, failed to adequately ad- dress some problems, and remained ambiguous on certain important issues such attorneys' liability for certain Medical-Legal costs.
This Committee recognized that it is important for all parties to separate "medical care" expenses from "legal care" expenses. The Committee, therefore, developed the following advisory opinion concerning these issues to guide their interprofessional relation- ship.
This advisory opinion, which will also be pub- lished in the Louisiana Bar Journal, will be proposed as a resolution at the 1987 House of Delegates for more formal acceptance by the membership of the Lou- isiana State Medical Society.
Also included herein is a sample letter for use by physicians in clarifying their role and fees in legal "expert" matters for which they are contracting with attorneys.
Michael S. Ellis, MD Medicolegal Interprofessional Committee
Many of the conflicts which arise between physi- cians and attorneys concern services rendered by physicians, including, but not limited to, court appearances, depositions, conferences, examinations of patients and the rendition of reports. These con- flicts involve three major areas: notice, fees and the conditions of payment for services.
In each major area, there are several troublesome situations which recur with predictable regularity. Most, if not all, conflicts between the professions can be avoided if each profession's expectations of the conduct of the other are tempered with realism and, most importantly, are arrived at through advance un- derstandings, mutually agreed upon and preferably confirmed in writing.
The medical and legal professions recognize that a physician who has treated a patient obligates him- self (and is subject to subpoena) to serve as a fact witness relative to litigation regarding that treatment. Both professions also recognize that the attorney and the physician may, by mutual consent, enter into a relationship wherein the physician serves in an expert capacity. In such a relationship, the physician may be expected to generate narrative reports, participate in conferences and/or depositions, appear in court to render his expert opinion, etc. In this relationship, the attorney will be expected to specify the service to be rendered, provide adequate notice, cooperate in scheduling meetings and depositions, and assure the payment of expert fees within the guidelines set out below.
I. NOTICE
A. Scheduling
Conferences, depositions, court appearances, etc. should be scheduled at the earliest time, and with at least two weeks advance notice whenever pos- sible, and confirmed in writing with all concerned
40
JOURNAL VOL 139 NO 2 FEBRUARY
SAMPLE PHYSICIAN LETTER TO ATTORNEY
(ESTABLISHES A CONTRACTUAL BINDING AGREEMENT)
Physicians are often uncertain as to the methodology of establishing clear communication with attorneys regarding their designated roles in legal matters and the advance establishment of fees for their expert services.
Attorneys’ methods for establishing fees were utilized in the attached “Sample Letter” to assist physicians in this endeavor. This type of letter can also act to establish a binding contractual relationship between the physician and attorney if mutual agreement to its terms can be established.
I have been notified that your are requesting my deposition regarding (case) on (date) at (place).
OR
I have received a subpoena to appear in court regarding (case) on (date) at (place).
Please let me know of any cancellations or settlements as soon as possible. It is also understood that your office will notify me as far in advance as possible of an expected time for my appearance.
Please be informed that my standard fees for time spent giving expert testimony are:
Review of records Photocopy records Telephone conference
$(fee) per hour $(fee) per hour $(fee) per hour (.3, .5, .8, 1.0, etc.)
Deposition Travel time Courtroom
$(fee) per hour $(fee) per hour $(fee) per hour
(From time of arrival at court)
I would appreciate your agreement to these amounts by signing and returning this letter. By your signing this letter, I will look to you, the attorney, for payment of my fees, notwithstanding any relationship between you and your client.
If this subpoena is not for my expert testimony as a (type of specialist), but only to testify as an interpreter and witness of fact, as presented in the patient’s records— without rendering a medical expert opinion, prognosis, etc.— please indicate this below.
If subpoenaed to appear in court or for a deposition and arrangements are made in my schedule to be available, failure to give adequate notification of continuance or cancellation will result in an appropriate charge based on amount of time lost from practice.
I would appreciate you contacting me for any pretrial questions you may have or to arrange a pretrial consultation in my office.
Cordially,
APPROVED AS MEDICAL EXPERT:
APRROVED AS WITNESS OF FACT ONLY:
JOURNAL VOL 139 NO 2 FEBRUARY
41
persons. Both the attorney and physician should provide the other with the name of any person in his/her office who has the authority to make such arrangements.
B. Cancellation
Notification of cancellation of conferences, dep- ositions, court appearances, etc., whether by the attorney or the physician, shall be communicated as early as possible to all concerned persons. The attorney and the physician may agree in advance as to appropriate compensation in the event of cancellation without adequate notice.
