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The South Dakota Journal of Medicine
CONTENTS
Editor
Robert Van Demark, M.D. Sioux Falls
Business Manager
Richard C. Erickson Sioux Falls
Commission on Communications and Liaison with Allied Organizations
J. F. Barlow, M.D., Chr. (’73) Mary E. Sanders, M.D. (’71)
Loren H. Amundson, M.D. (’71)
J. Vose, M.D. (’71)
William Hanson, M.D. (’71)
R. G. Belatti, M.D. (’72)
D. L. Scheller, M.D. (’72)
H. H. Theissen, M.D. (’72)
R. Auskaps, M.D. (’72)
R. E. Van Demark, M.D. (’73) Eldon Bell, M.D. (’73)
A. J. Tieszen, M.D. (’73)
Published Monthly by The South Dakota State Medical Association
711 North Lake Avenue Sioux Falls, South Dakota 57104
Subscription Rate Yearly $5.00 — Single Copy 50c
Controlled Circulation Postage Paid at Sioux Falls, South Dakota
Volume XXIV January 1971 Number 1
Ganglion Cyst Causing Ulnar Compression Syndrome at the Wrist 5
James B. Kullbom, M.D.; Robert E. Van Demark, M.D.
North American Blastomycosis 14
(Second Article in Series)
S. Sochocky, M.D, F.C.C.P.
Clinicopathological Conference
25
This Is Your Medical Association
35
Minutes of the Council Meeting
36
President’s Page
39
Editorial: “The Fainting on the John” — Syndrome . . 45
E. H. Heinrichs, M.D.
1
GANGLION CYST CAUSING ULNAR COMPRESSION SYNDROME AT THE WRIST*
James B. Kullbom, M.D. and
Robert E. Van Demark, M.D.
The symptoms of chronic nerve compression i are those of weakness, numbness, tingling, burn- ing and pain over the distribution of the nerves.
When the practitioner encounters a patient with these symptoms present in an extremity, he may be impressed with the severity of the complaints and the absence of visible organic disease. This may lead to a failure to properly i diagnose the problem, or to a diagnosis of hys- teria.
One of the more interesting nerve compres- sion syndromes is that of ulnar nerve compres- sion at the wrist.
The ulnar nerve is derived from the eighth cervical and first thoracic nerve roots. These branches join to form the largest branch of the medial cord of the brachial plexus. Six to eight , centimeters proximal to the wrist, the dorsal cutaneous branch to the hand leaves the main nerve. The ulnar nerve then passes through the ulnar carpal canal to the hand.
This narrow ulnar carpal canal was first des- } cribed by a French urologist, Felix Guyon, in 1861, and is also referred to as the Canal of Guyon. The canal is formed by the hook of the hamate laterally and distally, the pisiform prox- imally and medially. The floor is formed by the 5 volar carpal ligament and the roof is formed by the thick transverse carpal ligament. The canal contains a small amount of fat, an artery, and the ulnar nerve. There are no tendons or tendon sheaths in the canal.
* Paper presented at the annual meeting of the S. Dak. Chapter of the American College of Sur- geons, April 11, 1970, Aberdeen, S. Dak.
As it enters the canal, the nerve bifurcates into a superficial sensory and a deep motor branch. As the deep motor branch leaves the canal with the artery it turns sharply around the hook of the hamate and travels between the origins of the abductor digiti quinti and flexor digiti quinti brevis muscles. It then passes through the opponens digiti quinti and travels across the interossei, dorsal to the flexor ten- dons of the fingers and ends in the first dorsal interosseus muscles and occasionally the flexor pollicis brevis. The superficial branch leaves the canal, innervates the palmaris brevis muscle and passes through a fat pad deep to this mus- cle. It then continues on subcutaneously to provide sensory innervation to the ulnar surface of the hypothenar eminence and the ring and little fingers.
Three types of ulnar nerve compression syn- dromes have been described in relation to the location of masses at the Canal of Guyon.
Type I Syndrome
The Type I syndrome consists of a motor weakness of all the ulnar innervated muscles of the hand combined with a sensory deficit to the ulnar two fingers and the palmar surface of the hypothenar eminence. The Type I syndrome is caused by ulnar nerve compression in the Canal of Guyon or just proximal to it. This Type I syndrome can be differentiated from ulnar nerve compression at the elbow as normal sen- sation is still present on the medial side of the dorsum of the hand.
JANUARY 1971
5
2
Type II Syndrome
In the Type II syndrome the pressure on the nerve occurs where it leaves the Canal of Guyon in the region of the hook of the hamate. The superficial sensory branch is unaffected and the findings consist of motor weakness in ulnar in- nervated muscles of the hand. The number of muscles involved depends on the site of com- pression along the deep branch.
Type III Syndrome
In the Type III syndrome, the superficial branch is traumatized or compressed just as it leaves the Canal of Guyon. This may be a super- ficial mass or a blow to the area. The deep motor branch is spared. Findings include a sensory deficit over the ulnar two fingers and the volar surface of the hypothenar eminence. There is no associated motor weakness.
Case Report #1
A 35 year old white male farmer was seen for the first time on 11-29-69 with a chief complaint of numbness in the left hand extending into the ring and little fingers. He also had complaints of pain to a lesser extent between the thumb and first finger of the left hand. The patient stated that this numbness and pain began on about the 14th of September in 1969. On that date, he was
working with a power take-off at his farm and struck his hand against the power take-off pin. He denied any other known injury and stated that the hand became numb at the time of in- jury and he began to have pain in the thumb and 1st finger approximately two months later. He was seen by his local doctor and was referred to the Van Demark Clinic on 11-29-69. His past medical history included an old amputation of part of the middle finger on the left hand in- curred in a generator belt accident in 1953.
Physical examination on admission to the clinic revealed loss of sensation over the ring and little fingers on the left hand. Electromyo- graphic studies were performed on 11-29-69 and also on 12-3-69. The right ulnar nerve was studied first and at the conclusion of these studies, it was found that the right ulnar nerve NCV was 55.1 meters per second (normal is 40 to 60, plus or minus 5 meters per second). The left ulnar nerve was then studied and the NCV was found to be only 35.9 meters per second. Sensory studies of the right ulnar nerve re- vealed a conduction time of 2.3 milliseconds re- quired for response. On the left side sensory studies revealed no response to stimulation and typical fibrillation potential was present at rest.
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(Figure 1). These EMG studies were consistent with compression of the ulnar nerve at the level of the tunnel of Guyon. The patient was admitted
Figure 1.
Electromyographic study of the left ulnar nerve. Sen- sory studies revealed no response to stimulation. A typical fibrillation potential is shown.
to McKennan Hospital on 12-4-69 for explora- tory surgery on the ulnar tunnel of Guyon on the left side. Upon exposing the tunnel of Guyon on the left side, a ganglion was found lying in the tunnel and compressing the nerve. (Figure 2)
Figure 2.
A photograph of the ganglion cyst removed from the left Canal of Guyon of Case SI.
The ganglion was removed completely and the
nerve was restored to its original position. Microscopic examination proved the lesion to be a ganglion cyst. The patient was discharged the following day. He was seen on 12-13-69 and had noted cessation of pain and was getting some return of function in his 1st dorsal interos- seous muscle on the left side. The patient’s guitar playing talents had returned to normal by March of 1970.
The patient was last seen on August 12, 1970 at which time he had an excellent result and his left ulnar nerve sensory conduction time was 3.0 milliseconds as compared to the right of 2.4 milliseconds.
Case Report #2
A 45 year old married white female presented herself with complaints of weakness in the left hand with numbness and tingling in the left ring and little fingers. The symptoms first ap- peared in December of 1969. Her past medical history included a razor blade injury to the left wrist twenty years ago. She stated that she had no medical attention at the time of this injury and that healing was spontaneous. She also con- tracted rheumatic fever, scarlet fever, pneu- monia and hay fever as a child and has had seven pregnancies. Her father died of heart trouble at age 54 and her mother has hyperten-
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sion at the age of 81. Two of her sisters have multiple sclerosis and one brother and one sister are in good health. A maternal grandmother had cancer.
Physical examination revealed loss of sen- sation over the left little finger and the lateral side of the ring finger. The hand had the typical ulnar palsy picture with severe muscle atrophy of the hypothenar and interosseous muscles. (Figure 3) Electromyographic studies revealed a prolonged sensory conduction time of the left ulnar nerve (5.8 milliseconds).
Figure 3.
Severe muscle atrophy of the muscles of the left hand of Case #2. Note particularly the atrophy of the 1st interosseous muscle.
The patient was taken to surgery on 4-7-70 and a ganglion cyst measuring 6 mm. in dia- meter was located at the entrance of the Canal of Guyon compressing the left ulnar nerve. It was dissected free and removed. (Figure 4) Microscopic examination confirmed that it was a true ganglion cyst.
The patient was last seen on July 30, 1970 at which time her conduction time had improved and was now down to 2.4 milliseconds as com- pared to the opposite right ulnar nerve which had a sensory conduction time of 2.0 milli- seconds. Her function in her hand was excellent and she had no complaints.
Figure 4.
The ganglion cyst removed from the entrance of the left Canal of Guyon.
Discussion
A review of the literature reveals nineteen different lesions which have caused ulnar nerve compression at the wrist.
Shea and McClain tabulated 136 cases found in the literature and reported that thirty per cent were Type I, fifty-two per cent were Type II, and eighteen per cent were Type III. They found no correlation with age or sex. Most lesions cause reversible neuropathies. It is vir- tually impossible to determine the type of lesion causing the syndrome and it is recommended that each case should be thoroughly explored.
The syndromes are usually well developed when first seen because the onset of symptoms is very gradual. The action of the thumb and extrinsic muscles of the hand and wrist are not hampered and the motor deficit may go unno- ticed unless manual dexterity is used on the job.
When a patient presents symptoms of an ulnar compression syndrome, it is important to obtain a thorough history of systemic diseases present, such as rheumatoid arthritis, diabetes mellitus, connective tissue diseases, and any other neural disorders. A description of the pa- tient’s occupation may be enlightening. A des- cription of all injuries to the extremity is also important. Abnormalities of the cervical spine, shoulder, and elbow should also be excluded. Tests should include X-rays of the wrist and hand to rule out fractures or dislocations. Elec- tromyographic and nerve conduction studies should also be performed.
(Continued on page 11)
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8
SOUTH DAKOTA
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(Continued from page 8)
As was stated, once the diagnosis is made of ulnar nerve compression at the wrist, surgical exploration and decompression is the treat- ment of choice.
Summary
Three types of ulnar nerve compression at the wrist are discussed and two typical personal cases are presented. A guide to diagnosis and the recommendation of surgical exploration and decompression of the nerve are presented.
BIBLIOGRAPHY
1. Brooks, D. M.: Nerve Compression by Simple
Ganglion: A Review of Thirteen Collected Cases. J. Bone and Joint Surg., 34B:391-400, Aug., 1952.
2. Brooks, D. M.: Nerve Compression Syndrome. J.
Bone and Joint Surg., 45B:445-446, Aug., 1963.
3. Mallet, B. L. and Zilkha, K. J.: Compression of the
Ulnar Nerve at the Wrist by a Ganglion. Lancet, 1:890-891, 1955.
4. Richmond, D. A.: Carpal Ganglion with Ulnar
Nerve Compression. J. Bone and Joint Surg., 45B:513-515, Aug., 1963.
5. Seddon, H. J.: Carpal Ganglion as a Cause of
Paralysis of the Deep Branch of the Ulnar Nerve. J. Bone and Joint Surg., 34B:386-390, Aug., 1952.
6. Shea, J. D. and McClain, E. J.: Ulnar Nerve Com-
pression Syndrome At and Below the Wrist. J. Bone and Joint Surg., 51A:1095-1103, Sept., 1969.
7. Stein, A. H., Jr. and Morgan, H. C.: Compression
of the Ulnar Nerve at the Level of the Wrist. Am. Practit., 13:195-198, 1962.
8. Toshima, Y. and Kimata, Y.: A Case of Ganglion
Causing Paralysis of Intrinsic Muscles Inner- vated by the Ulnar Nerve. J. Bone and Joint Surg., 43A:153, Jan., 1961.
9. Vanderpool, D. W.; Chalmers, J.; Lamb, D. W.; and Whiston, T. B.: Peripheral Compression Le- sions of the Ulnar Nerve. J. Bone and Joint Surg., 50B:792-803, Nov., 1968.
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SECOND ARTICLE IN SERIES
NORTH AMERICAN BLASTOMYCOSIS
by
S. Sochocky, M.D.. F.C.C.P.*
Introduction:
North American blastomycosis is a systemic, granulomatous and suppurative infection caused by Blastomyces dermatitidis.
Gilchrist,1 in 1894, described a large, oval parasite in sections of skin from hand lesion of a patient. Later Gilchrist and Stokes2 isolated a fungus and named it Blastomyces dermatitidis, in 1896.
Bacteriology:
Blastomyces dermatitidis is a fungus 8-15 microns in diameter with thick refractory wall and may be isolated from soil, where it exists as a saprophyte. According to Schwartz and Baum,3 this disease is caused by inhalation of spores from a saprophytic source and systemic blastomycosis is secondary to the pulmonary in- fection. Incubation period of this disease has not been definitely settled. There has been no evi- dence that this infection may be transferred from animal to man, although this fungus is not uncommon in dogs and horses. J. Fred Denton4 et al. reported a case of laboratory assistant who probably acquired blastomycosis while handling cultures of mycelia form of Blastomyces derma- titidis. Michael W. Craig5 et al. described a mar- ried couple in which the husband had dissem- inated blastomycosis involving the prostate, epididymis and testicle and the wife concomit- antly had blastomycosis involving endometrium, fallopian tubes and peritoneum.
The incidence of infection is said to be highest in rural areas and among agricultural workers. North American blastomycosis is found in at
* Department of General Medicine, Veterans Ad- ministration Center, Sioux Falls, S. D. Assistant professor of Internal Medicine, University of South Dakota School of Medicine.
least 28 states in this country, however, it is more often found in Louisiana, Tennessee and North Carolina; Quebec and Ontario in Canada.
Pathology:
The histopathological reaction of tissue to Blastomyces dermatitidis is a combination of suppuration and epithelial cell granulomatous reaction with giant cells, Langhan’s type, which contain round or oval fungus. In lungs it is usually found as a round nodule or broncho- pneumonia, or thin walled cavity. Fibrosis may be present but calcification is not characteristic.
North American blastomycosis almost always begins as a pulmonary infection which may be asymptomatic or cause symptoms. Asympto- matic pulmonary lesions are often found on chest films. Primary pulmonary infection may progress as in any other granulomatous infec- tion to other forms, as chronic or acute, ful- minating, or become disseminated. Acute, ful- minating cases of blastomycosis, if not recog- nized early, may end fatally.
A 44 year old male was treated for pulmonary tuberculosis. However, as his progress was un- satisfactory, further studies of sputum showed Blastomyces dermatitidis. Treatment with am- photericin B was started but his general con- dition deteriorated and he died two weeks after admission to hospital. (See Figures 1 and 2).
From primary lesion in lung Blastomyces dermatitidis may disseminate throughout body by hematogenous or lymphatic route and invade almost any system of the body, e.g. skin, skeletal system, central nervous system and genito- urinary tract. In disseminated form North American blastomycosis usually presents itself as a disease of lungs and skin. The involvement
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SOUTH DAKOTA
7
of bones and joints varies between 27 - 50 per cent.
Urogenital infection may occur with systemic form of disease but diagnosis is rather difficult. Between January 1, 1952 and December 31, 1966,
Figure 1.
Chest film 11.14.62 shows a large density on left side with scattered infiltrations in middle and lower por- tion of right lung.
Figure 2.
Chest film 11.27.62 shows an increase of densities on the right, left side remains unchanged.
63 patients were treated for blastomycosis at JANUARY 1971
Duke University Medical Center.6 Systemic disease was noted in 25 cases, urogenital in- volvement found in 4. Urogenital infection with blastomycosis chiefly found in prostate gland and epididymis.
Skin lesions usually slowly develop into ulcers with serpinginous, elevated, advancing, vio- laceous borders. These ulcers may be associated with lymphoadenopathy.
Oral lesions due to North American blasto- mycosis are also described and may be more common than has been believed.
Disseminated blastomycosis with meningeal involvement was described by Robert L. Rainey7 et al.
Laboratory data:
There are no definite characteristic laboratory findings in North American blastomycosis. There may be secondary anemia, white cell count and sedimentation rate may be elevated.
Clinical Manifestations:
Signs and symptoms depend on the form of disease and the system of the body involved. The main symptoms of pulmonary blastomycosis are cough, purulent, sometimes blood tinged sputum and pain in chest, which quite often disappear without treatment. The patient may also have constitutional symptoms as a fever, general weakness, loss of appetite and weight. In our series8 of 15 patients, cough was the first symp- tom in 8 patients, spitting blood in 3, abnormal chest film in 1, shortness of breath in 1, chest pain in 1 and swelling of chest wall in 1. De- pending on degree of pulmonary involvement rhonchi, crepitations, consolidation with dull- ness and bronchial breathing may be found.
Radiological findings:
There are no characteristic radiological feat- ures of North American blastomycosis. Chest film may show infiltrations with or without cavity, diffuse mottled infiltration or a density with or without enlargement of mediastinum. Calcification is usually not found and pleural effusion is uncommon. Radiological findings in 15 patients in our series8 showed involvement of lungs in 8 patients, one lung in 7. Findings in chest film may be divided in the following groups: a) disseminated type of lesion in 3 pa- tients, b) chronic infiltration with thin walled cavities in upper parts in 4, c) “pneumonic” in 7 and “pleural changes” in 1 patient. No calcifica- tion was found but pleural fluid found in 1 pa- tient. Mediastinum was enlarged in 2 patients only.
17
8
Discussion:
History, residence of patient, course and lab- oratory investigations may help in diagnosis. North American blastomycosis may be found in any age, however, most frequently between 30- 50 with 80 per cent of cases occurring in males. In our series8 of 15 patients, there were 11 males and 4 females, the youngest <19 years and the oldest 69, remainder between 30-55.
In blastomycosis skin test may be of some help. This is different from tuberculin, histo- plasmin and coccidioidin skin tests which have considerable diagnostic value.
A complement fixation titer of 1 - 8 greater when associated with clinical signs may be a presumptive evidence of infection with Blas- tomyces dermatitidis and titer 1-32 may sug- gest active disease. This test is of diagnostic value if positive. In our series8 of 15 patients, blastomycin skin tests were positive in 4, nega- tive in 8 and complement fixation test was negative in all cases.
Blastomycosis may be complicated by other diseases and in E. J. Cherniss’9 et al. series of 40 patients, 16 had associated diseases “that oc- curred during the course of blastomycotic infec- tion, 3 had syphilis, 4 had pulmonary tuber- culosis, and other diseases.”
In our senes8 of 15 patients, 2 had pulmonary tuberculosis. The first patient had blastomycosis
Figure 3.
Photograph shows skin lesions with sinuses in left groin and probe inserted in sinus.
of skin and lungs in 1949, treated successfully with potassium iodide. In 1950 he developed tuberculosis of lungs, genito-urinary and skeletal systems. The second patient had pul- monary tuberculosis since December 1961, treated with isoniazid and para-aminosalicylic acid with satisfactory results. She developed swelling and abscess in groin which was dis- charging pus, in March 1962. (See Figure 3). Biopsy of this swelling and culture of pus showed Blastomyces dermatitidis. (See Figure 4). She received a course of 2-hydroxystilbami-
Figure 4.
Biopsy of a swelling in left groin and culture of pus from sinus showed Blastomyces dermatitidis.
Figure 5.
Sinuses healed following treatment with 2-hydroxy- stilbamidine.
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SOUTH DAKOTA
9
dine following which sinuses healed. (See Figure 5).
As signs and symptoms of pulmonary blas- tomycosis may mimic almost any granulomatous or neoplastic disease it should be suspected in any chronic pulmonary disease of undetermined etiology. Blastomycosis usually runs a chronic course but in some cases runs a fulminating course and if not recognized early ends fatally. Diagnosis should be based on isolation of Blas- tomyces dermatitidis from culture of tissue, e.g. blood, sputum or bone marrow.
Treatment:
Two drugs are available for treatment of blastomycosis, amphotericin B and 2-hydroxy- stilbamidine. Amphotericin B is the drug of choice in treatment of blastomycosis, especially in acutely ill patients with severe rapidly pro- gressive disease. According to some authors 2- hydroxystilbamidine is nearly as effective but is less toxic than amphotericin B. Both drugs are given intravenously over a period of weeks until 2 grams amphotericin B or 8 - 10 grams 2- hydroxystilbamidine have been given.
In our series8 of 15 patients, 10 received am- photericin B intravenously. A 33 year old female was treated for pulmonary tuberculosis but her progress was unsatisfactory (See Figure 6). Sputum was negative for tubercle bacilli and for fungus infection. However, lung biopsy
Figure 6.
Chest film 12.6.61 shows infiltrations involving both lungs, especially left lung. There is a cavity in left upper part.
showed a granulomatous inflammation with Blastomyces dermatitidis. She received a course of amphotericin B with improvement (See Figure 7). Nine patients were discharged and in follow up clinic later were well, the tenth died. Four patients received 2-hydroxystilbami- dine intravenously with success, one was treated with potassium iodide in 1949.
Figure 7.
Chest film 5.10.62 shows clearing of density in right lung and a large cyst in left upper part following course of amphotericin B.
REFERENCES
1. GILCHRIST, T. C.
Protozoan Dermatitis.
J. Cut. Gen. Urin. Dis. 12: 496, 1894.
2. GILCHRIST, T. C. and STOKES, W. R.
The Presence of an Oidium in the Tissues of a Case of Pseudolupus Vulgaris.
Bull. Hopkins Hosp. 7: 129, 1896.
3. SCHWARTZ, J. and BAUM, G. L.
Blastomycosis.
Am. J. Clin. Path. 21: 999, 1951.
4. DENTON, J. Fred, DI SALVO, Arthur F. and HIRSCH, Melvin L.
Laboratory Acquired North American Blastomycosis.
J.A.M.A. 199: 935, Jan.-March 1967.
5. CRAIG, Michael W., DAVEY, Winthrop N. and GREEN, Robert A.
Conjugal Blastomycosis.
Amer. Rev. Resp. Dis. 102, No. 1, 86, July 1970.
6. MALIN, Joseph M. Jr., ANDERSON, E. Everett, and WEBER, Carl H.
North American Blastomycosis of the Uro- genital Tract
The Journal of Urology — Vol. 102, No. 6, Dec. 1969.
7. RAINEY, Robert L. and HARRIS, T. Reginald
Disseminated Blastomycosis with Meningeal
JANUARY 1971
19
10
Involvement. Report of a Patient Cured by Amphotericin B Without Resort to Intrathecal Administration.
Arch. Int. Med. 117: 744, Jan.- June 1966.
8. SOCHOCKY, S.
North American Blastomycosis.
Laval Medical 35: 51, Jan. 1964.
9. CHERNISS, E. J. and WAISBREN, B. A.
North American Blastomycosis: a Clinical Study of 40 Cases.
Ann. Int. Med. 44: 105, 1956.
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20
SOUTH DAKOTA
CLINICOPATHOLOGICAL CONFERENCE
From the Intern and Resident Teaching Conferences at the Sioux Valley Hospital, conducted by the Department of Pathology of the Hospital and of the School of Medicine of the University of South Dakota
J. W. DONAHOE, M.D/
Internist - Discusser
JOHN F. BARLOW, M.D.* **
Pathologist - Editor
SIXTY-FIVE YEAR OLD FEMALE WITH AURICULAR FIBRILLATION AND SUDDEN ONSET OF COMA
CASE NO. 493594
This 65-year old Caucasian female was ad- mitted to Sioux Valley Hospital on 7-25-69 in coma.
The patient’s first admission had been six years previously for progressive intermittent epigastric pain of two months duration asso- ciated with nausea and vomiting. Physical ex- amination at that time showed a blood pressure of 130 systolic and 80 diastolic. The left cardiac border was at the midclavicular (left) line in the 5th intercostal space. The heart tones were regular and of good quality. A2 was greater than P2. There were no audible murmurs. There was exquisite point tenderness in the midepigas- trium but no other organs or masses. There were no other significant physical findings.
Clinical pathology data: Urinalysis: amber, clear, specific gravity 1.015, pH 6.0, negative for protein, glucose, sediment 0-2 leukocytes/hpf, hemoglobin 15.2 gm/100 ml., hematocrit 49 Vol.%, mean corpuscular hemoglobin concen- tration 32 micromicrograms, total leukocyte count 8,800 with 68% segmented neutrophils, 1% neutrophilic bands, 1% eosinophils, 23% lymphocytes and 7% monocytes. A serology was nonreactive. Erythrocyte sedimentation rate was 5 mm/hr. Blood urea nitrogen was 10 mgs/ 100 ml. An upper gastrointestinal series demon- strated a duodenal ulcer in the bulb. The patient responded to an ulcer regimen and was dis- charged.
The patient was next admitted on 12-17-65. She had been in good health until one week
*Specialist in Internal medicine, Sioux Valley Hos- pital, Assistant Professor of Medicine, School of Medicine, University of South Dakota.
**Pathologist, Sioux Valley Hospital, Professor of Clinical Pathology, School of Medicine, University of South Dakota.
Supported in part by Clinical Cancer Training Grant T12 CA 08032 from the National Cancer Institute of the National In- stitutes of Health, U. S. Public Health Service.
before entering the hospital when she developed “flu-like” symptoms. Three days before admis- sion she noted palpitations and sensation of fatigue and shortness of breath. Physical exam- ination revealed a well developed, well nour- ished normal appearing white female who was apprehensive and nervous. The blood pressure was 140 systolic and 70 diastolic, pulse was grossly irregular at 140/minute. There was no neck vein distention or other abnormalities of the head and neck. The lungs were clear to aus- cultation and percussion. The left cardiac bor- der was slightly to the left of the midclavicular line in the 5th intercostal space. The heart tones were grossly irregular with an apex rate of 140/ minute. A2 equalled P2. There were no audible murmurs. The liver was not palpable but there was tenderness in the right upper quadrant.