C. Delays
An attorney or physician who realizes that a de- lay will occur in the starting time of a conference, deposition, court appearance, etc. should promptly notify the other and make reasonable efforts to- ward coordinating with the other's office to min- imize the impact of the delay upon the attorneys, physicians, court reporters, or others who may be affected.
II. PAYMENT
A. Medical Services
1. It is entirely appropriate and acceptable for an attorney to guarantee payment for rendered Med- ical Services out of the proceeds of the litigation.
2. Since a situation may arise wherein the funds from the proceeds of the litigation are inade- quate, it is desirable that advance agreement be made to cover this situation by the physician and the patient.
3. It should be understood by the physician that response to a court-ordered deposition or court ap- pearance as a fact witness for a patient, for whom he has rendered medical service, cannot be con- ditional upon receipt of payment for those medical services because the physician's duty is the same as that of any other person to respond to judicial process.
4. It is not appropriate for a physician to require an attorney's personal guarantee or payment in advance for previously rendered medical services in advance of depositions, conferences, court ap- pearance or as a condition of the physician talking to the attorney.
B. Expert Services
1. Payment for expert services may be made in advance or deferred. By agreement, payment may
be deferred to the conclusion of the case, pro- vided that the amount is specified in advance and the amount is not dependent in any way on the outcome of the litigation.
2. It is considered appropriate for an attorney to pay or personally guarantee mutually agreed upon expert fees.
3. Attorneys should understand that a physi- cian's decision to become an expert witness and his agreement to produce medical reports with opinions, or to participate in conferences, dep- ositions or trials as an expert, can be conditional on receipt of payments or personal guarantees from the attorney for these expert fees.
4. With regard to any deferred payments for expert fees, there should be a clear understanding be- tween the physician and the attorney, preferably in writing, as to whether the deferred payment is guaranteed by the attorney and/or the patient/ client and/or both.
III. FEES FOR EXPERT SERVICES
A. Should be a specific amount mutually agreed upon, preferably in writing, and in advance of the event.
B. Fees may be at a reasonable hourly rate or reasonable flat rate.
C. Rates may differ for review of records, re- search, reports, during office hours conferences, in-office depositions, out-of-office depositions, travel, photocopies, court appearances, etc.
D. Mutual agreement as to the cost of and need for additional tests, procedures, or consultations employed by the physician/expert if the render- ing of his service is required. Such agreements should be confirmed in writing.
E. One reasonable guideline for determining an hourly rate could be a rate based on the physi- cian's normal average hourly office income.
DEFINITIONS
1. SUBPOENA — A written order of a Court of Law to appear at a certain time and place to give tes- timony upon a certain matter.
SUBPOENA DUCES TECUM — A process by which the court, at the instance of a party, orders a witness who has in his possession or control some document or object, to produce that docu-
JOURNAL VOL 139 NO 2 FEBRUARY
merit or object at a specific time and place.
2. FACT WITNESS — Any physician or other person who has had contact with a patient and may be called upon to testify regarding the facts and cir- cumstances surrounding that event. Facts include, but are not necessarily limited to: dates of contact, history given, physical findings, test results, work- ing diagnosis and treatment rendered.
3. EXPERT WITNESS — Any physician whose qual- ifications are accepted by the court may agree to render opinions including, but not necessarily lim- ited to: diagnosis, prognosis, causation, rehabili- tation and costs anticipated.
4. NARRATIVE REPORT — A written summary of the facts of a medical case and a physician's opin- ion of causation* * and other matters. The report is essential to an attorney in preparing for possible litigation. If done well, this report may obviate the need for depositions or even trial — resulting in settlements or avoidance of litigation as the case merits.
A report to the requesting attorney may include at least:
a) How, when and where the patient was first seen;
b) Name of any referring party;
c) The case history (i.e. chief complaint, date and circumstances of injury, previous eval- uations or treatments rendered, any signif- icant pre-existing conditions);
d) Initial general review of symptoms;
e) Any pertinent (positive or negative) past his- tory;
f) Physical examination;
g) Any laboratory or consultation results;
h) Therapeutic progress since initial evaluation, including present condition and limitations;
i) Diagnosis;
j) Opinion as to any causal* connection be- tween injury and condition diagnosed; ►
* A physician's opinion of causation should be based on his medical knowledge coupled with the histon / given and his findings.
* Legal cause need not be to a scientific certainty but only what is probably true (a reasonable medical probability). The incident complained of need not be the only (sole) cause of the condition. It may be coupled with pre- existing conditions and still be a sufficient factor to constitute legal cause.
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JOURNAL VOL 139 NO 2 FEBRUARY
43
BEN H. QUINNEY JR., M.D.