Clinical pathology data: Urinalysis: straw, clear, specific gravity 1.027, pH 5.0, protein 1 + , negative for glucose; sediment 1-3 leukocytes/ hpf, 3-5 hyalin casts/lpf, hemoglobin 14.4 gms/ 100 ml., total leukocyte count 6,100 with 70% segmented neutrophils, 4% eosinophils, 1% basophils, and 25% lymphocytes. Platelets were adequate on smear. The red cells were normo- chromic, normocytic. Atrial fibrillation was con- firmed on electrocardiogram.
The patient was admitted for cardioversion after digitalization. After a second discharge the patient developed a normal sinus rhythm. In the evening the patient developed sudden pain, numbness and coldness in the right leg below the knee. 5.0 cm. below the knee a sharp reddish dusky color appeared after initial pallor. On elevation the area blanched. There were absent pulses below the femoral. As she was being pre- pared for surgery, the pain disappeared and the pulses returned. She was discharged. She had reverted to auricular fibrillation after 2 days following cardioversion.
JANUARY 1971
25
The patient was next admitted one and one- half years prior to her final admission with pain, discomfort and tingling in the right calf, short- ness of breath and inability to gain weight. This was progressive over the several months prior to admission and was increased by exercise and relieved by rest. In addition, the symptoms became somewhat more exacerbated since she had had an infected tooth extracted. Pulse was 76/minute and grossly irregular, respirations 20/minute, temperature 98° F. Blood pressure 180 systolic, 92 diastolic. The lungs were clear to auscultation and percussion. The heart was normal in size. There was a blowing systolic murmur over the aortic area without a diastolic component. The rhythm was grossly irregular with a distinct pulse deficit. There was a gen- eralized rash. Abdominal examination was un- remarkable. The spleen was not palpable. Both lower extremities were thin. The dorsalis pedis and posterior tibial pulses were absent bilat- erally. The femoral pulses were present and equal. There was definite pain in the calves on walking.
Clinical pathology data: Urinalysis: straw colored, cloudy, specific gravity 1.016, pH 5.5, negative for protein, hemoglobin, sugar, ketone bodies, sediment 10-15 leukocytes/hpf, hemo- globin 14.4 gm/100 ml. total leukocyte count 9,300 with 71% segmented neutrophils, 3% bands, 1% eosinophils, 25% lymphocytes. The smear was normal. Erythrocyte sedimentation rate was 14 mm/hr. Fasting blood sugar was 94 mgs/100 ml., blood urea nitrogen 10 mgs/100 ml., creatinine 1.0 mgs/100 ml., cholesterol 190 mgs/ 100 ml., bilirubin 0.65 mgs/100 ml. total with 0.25 mgs/ 100 ml. direct. Resin triiodothyronine up- take 35% (normal 24-36%). Multiple blood cul- tures revealed no growth in 4 weeks. A throat culture revealed normal flora. The electro- cardiogram showed atrial fibrillation and left ventricular hypertrophy with T and ST segment changes involving both myocardial surfaces par- tially on basis of left ventricular hypertrophy but also on the basis of ischemia. Admission febrile agglutinins to salmonella, brucella, and tularemia: proteus OX2 and proteus OXK were negative. Proteus OX19 titer was 1:320. Repeat titers to proteus organisms OXK, OX2 and OX19 showed no change. Escherichia coli (over 100,000 colonies/ml.) was grown from the urine.
The patient was next admitted on 7-9-69 for nausea, vomiting and abdominal pain. Blood pressure was 154 systolic and 90 diastolic, res- pirations 20/minute, pulse 98/minute and ir- regular, temperature 98°F. There was no change
in physical findings. No cardiac murmurs were heard.
Clinical pathology data: Urinalysis: amber, turbid, specific gravity 1.024, pH 6.0, 1+ pro- teinuria; negative for glucose; moderate ketone bodies; trace hemoglobin, sediment 75-100 leu- kocytes/hpf, many bacteria; 0-1 erythrocytes/ hpf. Hemoglobin 18.3 gms/100 ml., hematocrit 52 Vol.%, mean corpuscular hemoglobin con- centration 35%, total leukocyte count 13,600/ mm3 with 83% segmented neutrophils, 2% neu- trophilic bands, and 15% lymphocytes. The smear was normal. Erythrocyte sedimentation rate was 5 mm/hr. Blood urea nitrogen was 14 mgs/100 ml. Stools for occult blood were nega- tive. Stools for ova and parasites and cultures for enteric pathogens were negative. A urine culture grew Escherichia coli over 100,000 col- onies/ml. An upper gastrointestinal series showed outlet obstruction in the duodenum. She was treated with antispasmodics, nasogastric suction, probanthine, gelusil and digitoxin.
Her last admission was one week later on 7- 25-69 to the Emergency Ward for coma. On the day of admission her right arm became stiff. She began shaking on the right side of her body and had a generalized seizure after which she became apneic and had to be ventilated. Hor- izontal nystagmus on one side started. Initial blood pressure was 210/140. She was given 2.5 mgs serpasil and shortly after blood pressure became unobtainable and she developed pallor, cyanosis and coldness in her left upper extrem- ity. A spinal tap revealed clear fluid with an opening pressure of 95 mm of Hg. She was given I.V. Ureaphil and started on papaverine and anticoagulation. She was transferred to the Special Care Unit.
The remainder of the physical examination showed temperature of 97 °F, respirations 20/ minute, and unobtainable blood pressure. She did respond to verbal questioning a few hours later. There was pallor and coldness of all ex- tremities, more marked on the left. The pupils were round and equal and normal size with slight response to light. The discs were flat. The lungs were clear to auscultation and percussion. Pulse was felt on the right radial artery. Fem- oral pulses were 4+ bilateral and carotid pulses 3+. The point of maximum intensity of the heart was shifted to the left and prominent. The rhythm was irregularly irregular. There were no murmurs. Abdominal examination was unre- markable. The plantar responses were extensor bilaterally. The right extremities moved poorly.
26
SOUTH DAKOTA
The stretch reflexes were more active on the right than on the left.
Clinical pathology data: Urinalysis: clear, specific gravity 1.010, pH 5.0, 1+ proteinuria, trace glucosuria, trace ketonuria, negative for hemoglobin. Sediment 40-50 leukocytes/hpf, 0-2 erythrocytes/hpf, Hemoglobin 15.0 gms/100 ml., hct. 44 Vol.%, mean corpuscular hemoglobin concentration 34%, total leukocyte count 28,500 with 74% segmented neutrophils, 9% neutro- philic bands, 1% eosinophils, 15% lymphocytes, and 1% monocytes. The red cells were normo- chromic normocytic. The platelets appeared adequate on smear. There were no cells in the spinal fluid. Protein was 20 mgs/100 ml., sugar 72 mgs/ 100 ml., culture of spinal fluid re- vealed no growth, carbon dioxide content 14 meq/L., sodium 144 meq/L., potassium 2.9 meq/ L., chloride 100 meq/L., pH 7.44, PCO2 21 mm. of Hg., PO2 81 mm. of Hg., O2 saturation 96%. Chest film showed possible cardiomegaly and mild vascular congestion. ECG showed atrial fibrillation, left ventricular hypertrophy and possible posterior infarction. She died one day after admission.
DR. DONAHOE: This is a long protocol but I think we can summarize it. The patient’s first admission was characterized by the signs and symptoms of a probable duodenal ulcer. There is a possibility, since a small bowel series was not done, that a carcinoid of the small bowel with secondary heart involvement was present. However, I doubt it. She responded to the treat- ment for duodenal ulcer and was discharged.
Approximately two years later the patient was admitted with “flu-like” symptoms. She had a normal blood pressure and a grossly irregular pulse with pulse deficit which strongly suggested auricular fibrillation. There was no neck vein engorgement and no enlarged liver, but there was some tenderness in the right upper quadrant. I imagine the patient had some early congestive failure as well as auricular fibrillation at this time. The latter was confirmed on electrocardiogram. The reason that I feel the patient was in failure was the dyspnea, protein- uria without other findings in the urinary sed- iment, fatigue, and tenderness in the right upper quadrant. Carcinoid heart disease or hyper- thyroidism could be the cause of the auricular fibrillation, but I am going to presume that the arrhythmia is due to arteriosclerotic heart disease.
The patient underwent cardioversion after digitalization. There is no mention of the pa-
tient having been anticoagulated prior to this. The auricular fibrillation disappeared for a while after cardioversion but reappeared two days later. This, unfortunately, is a common sequence after cardioversion. After cardiover- sion the patient developed what was probably an embolus to the leg, but just as the surgeon was sharpening his knife, the pulses returned and no surgery was necessary. I assume that the artery had gone into spasm and that the em- bolus later passed as the spasm relaxed. Then, the embolus went on down to a smaller vessel in the leg.
Three years later the patient came back into the hospital with pain in the right calf, short- ness of breath, and inability to gain weight of some months duration, the recent onset of a rash and probably fever (since febrile agglutins were ordered). There is no definite mention of temperature elevation. She had her first evi- dence of hypertension on this admission. To complicate the picture she had had the removal of an infected tooth prior to admission. She still had atrial fibrillation and she had a murmur for the first time. This was not diastolic but sys- tolic. We must consider subacute bacterial endo- carditis under this set of circumstances. How- ever, the patient does not have anemia, an ele- vated white count, or an elevated sedimenta- tion rate. Multiple blood cultures were negative. I think that the patient probably did not have bacterial endocarditis. The presence of a rash and an elevated proteus OX19 suggests the possibility of typhus. There is no evidence of contact with typhus and I do not know where the patient lived. I would suspect that the ele- vated titer is simply a red-herring. I might point out that she had evidence of a urinary tract in- fection, which she continued to have throughout the rest of her life. She evidently improved be- cause she was discharged.
She was admitted again — this time with nausea, vomiting, and abdominal pain and a somewhat lower blood pressure. She continued to have auricular fibrillation. The bacteriuria, proteinuria, and pyuria persisted. She had a slightly elevated white count. I think that the high white count could be explained as due to her urinary tract infection. The BUN was never elevated. I think the abdominal symptoms she had were due to an obstructed gastric outlet due to her chronic duodenal ulcer. The usual meas- ures brought about relief of these abdominal symptoms. She was discharged only to return one week later for her terminal admission with coma. I assume that this coma was rather sud-
vi
r •
JANUARY 1971
27
den in onset. Therefore, I suspect a vascular catastrophe in the cerebral circulation. The spinal fluid was not remarkable. Her blood pres- sure which was markedly elevated on admission had dropped to 0. I assume it stayed at zero un- til demise. She had good femoral and carotid pulses. She continued to have atrial fibrillation and had an enlarged heart. The high white count might suggest a bacterial infection, but there was certainly not a meningitis since there were no cells in the spinal fluid.
In seeking the cause of this patient’s auri- cular fibrillation, I see no evidence for rheu- matic heart disease. I do not think she had hy- perthyroidism. I think she had arteriosclerotic heart disease which caused the auricular fibril- lation and that her central nervous symptoma- tology was due to emboli from the heart due to the auricular fibrillation. I do not think her duodenal ulcer had much of a part to play. She could have had a perforated ulcer terminally, but I doubt this. Multiple emboli are certainly a frequent problem in people with auricular fibrillation. I’m sure that this patient had auri- cular fibrillation for a long period of time, per- haps intermittently, and may have had it for some time before her cardioversion.
*DR. JONES: The patient did have a normal sinus rhythm on her first admission six years previously.
DR. DONAHOE: Yes, but she did have auricular fibrillation a long period of time. The patient could have had a subacute bacterial endocar- ditis as a cause of her emboli, but I doubt it. I cannot support the diagnosis of hyperthyroidism or carcinoid heart disease. Periarteritis nodosa should be considered, but I have no evidence for that diagnosis.
DR. JACK DONAHOE'S DIAGNOSIS
1. Arteriosclerotic Heart Disease With Auri- cular Fibrillation
2. Emboli to Brain and Lower Extremities from Thrombi in Left Atrium
3. Urinary Tract Infection
4. Chronic Duodenal Ulcer, Not Perforated
**DR. LAURENS WILLIKES: I wonder if the initial hypertension during the last admission was not due to the emboli to the kidney. I also feel that we should more strongly consider bac- terial endocarditis or even a myocarditis.
DR. DONAHOE: I did consider an endocarditis
* Specialist in internal medicine, Sioux Valley Hos- pital, Assistant Dean, School of Medicine, Uni- versity of South Dakota.
** Intern, Sioux Valley Hospital.
on one admission, but think that the hyperten- sion in the last admission was probably due to her general condition. She probably did have emboli into the kidneys as I’m sure she had showers of emboli from her auricular fibrilla- tion.
***DR. WILLIAM O. ROSSING: You are mak- ing a diagnosis of arteriosclerotic heart disease in the absence of a history of angina pectoris or of an old myocardial infarction. This would be somewhat contrary to the criteria of the Amer- ican Heart Association.
DR. DONAHOE: Yes, this is true. However, I have a great deal of difficulty making a diag- nosis of rheumatic heart disease without a mur- mur. If rheumatic heart disease were present, I would think it would be mitral disease. fDR. EVERETT SANDERSON: I am a little suspicious, as is Dr. Willikes, of the diagnosis of bacterial endocarditis. However, I have to agree with Dr. Donahoe in his diagnosis and I would also support the diagnosis of arterio- sclerotic heart disease even in the absence of angina pectoris or a previous myocardial in- farction. I think we see cases like this rather frequently. An atrial myxoma might be a possi- bility also, but I have not got much to support it.
DR. DONAHOE: No, we only have a history of one transient systolic murmur.
DR. ROSSING: I am sure you can make the diagnosis of arteriosclerotic heart disease in the absence of previous myocardial infarction or angina pectoris. However, you have no more basis of making that diagnosis in this case than rheumatic heart disease without a murmur. I am just talking about the certainty of diagnosis and we cannot be certain of either arterio- sclerotic or rheumatic heart disease in this case. DR. DONAHOE: I could also suggest that the patient might have had a myocardial infarction terminally.
*DR. WALTER K. SOSSEY: I think that the times when the patient had an elevated white count were all times when she either had a urinary tract infection or some severe stress such as a convulsion. I also think the hyperten- sion on the last admission could have been due to cerebral edema.
DR, DONAHOE: I might also mention that the
***Specialist in internal medicine, Sioux Valley Hos- pital, Assistant Clinical Professor of Medicine, School of Medicine, University of South Dakota, t Specialist in internal medicine, Sioux Valley Hos- pital, Assistant Clinical Professor of Medicine, School of Medicine, University of South Dakota.
* Intern, Sioux Valley Hospital.
28
SOUTH DAKOTA
patient could have had a long standing pyone- phrosis and this could have been the explana- tion for her urinary tract findings and also a source of bacterial endocarditis. This is unlikely. Give me the bad news, John!
PATHOLOGIC FINDINGS
DR. BARLOW: I remember very well present- ing a case like this at cardiology grand round at the Massachusetts General Hospital. I think the striking thing about this case is that there was severe mitral stenosis with marked calci- fication of the valve cusps, and yet there was no murmur clinically. There were adherent throm- bi in the left auricular appendage which gave rise to many emboli. The whole right cerebral hemisphere showed infarction. There was also infarction of small areas in the right cerebral hemisphere and left occipital lobe. There were healed renal infarctions as well as a healed splenic infarct. There was focal bronchopneu- monia. In the heart in addition to the mitral stenosis and thrombi in the atrial appendage, there was moderately severe anterior descend- ing left coronary atherosclerosis. There was a small anterior wall healed myocardial infarction as well as a recent myocardial infarction of 1-3 days duration in the same area. The patient in- deed did have a chronic duodenal ulcer.
FINAL ANATOMIC DIAGNOSES
1. Mitral Stenosis With:
A. Myocardial Hypertrophy (480 Grams) and Dilatation
B. Mural Thrombus, Left Auricular Append- age With:
(1) Recent Thromboemboli to Brain Re- sulting In:
a. Infarction cf Right Cerebral Hemisphere
b. Focal Infarction of Cerebellum
c. Infarction of Part of Left Occipital Lobe
(2) Organizing Splenic Infarct
(3) Healed Renal Infarcts
2. Bronchopneumonia With Focal Microabscess Formation
3. Atherosclerosis of Anterior Descending Branch of Left Coronary Artery With:
A. Healed Anterior Wall Infarct (1-3 Days Duration)
B. Recent Anterior Wall Infarct, Small
C. Fibrous Pericardial Adhesions
4. Acute Renal Tubular Necrosis
5. Chronic Duodenal Ulcer
6. Moderate Arterial Nephrosclerosis
7. Mild Arteriolar Nephrosclerosis
8. Hemorrhagic Cystitis
9. Aortic Atherosclerosis, Mild
10. Fibrous Pleural Adhesions, Left
Figure I.
So-called fishmouth deformity of severe mitral sten- osis as viewed from left atrium.
Figure II.
Hemorrhagic infarct on right of picture from cerebral embolus probably secondary to left atrial thrombus.
Figure III.
Microscopic of hemorrhagic infarction of brain.
(Continued on following page)
JANUARY 1971
29
DR. DONAHOE: What is the significance of the high proteus 0X19 titer?
DR. BARLOW: This particular test using pro- teus 0X19 organisms is often called the Weil- Felix reaction. Titers to proteus 0X19, OXK, and 0X2 are commonly used in the diagnosis of rickettsial disease. This can be done because these particular strains of proteus organisms share antigens with the rickettsia. A big prob- lem, of course, is the nonspecificity of the re- action. Obviously, proteus or other gram nega- tive enteric bacillary infections will also cause a rise in titer of these antibodies since these organisms may possess the antigens mentioned. I think in this case although the patient had a high titer, there was no rise or fall in a subse- quent titer. What is more a gram negative in- fection was present. This would tend to make one believe that there was no rickettsial disease giving rise to this antibody response.
DR. ROSSING: Do you think that the valvulitis in this case could have been due to arterio- sclerosis and not due to rheumatic fever? In other words, is there a point at which the differential between rheumatic heart disease and arteriosclerotic valve disease is not distin- guishable?
DR. BARLOW: I think that the involvement of the valve was definitely rheumatic. There is arteriosclerotic disease causing calcification of the mitral annulus, but on an arteriosclerotic basis.
*DR. FREDRICKSON: What did the aortic valve look like in this case?
DR. BARLOW: The aortic valve was normal. DR. DONAHOE: What is the incidence of ar- terial emboli in a patient who has had mitral commissurotomy and is still fibrillating?
DR. JONES: I would think it would be very high. I feel that Dr. Donahoe did well in his dis- cussion of this CPC for what information ap- peared in the protocol. In fact, I did not do better than he even though I examined and observed this patient many times during the last few years of her life. I make these comments for whatever consolation it might be for our dis- cussant today. There are cases of this sort in which one tries to re-analyze on retrospect his way of thinking in order to ascertain whether or not he had really overlooked something that he ought to have found, and to see whether or not the treatment rendered might have been materially different had he been the wiser.
* Intern, Sioux Valley Hospital.
Therefore, I have a few comments to make at this time relative to several features of this case.
First of all, atrial fibrillation is a rhythm dis- turbance that usually occurs in the presence of underlying heart disease. Statistically, the chances are approximately 90% as opposed to 10% that the patient has underlying heart disease. The three most common causes for atrial fibrillation are: 1) Arteriosclerotic heart disease 2) Mitral stenosis and, 3) Hyperthyroidism. The latter is unlikely in this case, and mitral sten- osis certainly is not diagnosible on the basis of protocol information, so that Dr. Donahoe’s diagnosis of arteriosclerotic heart disease is cer- tainly the most likely on the basis of these statistics.
The second point is the fact that this lady had one and probably many arterial emboli. Arterial emboli usually arise from thrombi in the left atrium. Of a series of 1,200 patients1 with mitral stenosis, almost one third had experienced a systemic arterial embolism before mitral com- missurotomy. Among those patients with mitral stenosis, but with a sinus rhythm, in this series, the history of embolism was obtained in only 9.6%. To further amplify the high incidence of arterial embolization in patients with mitral stenosis and atrial fibrillation, a study by Daley and co-workers2 reported that 90% of the em- bolizations that occurred in patients with mitral stenosis was with associated atrial fibrillation. It was their conclusion that in patients with mitral stenosis and a sinus rhythm, arterial em- bolization is relatively rare.
Now, in order to reconcile the presence of a tight and severe calcific mitral stenosis without
Figure IV.
Shows relationship between the heart sounds (HS) and the electrocardiogram (ECG) and the components of the auscultatory findings in mitral stenosis: The diastolic murmur (DM), presystolic crescendo (PC), and the opening snap (OS) of the mitral cusps.
30
SOUTH DAKOTA
the usual auscultatory findings as found in our patient, let us first review the usual auscultatory findings in any patient with mitral stenosis. Referring to figure I, one will note that ordin- arily there is a loud amplified M-l, a normal M-2, an opening snap occurring from 0.08 to 0.11 seconds after the 2nd heart tone, and a diastolic rumble during the remainder of diastole with a presystolic crescendo.
These findings are characteristically obtained with the patient in the recumbent position, and listening carefully at the apex with the bell chest-piece. The more stenotic the mitral valve and the greater the pressure differential be- tween the left atrium and left ventricle during ventricular diastole, the greater the velocity blood flow and the louder the diastolic rumbl- ing murmur. The presystolic crescendo is created by the increase in velocity blood flow across the mitral valve at the time of atrial systole. Now, in this patient with atrial fibrillation, atrial sys- tole is noticeably absent, and therefore the pre- systolic crescendo would not be heard. It is stated that the diastolic murmur diminishes in intensity and may become inaudible when there is a very marked reduction in cardiac output, and consequently a change in the hemodynamics across the mitral valve. It may have been these hemodynamic changes that helped to create a “silent” mitral stenosis in this case. In ad- dition, the opening snap is created by the in- ordinate pressure gradient between the left atrium and left ventricle. This must be present in order to flex the rigid diseased mitral cusps. The opening snap tends to disappear with in- creasingly significant mitral regurgitation. It is also likely to be absent when calcification of the valve cusps is extensive enough to produce com- pletely rigid cusps. Therefore, one might ac- count for the absence of the opening snap in this case, which might otherwise have been a help- ful auscultatory finding. On these bases, there- fore, one might account for the possibility of the mitral stenosis without the usual auscultatory findings as was the case in this patient.
Antemortem, I had come to the same diag- nostic conclusions as Dr. Donahoe in his post- mortem analysis of this case.
BIBLIOGRAPHY
1. Friedberg, C. K., Diseases of the Heart, Third Ed., W. B. Saunders Co., Phila., 1966, p. 540.
2. Daley, R., Mattingly, T. W., et al, American Heart Journal, 42: 566, 1951.
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~fhiA fa tfCUf
MEDICAL ASSOCIATION
The annual symposium of the medical staff of the Sioux Valley Hospital was held in Sioux Falls on November 13 and 14. The theme of this year’s symposium was “Stroke — Its Diagnosis and Treat- ment.” Guest speakers in- cluded Adolph Sahs, M.D., Chairman of the Department of Neurology, University of Iowa; John Kennady, M.D., neurosurgeon from the Uni- versity of California and John Quast, M.D. from St. Joseph’s Hospital in Minneapolis. John F. Barlow, M.D., Sioux Falls, was chairman of the commit- tee which organized the pro- gram. Other supporters of the symposium were the South Dakota Regional Medical Pro- gram, the South Dakota Heart Association, and the South Da- kota Chapter of the American Academy of General Practice.
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The Yankton Diabetes De- tection Drive is being headed by R. I. Porter, M.D. Free dia- betes tests were given during Diabetes Week which was No- vember 15-21.
J. C. Smiley, M.D., 66 year old Deadwood physician, died recently following a brief illness. Dr. Smiley graduated from Rush Med- ical College in 1930. Follow- ing his internship and resi- dency training h e estab- lished his practice in Dead- wood and has been there for the past 36 years. Dr. Smiley is survived by his widow and a brother, R. A. Smiley of Deadwood.
F. E. Manning, M.D., died at age 78 in Custer. Dr. Manning graduated from Creighton University Med- ical School in 1915. He prac- ticed in Custer from 1926 to the time of his death. He served as county health of- ficer for more than 40 years, as coroner for 10 years, on the school board for 14 years, as mayor of Custer for 4 years and as a legisla- tor for Custer and Fall River counties for 6 terms. Dr. Manning is survived by his widow, Lucile, a son, Donald Manning, M.D., Sioux Falls, and a daughter, Mrs. Albert Tripet of Tucson, Arizona.
R. A. Buchanan, M.D.,
Huron, spoke to members of the Jerauld County Extension Club concerning Jerauld County’s participatory status in the Central South Dakota Mental Health Center.
YOUR
CONTRIBUTION TO THE
SOUTH DAKOTA MEDICAL SCHOOL ENDOWMENT FUND IS NEEDED
The Dakota State College Scholarship fund was pre- sented a two-story frame heme by J. R. Westaby, M.D., Madison.
^ ^ $
W. F. Slanage, M.D., Yank- ton, has been named by Presi- dent Nixon to serve as a dele- gate to the White House Con- ference on Children.
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Two Yankton physicians ap- peared on the scientific pro- gram of the American College of Obstetrics and Gynecology held in St. Paul, Minnesota. Brooks Ranney, M.D. pre- sented a paper on “Endome- triosis — Hereditary Tend- ency,” and David Holzwarih, M.D. participated in a round- table on “Surgical Steril- ization” and presented one of three papers on this subject.