ANNOUNCES THE RELOCATION OF HIS OFFICE FOR THE PRACTICE OF
MEDICAL ONCOLOGY
AND
HEMATOLOGY
TO
1800 BUCKNER SQUARE. SUITE 102 SHREVEPORT. LA. 71101
OFFICE HOURS
BY APPOINTMENT 227 - 1907
k) Opinions as to future prognosis, therapy, tests, and estimated costs;
l) Copy of patients' bill for services rendered to date;
m) Separate bill to attorney for rendering the narrative report if not previously paid;
n) Copy of curriculum vitae if expected to be used as an expert witness.
5. CANCELLATION — Refers to the elimination or continuance (postponement) of the scheduled con- ference, deposition or court appearance.
6. MEDICAL SERVICES — Those services rendered by a physician to a patient which would be ren- dered regardless of the existence or non-existence of litigation.
7. EXPERT SERVICES — Those services rendered by a physician as contracted for by the attorney with regard to litigation.
in the
JOURNAL
The nonspecific sonographic nature of a chronic renal infarct
CAUTIONARY NOTES
1. DEPOSITIONS — RIGHT TO READ AND SIGN
Under both the Federal and Civil Rules of Proce- dure, any witness has the right to read and sign his or her deposition. When the witness reads a deposition and finds an inaccuracy in recording an answer, a typographical mistake, or other matters that need to be clarified, the witness may write out a “process verbal." A process verbal is a list of the page number and the line number of the deposi- tion, spelling out what changes the witness desires to be made in the transcript. That process verbal will then be forwarded to the court reporter and attached to the deposition. In some instances, an expert witness ought to reserve the right to read and sign his or her deposition. The expert witness who reads and signs the deposition ought to re- alize that some time will be involved in doing this and ought either to gauge his or her expert fee to cover this requirement or should reach an agree- ment in advance with the attorney taking the dep- osition for payment of the said time. ■
JOURNAL VOL 139 NO 2 FEBRUARY
STACKS
HEALTH SCIENCES LIBRARY UNIVERSITY OF MARYLAND BALTIMORE
MAR 19 198?
BEC’B,
NOT TO CIRC.
ACES
TOURNAL
STACKS
OF THE LOUISIANA STATE MEDICAL SOCIETY
March 1987
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EDITOR
MANNIE D. PAINE, JR, MD
GENERAL MANAGER RENE G. ABADIE
MANAGING EDITOR
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JOURNAL COMMITTEE
CONWAY S. MAGEE, MD Chairman
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Copyright 1987 by The Journal of the Loui- siana State Medical Society, Inc.
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VOLUME 139 / NUMBER 3 / MARCH
ARTICLES
|
3 |
107th Annual Meeting Schedule of Events |
|
|
Neil Wolfson, MD, FACOG Carlton Hodgson, MD, PhD |
35 |
Clinical toxicology of one-day administration of 500 mg of clotrimazole |
|
Harley Ginsberg, MD Irwin Cohen, MD |
39 |
Late onset Group A streptococcal bacteremia in a neonate |
|
Gault H. Townsend, MD Deba P. Sarma, MD |
47 |
Signet-ring cell carcinoma of the urinary bladder |
DEPARTMENTS
5
13
19
28
61
ECG of the Month Otolaryngology /Head
and Neck Surgery Report Book Reviews Calendar
Classified Advertisements
Cover illustration by Eugene New, New Orleans, LA
INFORMATION FOR AUTHORS
MANUSCRIPTS should be of a reasonable length and double spaced on firm white paper 8V2 x 1 1 inches with adequate margins. This applies to all text elements: references, legends, footnotes, etc. Single spaced manuscripts and photo copies will not be considered. The original and one duplicate should be submitted. Manuscripts are received with the explicit understanding that they are not simultaneously being considered by any other pub- lication. Accepted manuscripts become property of THE JOURNAL and may not be published else- where without permission from the author and THE JOURNAL. Manuscripts are subject to copy edit- ing.
TITLE PAGE should carry (1 ) the title of the article, which should be concise but informative; (2) first name, middle initial, and last name of each author, with highest academic degree(s); (3) name and address of author to whom requests for reprints should be addressed, or statement that reprints will not be available from the author.
ABSTRACT should be the second page consisting of no more than 1 50 words. The abstract should be a factual (not descriptive) summary of the work and should contain: 1) a brief statement of the paper's purpose, 2) the approach used, 3) the material stud- ied, and 4) the results obtained. Emphasize new and important aspects of the study or observations.