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Featured speakers at the Cancer Conference for Nurses held in Huron included B. T. Lenz, M.D., Huron, president of the South Dakota Division of the American Cancer So- ciety, and James Vose, M.D., Mitchell, Chairman of the American Cancer Society Service Committee.
Charles L. Combe, M.D.,
38, assistant professor o f pathology at the University of South Dakota, died fol- lowing a car accident near Vermillion. He is survived by his widow, Margaret, two sons, Charles, 5, and Robert, 2, and a daughter, Teresa, 1 month.
JANUARY 1971
35
Karlis Zvejnieks, M.D.,
Aberdeen, spoke to members of the Corona Community Club on the hardships of the Russian civil war and the communist atrocities.
sj; :j:
Arthur Semones, M.D.,
director of the Homestake Hospital staff, participated in
a panel discussion on drug use and abuse which was held in
the Lead High School.
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Bruce Lushbough, M.D.,
Brookings, was elected the 65th president of the Univer- sity of South Dakota Alumni Association at its annual meet- ing.
Professional dieticians at- tending the 21st annual meet- ing of the South Dakota Die- tetic Association heard Robert Hayes, M.D., state health of- ficer, put forth “A Plan for Action” relating to ‘‘The Health Crisis in South Da- kota.”
MINUTES OF THE COUNCIL MEETING SOUTH DAKOTA STATE MEDICAL ASSOCIATION December 5, 1970
Cataract Hotel, Sioux Falls, South Dakota
The meeting was called to order at 1:45 p.m. by Dr. Harvard Lewis, Chairman of the Council. Present for roll call were the following physicians: J. A. Muggly, G. Robert Bartron, W. R. Taylor, A. P. Reding, R. H. Quinn, G. E. Tracy, Fred Leigh, H. R. Lewis, E. T. Lietzke, and E. T. Ruud.
Dr. Taylor moved that the minutes of the Septem- ber meeting be approved as published in the Journal. The motion was seconded by Dr. Ruud and carried.
A discussion of the proposed budget for the School of Medicine was held. Dr. Tracy moved that the Coun- cil be in favor of urging the adoption of the 1972 fiscal year budget for the Medical School as submitted by the University of South Dakota by the State Legis- lature. The motion was seconded by Dr. Ruud and car- ried.
Dr. Tracy reported on the meeting of the Commis- sion on Medical Service which had been held that morning.
To: COMMISSION ON MEDICAL SERVICE From: FACULTY, UNIVERSITY OF SOUTH DAKOTA SCHOOL OF MEDICINE Subject: THE FUTURE OF MEDICAL EDUCATION IN SOUTH DAKOTA
Although the possibility of establishing a four-year school has been considered several times in the past, the grinding necessity of adequate financing for our two-year school continually pushes this into the back- ground. I am sure you are all aware that last year’s appropriation for the Medical School would never have been obtained without the solid backing of the Medical Association.
A number of actions and events, recently, on the local, regional, and national scene have again focused the attention of the faculty upon the future of the University of South Dakota School of Medicine, and medical education in South Dakota.
The most immediate and pressing concern has to do with N.A.M.E. There are several people present who are more knowledgeable than I regarding N.A.M.E.; but, briefly, this is an attempt to form a regional medical school in St. Paul. They would use St. Luke’s Hospital in St. Paul as a central, or core, hospital, and then use other hospitals and doc- tors’ private practices in the region as ancillary teaching units. No school can start without money, and so they want to enter into compacts with ad- jacent states to finance it. To begin with, this would be a medical school for only the last two years, much as Rush Medical School was many years ago. The initial amount is not clear to me, but I have heard figures between 200,000 and 400,000 dollars from each state. In addition to some preliminary meetings in St. Paul, Dr. Davitt Felder has recently met with the South Dakota Board of Regents. An additional and very disturbing rumor is that there are those who would like to get rid of the medical school, com- pletely, because of the money it costs. The faculty of the Medical School is concerned that such a com- pact will be brought up during the next session of
the legislature; and this is the reason for calling this special meeting of the Commission on Medical Serv- ice. Thus far, at least, the Medical Association, the Medical School faculty, and those knowledgeable about medical education, have not been consulted by the Regents, Mr. Gibb, or the Governor.
On the national and regional scene, there are fast- moving developments:
1. The Carnegie Foundation’s Commission on High- er Education report (a second Flexner-type re- port) which has recently been released, will have profound and far-reaching effects upon medical education in this country. From this report, plus the growing demands of the people, plus the attitude of H.E.W., it is apparent that academic excellence is a luxury that we can no longer afford, and perhaps, realistically, a doctor should not be expected to absorb all of the new medi- cal information. Without going into detail, it is their recommendation that medical school and residencies be shortened by one year each. Ad- ditionally, they recommend that the doctor going into research or academic teaching branch off after the second year of medicine.
2. Medical school curricula have already changed
radically, and the isolated internship, as such, will be gone by 1975. At this time, the fourth year of medical school is actually the same as the rotating or mixed internship that most of us knew. Therefore, a repetition of this type of training is already redundant. i
3. Dr. Walter C. Bomemeier’s inaugural address to the American Medical Association should not be ignored, as he is the spokesman this year for organized medicine. Briefly, he would do away with the large medical center concept of grad- uate training, and disperse young doctors about j the country as preceptees.
4. We do have some existing guidelines which point to the future:
a. The existing Indiana Program
b. The new Michigan State Program
c. The planned new University of Missouri, at Kansas City, is a radical departure from present norms of medical school curriculum.
5. In my opinion, the existing Family Practice Res- idency will not work. The time (3 years) is too long, and the curriculum too rigorous. Those of you who have studied the Family Practice Res- idency Programs, I am sure would agree with me, that if I were a medical student it would terrify me, and for the same amount of time I could go into one of the specialties. There is currently a revolution brewing among the Cali- fornia A.A.G.P.
With the foregoing as a preamble, and to avoid the position of being negative regarding the compact with N.A.M.E., the Clinical Faculty would like to make a positive recommendation to the doctors and the people of South Dakota. We do not think it is unrealistic, with the foregoing points of reference, to plan for complete medical education in South Dakota. With the pressures to establish Health Training Cen- ters for all health-related programs, the only way that we can possibly retain doctors and related per- sonnel in South Dakota is to train them here. The
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financing of the following proposal I must leave to others; but if we are talking about $200,000-$400,000 for a compact with N.A.M.E., with the same amount of money we can get a complete medical training program for doctors started, and if H.E.W. and the Carnegie Report mean what they say, there should be federal money available, also. We cannot do it with the present personnel. You are all aware of the demands of private practice; and although many have given generously of their time and energies to teach at the Medical School, the additional time it would take to teach and supervise third and fourth-year medical students is a practical impossibility; and yet, we have a nucleus that could do the job if there were full-time men to direct and coordinate our ac- tivities. Already, there are two internships in Sioux Falls, and residencies in Obstetrics & Gynecology and General Surgery in Yankton. I can tell you from long experience that it is easy to incorporate under- graduate teaching into an existing graduate program. Our summer clerks and former students who have returned for an elective quarter in their fourth year would testify to the fact that it works well, and meshes with the curriculum of their school.
Therefore, the faculty would propose that a pilot program for complete medical education in South Dakota should be considered. If the legislature would make a special appropriation for a full-time staff, if federal aid were available, if the Council on Medical Education, and the Association of American Medical Colleges would give provisional approval, and if Sa- cred Heart Hospital, McKennan Hospital, and Sioux Valley Hospital and staffs would agree to participate, we could certainly start with a pilot group of 16 to 24 of our own students. These hospitals already have graduate programs and part-time Directors of Med- ical Education. Then, if the pilot program worked, and additional financing were made available, other areas of the state could be incorporated into the pro- gram for handling all of our medical students. If the above suggestion would prove too cumbersome to begin with, we could start a pilot program with 8 students at Sacred Heart Hospital and call upon the Sioux Falls hospitals or other hospitals in the state to help us in areas of training in which we are de- ficient. With developments on the national scene, I think now is the time to expand our school, and the matter is most urgent.
You will remember that Bob Hayes proposed a pre- ceptor-type program several years ago. I was unal- terably opposed to it, because I thought it would pro- duce second-class doctors. However, gentlemen, and as the Carnegie Report makes clear, the American people can no longer afford the luxury of academic excellence for every physician.
With the fading out of the internship as such, we must not only provide a complete medical school which may eventually be just three years, but pro- vide graduate training in the specialties, and espe- cially in some type of Family Practice. That intern- ships and residencies can work in South Dakota has been proved; and in line with the foregoing, other areas in the state should plan for graduate training. They cannot do it, though, without teaching affilia- tion with the Medical School. I have briefly outlined a future for Medical Education in the State of South Dakota. I believe it is desirable, possible, and much better than out-of-state alliances. The future of Med- icine in South Dakota depends upon us — the doctors of South Dakota. Let us not be the victims of polit- ical expedient.
Respectfully submitted,
C. B. McVay, M.D., Ph.D.
Clmical Professor of Surgery and
Associate Professor of Anatomy
University of South Dakota School of Medicine
University of South Dakota School of Medicene
PLANNING FOR AN EXPANDED MEDICAL EDUCATION PROGRAM
There continues to be great concern, both locally and nationally, over the growing shortage of health
manpower and the need for improvements in the de- livery of health care. Recommendations that this med- ical school’s programs be expanded to meet these needs continue to come from various sources. At the national level, recent recommendations of the Asso- ciation of American Medical Colleges and of the Car- negie Commission on Higher Education call for in- crease in the number of medical graduates, short- ening of medical training, and greater involvement of medical schools in the systems for providing health care.
The School of Medicine has held back in its plan- ning for expansion in order to concentrate its efforts on obtaining adequate financial support for the cur- rent two-year program. An urgent need still exists to strengthen this basic support, inasmuch as we share with all other medical schools the financial problems posed by decreasing support for higher education and withdrawal of federal support for research and other programs. Nevertheless, the pressures continue to mount for action to offset the growing health care crisis especially as it relates to South Dakota. In consideration of this, the Executive Committee of the School of Medicine has concluded that it is now time to formulate more clearly and present some of the plans for expansion of the educational program which we have had under consideration for the past three years. While our major efforts will still be to con- tinue strengthening the two-year program, we recog- nize its limitations in meeting the long-term needs of South Dakota. Therefore, we consider it essential that new concepts for development of the school be explored. Also, recent developments in medical edu- cation and in medical practice provide opportunities which did not exist before for serious study of in- novative approaches to a complete medical education program.
One approach, which is presently under considera- tion, would be to provide a complete course of med- ical education in South Dakota through expansion of the present clinical instruction program, with eventual extension to incorporate teaching resources throughout the state and region. The curriculum would be designed to incorporate various new ap- proaches in clinical teaching, including the provision of elective courses in various fields of medicine. The emphasis would be on educating the student in the setting of his future practice relationships so as to encourage an interest in providing comprehensive family health care. Such a plan could be carried out in phases, with the first consisting of a “pilot pro- gram” for 8 or 12 students who have completed the present two-year program. The remaining sophomore students would transfer as usual to other four-year schools. During the second phase the clinical enroll- ment could be increased by increments over a period of years to eventually include all of the students en- tering medical school. There would also be con- solidation and any needed restructuring of the cur- riculum during this period. A third phase would be one of extension of the clinical instruction to incor- porate other hospitals and teaching facilities in the state and region. Obviously the various phases would overlap, for it would be expected that concurrently there would be:
— Development and refinement of the program.
— Expansion and extension of clinical instruction.
— Increase in number of clinical students enrolled.
— Reorganization and modernization of the cur- riculum, with integration of basic and clinical sciences.
In the development of any expanded clinical in- struction program attempts would be made to in- corporate desirable and practicable aspects of cur- ricular improvements being made at other medical schools. Efforts would be made to shorten the time necessary for the medical degree, to better integrate basic and clinical sciences and medical and premedical instruction, to make greater use of sophisticated com- munications media, etc. It would be understood that although new concepts would be applied there would also be careful ongoing evaluation of the program with modification made as indicated.
JANUARY 1971
37
The Administrative Committee of the School of Medicine in December, 1967, recommended eventual establishment of a medical degree-granting program and urged that feasibility studies be made. We be- lieve that the climate in medical education and the pressures for medical manpower make it increasingly important to devote intensive study to this matter. Of course, fundamental to the development of a specific plan for a medical degree-granting program would be strengthening of the present Department of Clinical Instruction and full support of the basic science departments and other fundamental programs of the present two-year medical school. This should include establishment of the long recommended De- partment of Community Medicine and the develop- ment of the school’s capabilities to respond to the demands for continuing medical education. For initiating an expanded program, it would be essential to have a department of educational planning and assessment or some other form of planning assist- ance.
The recommendations of the Carnegie Commission lend immediacy to our planning efforts. The prin- cipal goal of the Commission to be achieved by 1980 is “Expansion of the functions of university health science centers so that they can play a central role in coordinating and guiding health manpower educa- tion and cooperating with other agencies in the de- velopment of improved health care delivery systems in their regions.” Other major goals call for develop- ment and expansion of programs for physicians and dentists’ associates and assistants, for acceleration of medical education, and for integration of basic sciences with premedicine, and of professional educa- tion with programs of postgraduate training. It is recommended that medical education be more respon- sive to the expressed needs of students and more concerned with problems of delivery of health care. In South Dakota, the School of Medicine is iden- tified by the Carnegie Commission as a University Health Science Center which should be developed and expanded, and it is the Commission’s goal that area health education centers affiliated with our medical school be established in Rapid City and Sioux Falls by 1980.
In view of the opportunity and the potential which now exists, we believe that plans should be formu- lated for adapting new concepts in medical education to provide a complete medical degree-granting pro- gram in South Dakota. We believe that these de- velopments also provide a strong argument for giving firm support to the present two-year program so as to create a firm foundation for expansion.
G. W. Knabe, M.D., Dean
Dr. Tracy presented the recommendation of the Commission as follows:
The Commission on Medical Service recommends to the Council that the philosophies, goals and concepts of the 1970 USD Medical School pro- gram for an M.D. degree granting program be approved by the Council; and that if the Council approves this recommendation, that the presi- dent of the University of South Dakota, the Board of Regents and the Governor be apprised of this report and urged to proceed with the study and implementation of a degree granting program at the University of South Dakota Med- ical School.
Following a discussion of this recommendation, Dr. Taylor moved that the recommendations of the Commission on Medical Service be adopted and that the Council reaffirm its firm support of the two- year school. The motion was seconded by Dr. Leigh and carried.
Mr. Erickson read a letter from the Eighth District Medical Society with their nominations for Coun- cilor to complete the term of Dr. Clark Johnson who has resigned. Dr. Leigh moved that Duane Reaney be named to complete the term of Dr. Johnson which will expire at the 1971 annual meeting. The motion was seconded by Dr. Reding and carried.
Mr. Erickson read a letter from C. S. Richter,
D.D.S. of Huron, requesting sample drugs from phys- icians for distribution in Central America. Dr. Leigh moved that announcement of this request be included in a future issue of the Grab Bag. The motion was seconded by Dr. Lietzke and carried.
The meeting adjourned at 3:30 p.m.
ANNOUNCEMENT
The Department of Postgraduate Medicine of Albany Medical College announces Reservations Now Being Accepted for a Spring Postgraduate Medical Seminar Cruise to the Mediterranean April 30-May 20, 1971.
A 20-day cruise from New York aboard the luxurious and distinguished ship “Raffaello” of the Italian Line.
Ports of call include Casablanca, Naples, Genoa, Cannes, Barcelona and Lisbon.
Faculty of the Albany Medical College will pre- sent a comprehensive shipboard postgraduate pro- gram, covering subjects in internal medicine, cardiology, obstetrics and gynecology, pathology and surgery.
Request has been made for continuation study credit by the American Academy of General Prac- tice.
For information write to:
William P. Nelson, III, M.D.
Department of Postgraduate Medicine Albany Medical College Albany, New York 12208
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38
SOUTH DAKOTA
(
Legislative activities continue to play a big role in the over-all concerns of organized medicine.
Over the years, the South Dakota State Medical Association has worked hard with our State Legislature to develop programs aimed at better health care for our citizens. It is important that this work and interest be continued by our Association.
Each year more and more bills are introduced which affect medicine and we can expect between thirty and thirty-five bills to be introduced during the ’71 Session.
Our executive secretary, attorney and director of public relations will again be in Pierre, during the Session. If you have ideas or comments on legislative matters anytime during the Session, let these people know your thoughts. Headquarters are at the Holiday Inn.
J. A. Muggly, President
JANUARY 1971
39
DIRECTORY
THE SOUTH DAKOTA STATE MEDICAL ASSOCIATION Organized 1882 711 North Lake Avenue
Sioux Falls, South Dakota 57104
1970-1971 OFFICERS
President
J. A. Muggly, M.D. Madison
President-Elect
G. Robert Bartron, M.D Watertown
Vice President
W. R. Taylor, M.D. Aberdeen
Secretary-Treasurer (1970-1971)
A. P. Reding, M.D. Marion
AMA Delegate (1970-1971)
R. H. Quinn, M.D. Sioux Falls
Alternate AMA Delegate (1970-1971)
J. J. Stransky, M.D. Watertown
Chairman of the Council
Harvard Lewis, M.D. Mitchell
Speaker of the House
J. T. Elston, M.D. Rapid City
Councilor-at-Large
R. H. Quinn, M.D. Sioux Falls
COUNCILORS
First District (Aberdeen)
David Seaman, M.D. (1971) Aberdeen
Second District (Watertown)
Gerald E. Tracy, M.D. (1971) Watertown
Third District (Brookings-Madison)
Bruce Lushbough, M.D. (1972) . Brookings
Fourth District (Pierre)
C. L. Swanson, M.D. (1971) Pierre
Fifth District (Huron)
Fred Leigh, M.D. (1972) Huron
Sixth District (Mitchell)
Harvard Lewis, M.D. (1972) Mitchell
Seventh District (Sioux Falls)
E. T. Lietzke, M.D. (1972) Beresford
Eighth District (Yankton)
Duane Reaney, M.D. (1971) Yankton
Ninth District (Black Hills)
E. T. Ruud, M.D. (1970-1971) Rapid City
Tenth District (Rosebud)
M. R. Cosand, M.D. (1970-1971) Winner
Eleventh District (Northwest)
James Ryan, M.D. (1970-1971) Mobridge
Twelfth District (Whetstone)
E. A. Johnson, M.D. (1970-1971) Milbank
1970-1971 COMMISSIONERS
Commission on Legislation and Governmental Relations
J. B. Gregg, M.D., Chr., (’73) Richard G. Gere, M.D., (’73) Thomas Bunker, M.D., (’73) Charles E. Tesar, M.D. (’73) Harold Frost, M.D. (’72)
R. W. Honke, M.D. (’72)
R. J. Foley, M.D. (’72)
Bill Church, M.D. (’71)
G. Robert Bartron, M.D. (’71) Robert Hayes, M.D. (’71) Howard Wold, M.D. (’71)
J. E. Ryan, M.D. (’72)
Executive Committee
Robert H. Quinn, M.D., Chr. J. T. Elston, M.D.
G. Robert Bartron, M.D. William Taylor, M.D.
A. P. Reding, M.D. J. A. Muggly, M.D.
Grievance Committee
Paul Hohm, M.D., Chr. (’71) James P. Steele, M.D. (’72) R. H. Quinn, M.D. (’75) John T. Elston, M.D. (’74)
John J. Stransky, M.D. (’73)
Utilization and Insurance Review Committee C. B. McVay, M.D., Chr. E. S. Palmerton, M.D.
Harvard Lewis, M.D. H. Russell Brown, M.D.
Roscoe E. Dean, M.D. Wm. Rossing, M.D.
DISTRICT OFFICERS
DISTRICT 1
President John C. Rodine, M.D., Aberdeen, S. D.
Vice President Mary Sanders, M.D., Redfield, S. D.
Secretary-Treasurer Karl Kosse, M.D., Aberdeen, S. D.
DISTRICT 2
President J. C. Larson, M.D., Watertown, S. D.
Vice President Alden Heupel, M.D., Watertown, S. D.
Secretary-Treasurer T. J. Wrage, Jr., M.D., Watertown, S. D.
DISTRICT 3
President H. J. Stensrud, M.D., Madison, S. D.
Vice President F. X. McCabe, M.D., Brookings, S. D.
Secretary- Treasurer C. M. Kershner, M.D., Brookings, S. D.
DISTRICT 4
President A. J. Tieszen, M.D., Pierre, S. D.
Vice President Dai H. Park, M.D., Pierre, S. D.
Secretary-Treasurer J. T. Cowan, M.D., Pierre, S. D.
DISTRICT 5
President W. R. J. Kilpatrick, M.D., Huron, S. D.
Vice President James Monfore, M.D., Miller, S. D.
Secretary-Treasurer Emil Hofer, M.D., Huron, S. D.
DISTRICT 6
President _ D. W. Weatherill, M.D., Mitchell, S. D.
Vice President F. D. Gillis, M.D., Mitchell, S. D.
Secretary-Treasurer E. A. Schabauer, M.D., Mitchell, S. D.
DISTRICT 7
President Paul Aspaas, M.D., Dell Rapids, S. D.
Vice President R. B. Leander, M.D., Sioux Falls, S. D.
Secretary James Shaeffer, M.D., Sioux Falls, S. D.
Treasurer Robert Giebink, M.D., Sioux Falls, S. D.
DISTRICT 8
President . — L. G. Behan, M.D., Yankton, S. D.
Vice President R. W. Honke, M.D., Wagner, S. D.
Secretary C. R. Herbrandson, M.D., Vermillion, S. D.
Treasurer R. Porter, M.D., Yankton, S. D.
DISTRICT 9
President W. N. Golliher, M.D., Spearfish, S. D.
Vice President George Angelos, M.D., Hot Springs, S. D.
Secretary-Treasurer Russell Harris, M.D., Rapid City, S. D.
DISTRICT 10
President M. R. Cosand, M.D., Winner, S. D.
DISTRICT 11
President Gus Torkildson, M.D., McLaughlin, S. D.
Secretary-Treasurer B. P. Nolan, M.D., Mobridge, S. D.
Commission on Communications and Liaison With Allied Organizations
J. F. Barlow, M.D., Chr. (’73) Mary E. Sanders, M.D. (’71) Loren H. Amundson, M.D. (’71) J. Vose, M.D. (’71)
William Hanson, M.D. (’71)
R. G. Belatti, M.D. (’72)
Commission on
B. J. Begley, M.D., Chr. (’72) Saul Friefeld, M.D. (‘71)
Bruce Allen, M.D. (’71)
Charles S. Roberts, M.D. (’71) David Seaman, M.D. (’71)
C. Rodney Stoltz, M.D. (’73)
Commission on
Gerald Tuohy, M.D., Chr. (’72) G. E. Tracy, M.D. (’73)
Edward T. Ruud, M.D. (’71) Roland F. Hubner, M.D. (’71) Judson O. Mabee, M.D. (’71)
F. R. Williams, M.D. (’71)
D. L. Scheller, M.D. (’72)
H. H. Theissen, M.D. (’72)
R. Auskaps, M.D. (’72)
R. E. Van Demark, M.D. (’73) Eldon Bell, M.D. (’73)
A. J. Tieszen, M.D. (‘73)
Internal Affairs
R. Giebink, M.D. (’73) Edward A. Pasek, M.D. (’73)
A. Shousha, M.D. (’73)
B. T. Lenz, M.D. (’72)
James Shaeffer, M.D. (’72)
E. A. Rudolph, M.D. (’72)
Medical Service
W. B. Odland, M.D. (’73) Bernard C. Gerber, M.D. (’73) Warren Jones, M.D. (’72)
T. H. Sattler, M.D. (’72) George Wood, M.D. (’72)
M. Mutch, M.D. (’73)
Commission on Scientific Medicine
James C. Larson, M.D., Chr. (’73) Jose Michieli, M.D. (’71)
John Tidd, M.D. (’71)
C. C. Lardinois, M.D. (’73)
Noel deDianous, M.D. (’71)
Karl Wegner, M.D. (’71)
G. Paulson, M.D. (’73)
H. Phil Gross, M.D. (’73)
E. H. Heinrichs, M.D. (’72) N. B. Saoi, M.D. (’72) Richard Leander, M.D. (’72) R. J. Zakahi, M.D. (’72)
DISTRICT 12
President E. J. Batt, M.D., Sisseton, S. D.
Secretary - - Joseph Kass, M.D., Rosholt, S. D.
THE SOUTH DAKOTA JOURNAL OF MEDICINE
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40
SOUTH DAKOTA
"THE FAINTING ON THE IOHN" - Syndrome
E. H. Heinrichs, M,D.
A syndrome is the summation of “symptoms characteristic of a specific condition, disease or the like”1 and as such the shorthand of med- icine. With it we are able to describe briefly and precisely, complex findings or groups of diseases that have common denominators. Un- fortunately the names of syndromes are often not related to the disease they represent but named after their first or subsequent describer. Thus “name calling” has resulted in a lingo be- tween pediatricians, comparable to the special dialect in psychiatric circles.
The Fainting-on- the- John syndrome is des- cribed here not to add the authors name to the long list of eponyms, but to point out that sev- eral disease complexes have one important find- ing in common: the syncope in the bathroom. When this important clue is given, circumstan- tial evidence should lead the medical detective on the way to the right diagnosis.
There are probably many causes for this syn- drome and this description claims not to be com- plete by any means. It should, however, be pointed out that small details in the history can lead to the correct diagnosis, save a gamut of laboratory tests, referrals to specialists, etc.