KEY WORDS should follow the abstract and be identified as such. Provide three to 1 0 key words or short phrases that will assist indexers in cross- indexing your article. Use terms from the Medical Subject Headings list from Index Medicus when possible.
SUBHEADS should be used to provide guidance for the reader. This format is flexible but the subheads would ordinarily include: Methods and Materials, Case Reports, and Discussion.
REFERENCES must be limited to a reasonable num- ber. They will be critically examined at the time of review and must be kept to a minimum. Personal communications and unpublished data should not be included. The following form can be followed:
Journals
(1) Authors: Use the surname followed by initials without punctuation. The names of all authors should be given unless there are more than three, in which case the names of the first three authors are used, followed by "et al." (2) Title of article. Capi- talize only the first letter of the first word. (3) Name of journal. Abbreviated according to Index Medi- cus. (4) Year of publication; (5) Volume number: (6) Inclusive page numbers.
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All references must be cited in the text and the list should be arranged in order of citation, and not alphabetically.
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2
JOURNAL VOL 139 NO 3 MARCH
Norton W. Voorhies, MD, Editor
ECG OF THE MONTH
TRIPARTITE BLOCK
JORGE I. MARTINEZ-LOPEZ, MD
The rhythm strip shown below, precordial lead VX/ belongs to a 92-year-old black woman. It was recorded shortly after she was admitted to the MICU in an obtunded mental state. No other medical information was available.
What is your diagnosis? Elucidation is on page 7.
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ECG of the Month
Case presentation on page 5.
DIAGNOSIS — First and second-degree AV block, and defective intraventricular conduction
Sinus arrhythmia, at 88 times a minute, is associated with a regular ventricular rate of 44 a minute, half that of the sinus rate. The PR interval (0.22 sec) and the QRS interval (0.12 sec) are both abnormally long. Measurement of the QT interval cannot be made with precision because non-conducted P waves are re- corded near the end of the T wave, but it has to measure at least 0.44 sec, ie, it is also prolonged.
Prominent in the rhythm strip is the presence of two P waves for every QRS complex. This 2:1 AV ratio raises two diagnostic possibilities: either non- conducted atrial premature impulses in bigeminy or second-degree AV block. The first possibility can be promptly rejected by measuring P-P intervals. Note that P-P intervals which contain QRS complexes are not shorter, but longer than P-P intervals without QRS complexes. Therefore, the non-conducted P waves do not occur prematurely and do not represent non-con- ducted atrial premature impulses in bigeminy. In- stead, they represent non-conducted sinus impulses. This finding leads to the diagnosis of second-degree AV block.
DISCUSSION
Components of the normal cardiac conducting system (CCS) include: the SA node, three internodal tracts, an interatrial tract (Bachmann's bundle), the AV node, the bundle of His, a right and left bundle branch, and myriad Purkinje fibers located in the ventricular mus- culature. Electrical impulses generated in the SA node exit from this structure and propagate by way of the components of CCS to both atria and to both ventri- cles. Although CCS primarily functions as an anter- ograde pathway, retrograde conduction can occur un- der certain circumstances.
Disturbances of impulse conduction occurring anywhere in CCS are collectively designated as "blocks," even though the so-called block may only be a delay in impulse conduction rather than complete failure of the impulse to traverse components of CCS. Conduction block may be present simultaneously at
more than one site. Three forms of conduction block are recognized: first-degree, second-degree, and third- degree. This distinction, however, is often misleading and is an oversimplification of a rather complex sit- uation that frequently results in overtreatment.
First-degree AV block is said to be present when the length of the PR interval on the surface ECG ex- ceeds 0.20 sec. Virtually always, lengthening of the PR interval indicates an abnormal conduction delay of the supraventricular impulse that occurs at the level of the AV node. On rare occasions, the abnormal conduction delay takes place at the level of either the bundle of His or both bundle branches. However, the surface ECG does not furnish clues from which the precise location of the impulse conduction delay can be specified.
Second-degree AV block is a conduction abnormality in which not every supraventricular impulse is prop- agated into the ventricles. There are four varieties of second-degree AV block: Mobitz types I and II, 2:1, and advanced AV block. Earlier in this presentation, it was established that the tracing shown here rep- resented 2:1 AV-block. This type of conduction block is considered as a "separate" entity because, in the presence of sustained 2:1 AV block, it is not possible to define whether the conduction abnormality is of the Mobitz type I or Mobitz type II variety. On the surface ECG, the distinction can be made if changes in the A:V ratio occur. Typical Mobitz type I block shows progressive prolongation of the PR interval and the sequence ends with a non-conducted sinus P wave. By contrast, the PR interval remains constant before the sinus P wave is blocked in Mobitz type II block. When the 2:1 A:V ratio is sustained, one type block may be favored over the other by measuring the duration of the QRS complexes. Because in the vast majority of cases with Mobitz type I block the site of the block takes place at the level of the AV node, this block is usually associated with narrow QRS complexes. On the other hand, Mobitz type II block is almost always associated with wide QRS com- plexes because block occurs in the distal CCS.