Orthostatic hypotension is probably the most common cause for this type of syncope.2 Usually it concerns a very healthy male ado- lescent, tall and slender, the typical Aqua Velva man. He will tell you that he got out of bed in the morning feeling great and while standing in the bathroom shaving, 3-7 minutes later, be- came dizzy and blacked out. This phenomenon can be repeated in the office when after 20-30 minutes rest with blood pressure and pulse
measurements for base line, the patient is asked to stand up freely. Continued measurements will show that the pulse pressure widens and within 3-7 minutes the systolic pressure fades, while the pulse rate goes up and the patient down or at least becomes dizzy. The treatment is simple: just avoid sudden changes of position after prolonged rest (sit on the bedside for 5 minutes) and usually methylphenidate hydro- chloride (10-20 mg. in a.m. and at noon) appears to be helpful. The prognosis is favorable: as the patient matures the circulatory system becomes more responsive to sudden changes of position.
Less frequent are all other causes for the syn- drome. For more than a decade we have known the micturition syncope as a separate entity.3 The mechanism is not entirely clear but it is presumed to be of vasovagal nature re- sulting in hypotension and cerebral anoxia. The usual history is that the patient, after several hours of sleep went to the bathroom, urinated while standing and lost consciousness during or immediately after terminating the act of void- ing. The very nature of this history indicates that these attacks occur usually about midnight and involve mostly male individuals of no par- ticular age group who are otherwise healthy and who have no similar attacks associated with straining at defecation, heavy lifting or other activities involving Valsalva’s maneuver. The particular test which has been helpful to diag- nose the condition is to have the patient void standing under EKG control after prolonged bedrest. One will notice even if the patient is not fainting a remarkable slowing of the pulse, including occasionally A-V blocks and sinus
>(
JANUARY 1971
45
arrhythmias. The treatment is very simple again: just advise the patient to sit on the toilet stool when voiding.
tract may be helpful and of course the good physical examination including the rectal “digi- talization.” -
Rather rare is the psychomotor epileptic attack with micturition.4 This problem involves both sexes, frequently there is a history of al- cohol consumption prior to the event, the attack occurs independent from the erect position and has happened even when voiding in bed and occurs at the end, rather than during micturi- tion. After the usual akinetic seizure, the patient shows post-ictal confusion, sleeps and is un- aware of what has happened. The critical diag- nostic test is the encephalogram with the typical changes after micturition. Anticonvulsant therapy is the therapy of choice. The causal con- nection between the micturition and the epilepsy is not fully understood.
A fourth cause to be considered concerns the patient with massive upper gastro-intestinal bleeding.5 He may have increased peristalsis, cramps and an urge to defecate. Sitting on the toilet he strains, performs Valsalva’s maneuver and faints shortly after standing up again. By that time the evidence has either been flushed or the patient has been unaware of it, especially when using outhouses, still in wide use in our area. A history of symptoms related to the G.I.
In any of these syncopes, the situation may be aggravated by head injuries due to the fall re- sulting in coma. One should not accept the diag- nosis of head injury by itself but investigate why the person fell in the bathroom to begin with. After asking a few pointed questions, the diagnosis may become clear very soon and proper treatment can be instituted immediately.
So, when encountering the Fainting-on-the- John syndrome, just get the facts. The rest is quite elementary, dear Dr. Watson!
BIBLIOGRAPHY
1. The Random House Dictionary of the English Language, Random House Publications, New York. 1967.
2. A. Heyman in Cecil-Loeb Textbook of Medicine, W. B. Saunders, Philadelphia - London, 1963, 11th edition, pg. 1549.
3. C. H. Loggins, G. A. Lillington and C. P. Gray, Micturition Syncope.
Arch. Int. Med. 113 (1964) pg. 14-18.
4. I. Zivin and W. Rowley
Psychomotor Epilepsy with Micturition, Arch. Int. Med. 113 (1964) pg. 8-13.
5. H. Jeghers, St. Vincent Hospital, Worcester, Mass, and Tufts Medical Service, Boston City Hospital, Boston, Mass.
GLOSSARY
Methylphenidate hydrochloride: Ritalin.
Noludar300
(methyprylon)
l one capsule L for the rest
k. of the night j
Roche
Before prescribing, please consult complete product information, a summary of which follows: INDICATION: Relief of insomnia of varied etiology. CONTRAINDICATIONS: Patients with known hyper- sensitivity to the drug.
WARNINGS: Caution patients about combined ef- fects with alcohol and other CNS depressants. Caution against hazardous occupations requir- ing complete mental alertness, such as- op- erating machinery or driving a motor vehicle I shortly after ingesting the drug.
Physical and Psychological Dependence: Physical and psychological dependence rarely re- ported. If withdrawal symptoms do occur they may resemble those associated with withdrawal of barbiturates and should be treated in the same fashion. Use caution in administering to individuals known to be addiction-prone or those whose history sug- gests they may increase the dosage on their own initiative. Repeat prescriptions should be under adequate medical supervision.
Usage in Pregnancy: Weigh potential benefits in pregnancy, during lactation, or in women of child- bearing age against possible hazards to mother and li Id.
PRECAUTIONS: If sleeplessness is pain-related, an anal- gesic should also be prescribed. Perform periodic blood counts if used repeatedly or over prolonged periods. Total daily intake should not exceed 400 mg, as greater amounts do not significantly increase hypnotic benefits.
| ADVERSE REACTIONS: At recommended dosages, there have r been rare occurrences of morning drowsiness, dizziness, mild to moderate gastric upset (including diarrhea, esopha- gitis, nausea and vomiting), headache, paradoxical excita- tion and skin rash. There have been a very few isolated reports of neutropenia and thrombocytopenia; however, the evidence does not establish that these reactions are re- lated to the drug.
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His wife has a lot of different menopausal symptoms, but only a few really irritate him. Her hot flashes, her vertigo, her palpitations— that’s her problem. What really bothers him is her nervousness, her irritability and her excessive anxiety, often expressed by endless “book-shuffling, chain- smoking, reading-lamp” insomnia!
Menrium takes care of hot flashes, vertigo, palpitations in most menopausal v/omen. Menrium provides the well-known antianxiety action of chlordiazepoxide (Librium®) and water-soluble esterified estrogens. It therefore relieves more symptoms than either component separately.
It takes care of the vasomotor symptoms as well as the emotional symptoms. This means the symptoms that bother his wife most. And the symptoms that irritate him most.
So, to help them both get through her menopause, remember Menrium.
Before prescribing, please consult complete product informa- tion, a summary of which follows:
Indications: Management of manifestations generally associated with the menopausal syndrome — anxiety and tension, vasomotor complaints and hormonal deficiency states.
Contraindications: Women with cancer of breast or genitalia, except inoperable cases, and those with known hypersensitivity to chlordiazepoxide and/or esterified estrogens.
Warnings: Caution patients about possible combined effects with alcohol and other CNS depressants. As with all CNS-acting drugs, caution patients against hazardous occupations requiring complete mental alertness ( e.g ., operating machinery, driving). Exclude other possible causes of menopausal syndrome manifestations, such as pregnancy. Though physical and psychological dependence have rarely been reported on recommended doses, use caution in administering to addiction-prone individuals or those who might increase dosage; withdrawal symptoms (including convulsions) similar to those seen with barbiturates have been reported following discontinuance of chlordiazepoxide HC1. Potential benefits of use in pregnancy, lactation or women of childbearing age should be weighed against possible hazards to mother and child. Clinical data inadequate on safety in pregnancy.
Precautions: In elderly and debilitated patients, limit dosage to smallest effective amount of chlordiazepoxide (initially 10 mg or less per day) to preclude ataxia or oversedation; increase gradually as needed and tolerated. Though generally not recommended, if combina- tion therapy with other psychotropics seems indicated, carefully consider individual pharmacologic effects — particularly in use of potentiating drugs such as MAO inhibitors and phenothiazines. Observe usual precautions in patients with impaired renal or hepatic function. Paradoxical reactions to chlordiazepoxide (e.g., excitement, stimulation and acute rage) have been reported in psychiatric patients. Employ usual precautions in the treatment of anxiety states with evidence of impending depression; suicidal tendencies may be present and protective measures necessary. Variable effects on blood coagula- tion very rarely reported in patients receiving Librium® (chlordiaz- epoxide) and oral anticoagulants.
Adverse Reactions: Untoward effects seen with either compound alone may occur with Menrium. With chlordiazepoxide, drowsiness, ataxia and confusion reported in some patients, particularly in the elderly and debilitated; while usually avoided by proper dosage adjust- ment, these are occasionally observed at lower dosage ranges. Also reported have been a few instances of syncope; isolated occurrences of skin eruptions, edema, minor menstrual irregularities, nausea and constipation, extrapyramidal symptoms, increased and decreased libido, and occasional reports of blood dyscrasias, including agranu- locytosis, jaundice and hepatic dysfunction. Periodic blood counts and liver function tests advisable during protracted treatment. Changes in EEG patterns (low-voltage fast activity) observed during and after chlordiazepoxide treatment.
With estrogens, headache, nausea and vomiting, anorexia, gastrointestinal discomfort, dysuria and urinary frequency, jitteriness, breast engorgement, formation of breast cysts, skin rashes and pruritus occasionally seen. Administration may also be associated with uterine bleeding and/or followed by withdrawal bleeding.
Usual Dosage: One tablet t.i.d. for 21 days, followed by one-week rest periods.
5 mg chlordiazepoxide
5 mg chlordiazepoxide
10 mg chlordiazepoxide
0.2 mg water-soluble esterified estrogens
0.4 mg water-soluble esterified estrogens
0.4 mg water-soluble esterified estrogens
The South Dakota Journal of Medicine
Editor
Robert Van Demark, M.D. Sioux Falls
Business Manager
Richard C. Erickson Sioux Falls
Commission on Communications and Liaison with Allied Organizations
J. F. Barlow, M.D., Chr. (’73) Mary E. Sanders, M.D. (’71)
Loren H. Amundson, M.D. (’71)
J. Vose, M.D. (’71)
William Hanson, M.D. (’71)
R. G. Belatti, M.D. (’72)
D. L. Scheller, M.D. (’72)
H. H. Theissen, M.D. (’72)
R. Auskaps, M.D. (’72)
R. E. Van Demark, M.D. (’73) Eldon Bell, M.D. (’73)
A. J. Tieszen, M.D. (’73)
Published Monthly by
The South Dakota State
Medical Association
711 North Lake Avenue Sioux Falls, South Dakota 57104
Subscription Rate Yearly $5.00 — Single Copy 50c
Controlled Circulation Postage Paid at Sioux Falls, South Dakota
CONTENTS
Volume XXIV February 1971 Number 2
Pulmonary Candidiasis 5
(Third Article in Series)
S. Sochocky, M.D., F.C.C.P.
This Is Your Medical Association
11
Family Practice: Present and Future A. Sherwood Baker, M.D.
12
President’s Page
22
Clinicopathological Conference
27
Letters to the Editor
36
Economics: Regional Medical Library —
Regional Medical Program Cooperation 37
E. N. Jyvaskyla, M.S.; James R. Nordstrom, MSPH; Henry M. Parrish. M.D.. Dr. P.H.
Minutes of the Council Meeting .
43
11
3rd Article in Series
PULMONARY CANDIDIASIS
by
S. Sochocky, M.D., F.C.C.P.*
Introduction:
Candidiasis or moniliasis is an acute, subacute or chronic infection caused by species of Candida. There are about 150 strains of candidiasis but Candida Albicans is mainly pathogenic for man. Candida Albicans exists usually in three mor- phological forms; yeast cells, mycelium or pseu- domycelium and chlamydospores which grow on various cultures of media. According to Win- ner and Hurley,1 Langenbeck, in 1839, dis- covered Candida Albicans which is usually seen as small budding yeast-like cells with thin walls about 2-4 microns in diameter.
Pathogenesis:
Candida Albicans is often present in mouth and throat of normal persons, where it exists as a saprophyte. However, it may become a parasite and produce a rather severe infection under cer- tain circumstances. There are several con- tributing factors but the most important are pre- existing disease, treatment with antibiotics, steroids, cytotoxic, immunosuppressive drugs and a malnutrition.
Infection with Candida Albicans occurs in all ages, races and in both sexes, common in chil- dren and between 30 and 40 years of age. Candidiasis may affect almost any system of the body but most common are the skin, mucous membranes and respiratory system, or may become disseminated. Disseminated and fatal cases of candidiasis occur with an increasing frequency following treatment with antibiotics and steroids. E. R. Harrell2 et al. described two
* Department of General Medicine, Veterans Admin- istration Center, Sioux Falls, S. D. Assistant Pro- fessor of Internal Medicine, University of South Dakota School of Medicine.
patients with bacterial endocarditis due to coa- gulase positive Staphylococcus aureus. These patients were treated with large doses of broad spectrum antibiotics and cultures of their blood showed Candida Albicans. Kaufman3 et al. des- cribed a case of esophagitis due to Candida Al- bicans in patient with leukemia.