Defective intraventricular conduction encompasses incomplete and complete bundle branch blocks as well as nonspecific intraventricular blocks. In the tracing shown here, the term denotes increased duration of the QRS complex (0.12 sec). The 12-lead ECG showed it to be due to complete left bundle branch block.
JOURNAL VOL 139 NO 3 MARCH
7
Finally, the tracing recorded in the patient pre- sented here is complex because of the existence of a tripartite block. Such a complex conduction disturbance usually has serious clinical, prognostic, and thera- peutic implications, particularly when it coexists with organic heart disease. The patient's obtunded mental state was attributed to hemodynamic alterations brought about by the tripartite block. Attempts to improve AV conduction with pharmacologic agents proved futile. Because temporary cardiac pacing im- proved her clinical status, a permanent pacemaker was implanted before a complete cardiac diagnosis was established. ■
SELECTED REFERENCES
1. Dhingra RC, Denes P, Wu D, et al: The significance of second degree atrioventricular block and bundle branch block. Circu- lation 1974;49:638-646.
2. Zipes DP: Second-degree atrioventricular block. Circulation 1979;60:465-472.
3. Reddy CP: Diagnosis and implications of atrioventricular block. Practical Cardiol 1980;6:180-190.
4. Strasberg B, Amat-y-Leon F, Dhingra RC, et al: Natural history of chronic second-degree atrioventricular nodal block. Circula- tion 1981;63:1043-1049.
5. Marriott HJL: Second-degree AV block. Primary Cardiol 1981;(Oct):33-46.
6. Gomes JAC, EL-Sherif N: Atrioventricular block. Med Clin NA 1984;68:955-96 7.
From the Cardiology Service, Department of Medicine, William Beaumont Army Medical Center, El Paso, TX 79920-5001.
The opinions or assertions contained herein are the private views of the author and are not to be construed as official or as reflecting the views of the Department of the Army or Department of Defense.
LSU MEDICAL VIDEOCASSETTE SERVICE
The Division of Learning Resources of Louisiana State University's School of Medicine in New Orleans is offering a new educational videocassette service. We will publish, monthly, a videotape catalog from which you may purchase a variety of interesting topics presented during weekly video conferences held by LSU Medical School's departments of Ob-Gyn, Pediatrics and Surgery. Recent examples include:
OB-GYN
Urinary Incontinence The various forms of urinary incontinence and their diagnosis are described. Treatment methods and their complications are also discussed, (approx. 60 min.) 1 1/17/86
PEDIATRICS
Pediatric Dentistry A faculty member of the LSU School of Den- tistry gives an overview of dental problems in children from birth to teens, (approx. 60 min.) 1 1/19/86
SURGERY
Thyroid Disease Included in this discussion of thyroid disease is thyrotoxicosis, thyroiditis, and carcinoma. Surgical management is also discussed, (approx. 60 min.) 12/1/86
Occasionally, topics of special interest in other clinical fields may also be offered. All programs are offered for a limited time and will be regularly replaced by new programs. After you have viewed the program, THE VIDEOCASSETTE IS YOURS TO KEEP for future reference or to reuse for your own purposes. All programs are recorded on Vi inch VHS or BETA formats. The purchase price is only $20.00 per program.
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JOURNAL VOL 139 NO 3 MARCH
OTOLARYNGOLOGY/
HEAD AND NECK SURGERY REPORT
UNILATERAL TONSILLAR SWELLING
IN ADULTS
JOHN A. WHITE, MD; MACK L. CHENEY, MD;
RICHARD M. WEIR, MD; HOLLIS T. REED, MD
The presence of unilateral tonsillar swelling in adults often causes alarm because of the possibility of neoplastic disease. The usual cause, if not inflammatory, is a mass arising in the parapharyngeal space. Following a case presentation, we will discuss the anatomy and pathological processes of the parapharyngeal
space.
A 36-year-old white male presented to his physi- cian with a complaint of a swelling in the right tonsillar area associated with minimal discomfort and a change in voice. Antibiotics were prescribed and after one week there was no improvement. He was referred to an otolaryngologist