Clinical Manifestations:
Candida Albicans causes two forms of lung infection, a bronchopulmonary and a pulmonary. Bronchopulmonary candidiasis is not uncom- mon, produces signs and symptoms of a bron- chitis. This infection is limited to bronchial tree and peribronchial tissue is little affected. Cough, dry or with sputum which may be mucoid or gelatinous and elevation of temperature are most common symptoms.
Symptoms are more severe in pulmonary can- didiasis as parenchyma of lungs is involved. The common symptoms are cough, with or without sputum, fever, a shortness of breath and chest pain. Cough may be dry, hacking or productive, sputum may be mucoid, mucopurulent or blood stained. There also may be present general mal- aise, anorexia, loss of weight and fever up to 106 degrees has been reported. Signs depend on amount of lung tissue involved, may reveal signs of consolidation which may be scattered or confluent. Moist rales with dullness and changes in breath sounds may be present. Signs of bronchitis or involvement of pleura, as pleural effusion, may also be found. Clinical manifes- tations of anaphylactic hypersensitivity may de- velop during infection with Candida Albicans. Edmund L. Keeney4 reported bronchial asthma which followed a bronchial infection. The symp-
ii
FEBRUARY 1971
12
toms of asthma disappeared when infection was controlled.
Radiological findings:
Chest film reveals slight to moderate peri- bronchial thickening in bronchopulmonary candidiasis. In pulmonary candidiasis chest film shows shadows varying in size and shape, soft, patchy infiltration, bronchopneumonic or mil- iary densities. These lesions are usually bilateral and widespread. The enlargement of mediastinal glands, atelectasis, cavitations and pleural effusion may be found. Alvis E. Greer5 reported a series of 9 autopsied cases of disseminated can- didiasis in which lungs were involved in 9 and pleura in 7.
Laboratory data:
Secondary anemia may be present and white cell count is usually elevated. In severe infec- tion complete blood count may show changes comparative with leukemoid reactions. High globulin level in blood may also be present. Skin tests are of no great value because of high percentage of positive reactions in patients with- out active infections. Agglutinins and pre- cipitins may be present in patients with severe form of systemic infections. Cultures of sputa, bronchial and gastric washings usually show Candida Albicans on repeated examination. The urine may show albumin, leukocytes and hyaline casts.
Illustrative case:
A 24 year old non-white male was admitted to a hospital with a presumptive diagnosis of pulmonary tuberculosis of 2 weeks duration. On admission he was acutely ill and his temp- erature was 106 degrees. He complained of a dry cough, a shortness of breath, poor appetite and loss of weight. Chest respiratory movements equal and fair and rhonchi heard in both lungs. Family and past history not remarkable. Laboratory investigations:
Skin test OT 1:2000, coccidiodin and histo- plasmin negative. Sputa negative on direct smear and culture for tubercle bacilli but re- vealed Candida Albicans. No malignant cells were found in sputum. Chest film showed mil- iary shadows in both lungs which were con- fluent in both upper parts (See Figure 1). As a presumptive diagnosis of miliary tuberculosis was accepted he received 1 gram streptomycin and 300 milligrams isoniazid daily. Chest film 11-5-63 shows an increase of shadows in both lungs (See Figure 2). Repeated examinations on direct smears and cultures showed only Candida Albicans and failed to show any bacterial or other fungus infections. In review of results of
Figure 1.
Chest film 10-23-63 shows miliary shadows involving both lungs.
Figure 2.
Chest film 11-5-63 shows an increase in shadows in both lungs.
cultures of sputa streptomycin and isoniazid were discontinued after 3 weeks; course of Am- photericin B was given. However, his condition steadily deteriorated and chest film 12-10-63 showed further increase of shadows in both lungs (See Figure 3). He died 6 weeks after ad- mission to hospital.
Pathologist reported by using special stains
6
SOUTH DAKOTA
13
Figure 3.
Chest film 12-10-63 shows an increase of shadows in- volving almost every part of both lungs.
“there are foci of granulomatous inflammation with epithelioid and giant cells seen throughout lung parenchyma. A severe focally confluent bronchopneumonia is also present. Alveoli spores are filled with neutrophils and sur- rounded by epithelioid and giant cells. Eosino- philic fibrillar and granular material is in many alveoli and a large cyst filled mainly with sim- ilar material is noted. Macrophages with foarny cytoplasm fill many alveoli. A few foci of ne- crosis are seen but typical necrosis is not noted. There is a marked focal pulmonary fibrosis and subpleural blebs are seen. There is no evidence of malignancy or other infection. Examination
Figure 4.
Photomicrograph of section of lung shows granuloma- tous tissue with Candida Albicans.
of special stains reveals organisms morpho- logically identical to Candida Albicans. The sig- nificant findings are the acute and granuloma- tous inflammation of the lungs. The etiologic agent of this granulomatous inflammation is morphologically identical with Candida Al- bicans (See Figure 4). There is no evidence of malignancy or of other infection.”
Discussion:
Candida Albicans is frequently found in spu- tum as a saprophyte without causing any signs or symptoms. The frequency of Candida Albi- cans found in sputum of normal persons varies according to various statistics. According to Scott6 the fungus may be found in sputum of 30 - 40 per cent of population and according to Abrams7 in 3 per cent. In our series8 of 200 pa- tients Candida Albicans was found in 30 pa- tients, or 15 per cent.
Diagnosis of pulmonary infection with Can- dida Albicans is rather difficult as it may mimic any other pulmonary disease, bacterial, as pul- monary tuberculosis, virus infection or fungus diseases. It is also rather difficult as Candida Albicans is often present in sputa of normal per- sons.
As there are no pathognomonic signs and symptoms of pulmonary candidiasis it is essen- tial to exclude presence of any other cause of lung disease, especially tuberculosis. Candida Albicans must be found on repeated examina- tion of sputa or preferably bronchial washings. Cultures of sputa should be negative for pyo- genic bacteria, tubercle bacilli and negative for malignant cells. Skin tests are not of any value but serological tests may help in diagnosis of visceral candidiasis. According to Preisler9 et al. there is a rise of titer in agglutinating and precipitating antibodies against Candida Al- bicans in visceral candidiasis. In his series of 33 patients dying of acute leukemia, 23 with vis- ceral candidiasis on autopsy had significant rise of agglutinating antibody titer before death but none of 10 patients who did not have vis- ceral candidiasis on autopsy had a rise in agglu- tinating titer before death. However, diagnosis may be finally established by lung biopsy.
Prognosis is fair to good in bronchopulmonary form but grave in pulmonary form.
Treatment:
Various drugs have been used in treatment of pulmonary infections with Candida Albicans. Bronchopulmonary candidiasis responds t o treatment with potassium iodide but in pulmon- ary and disseminated forms Amphotericin B
FEBRUARY 1971
7
14
should be given. E. R. Harrell2 et al. described one patient with septicemia due to Candida Al- bicans who was treated by use of mycostatin parenterally. He suggested prophylactic treat- ment with mycostatin in patients receiving a broad spectrum antibiotic for a long time. John H. Kennedy10 treated a patient with cavitary bronchopulmonary moniliasis by resection of affected segment and post-operative brilliant green aerosol therapy.
REFERENCES
1. WINNER, H. I. and HURLEY, Rosalinde
Candida Albicans.
Little, Brown & Co., Boston, 16, 1964.
2. HARRELL, E. R. and THOMPSON, G. R.
Systemic Candidiasis (Moniliasis)
Complicating Treatment of Bacterial Endo- carditis, with Review of Literature and Report of Apparent Cure of One Case with Parenteral Mycostatin.
Ann. Int. Med. 49: 1, 207-215, July-Dee. 1958.
3. KAUFMAN, S. A. and LEVENE, G.
Esophageal Moniliasis: Report of a Case with Roentgenographic Findings.
Ann. Int. Med. 49: 3, 684-687, July-Dee. 1958.
4. KEENEY, Edmund L.
Practical Medical Mycology.
Charles C. Thomas, Springfield, 111. 78, 1955.
5. GREER, Alvis E.
Disseminating Fungus Diseases of the Lung. Charles C. Thomas, Springfield, 111. 163, 1962.
6. SCOTT, P. W.
A Possible Case of Pulmonary Moniliasis.
Amer. Rev. Tuberc. 77: 329-337, Jan. -June, 1958.
7. ABRAMS, W. W.
Pulmonary Moniliasis.
J. Kans. Med. Soc. 51: 562-564, 1950.
8. SOCHOCKY, S.
Pulmonale Candidiasis.
Medizinische Klinik 61: 13, 492-497, April, 1966.
9. PREISLER, Harvey D.
HASENCLEVER, Herbert F. and LEVITAN, Alexander A.
Serologic Diagnosis of Disseminated Candidiasis in Patients with Acute Leukemia.
Ann. Int. Med. 70: 1, 19, Jan.-June, 1969.
10. KENNEDY, John H.
Bronchopulmonary Moniliasis. Treatment by Segmentectomy.
J. Thorac. Surg. 37: 2, 231-235, Jan.-June, 1959.
HEALTH SPENDING ON RISE
Spending for health and medical care con- tinued to increase, reaching $60.3 billion in the fiscal year that ended June 30, 1969, according to the Division of Health Insurance Studies, Office of Research and Statistics. Highlights of the re- port include: (1) The nation’s health expend- itures accounted for 6.7 percent of the GNP; (2) Total outlays rose $6.4 billion, or 12 percent in one year; (3) Increases in spending were re- ported for all public programs except medical research; (4) Health spending per person amounted to $294 a year ($184 from private sour- ces and $110 from public funds).
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SOUTH DAKOTA
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MEDICAL ASSOCIATION
News Notes •
Changes • Births • News
The Black Hills District Medical Society presented a 50 year pin to Frieda J. Radusch, M.D., Rapid City, on behalf of the South Dakota State Medical Association in tribute for the 50 years she has practiced medicine i n South Dakota.
^ ^ ^
Gerald F. Tuohy, M.D.,
former anesthesiologist at McKennan Hospital in Sioux Falls, has been named Chair- man of the Department of Anesthesia at St. Luke’s Hos- pital in Kansas City, Missouri.
Dr. Anthony Castillo Lopaz, Altamirano, Chiapas, Mexico, has returned to the American mission hospital there after working with William De- laney, M.D., Mitchell, for one month. Last year Dr. Delaney worked with Dr. Castillo at the mission hospital for two weeks.
The American Medical Asso- ciation Board of Trustees has announced the reappointment of A. A. Lamperi, M.D., Rapid City, to a two-year term on the Council on Legislation of the American Medical Asso- ciation.
YOUR
CONTRIBUTION TO THE
SOUTH DAKOTA MEDICAL SCHOOL ENDOWMENT FUND IS NEEDED
J. C. Murphy, M.D., form- erly of Hot Springs, has re- tired from active practice and is now residing in Bettendorf, Iowa. Dr. Murphy practiced in Murdo for a number of years before joining the staff at the V.A. Hospital in Hot Springs. ❖ ❖ ❖
C. B. McVay, M.D., Yankton, has been named one of 26 doc- tors whose work has contrib- uted to the outstanding ad- vances made in surgery dur- ing the past 20 years. The American College of Surgeons has credited Dr. McVay with making “fundamental contri- butions for the anatomical re- pair of hernias.”
# sH
Creighton University hon- ored Francis J. Tobin, M.D.,
Mitchell, on his 50th anniver- sary as a graduate of the Uni- versity’s Medical School. Dr. Tobin and other members of the class of 1920 received special citations at the annual Medical Alumni Banquet.
k
n
FEBRUARY 1971
11
15
.
wgmmm
ilik
FAMILY PRACTICE: PRESENT AND FUTURE’
by
A. Sherwood Baker, M.D.* **
I want to talk to you about Family Medicine, something that affects us all, because no matter where we live or what we do, at one time or an- other we are members of a family. Despite the assaults of the “new morality” (neither new nor moral), pre-packaged foods and jet planes, we still are identified at intervals with a cultural group known as the family.
I submit that there is an existence of a body of medical knowledge and skills that are called “family medicine.”
The family and home are still, quite obviously, evident. A bit ago, I watched a harried house- wife in a store having some of her children fitted for shoes. Looking at her 4 pre-schoolers she commented, “Sometimes I wish I’d loved and lost.”
That family has to go somewhere for its med- ical needs. The general practitioner of America, particularly rural America, that we have known and identified has been a very special breed. (Usually about here the speaker paints a glowing landscape of medicine to include black bags, horses and buggies, World War II, the computer and specialization). I will leave my paint behind and you can draw your own landscape.
This physician has not had an actual counter- part outside of the North American continent. Our British and Continental cousins have been somewhat different, particularly in their rela- tionship to hospital medicine. The American GP had to be self-reliant and self-taught in many in- stances. His academic mothers are totally un-
*A talk presented at the Annual Awards Banquet of the University of South Dakota School of Medicine, Sioux Falls, South Dakota, April 4, 1970.
**Professor and Chief of the Section on Medical Prac- tice, Department of Community Health and Medical Practice, School of Medicine, University of Mis- souri, Columbia, Missouri 65201.
able to understand him or at times to forgive him for what he has become, have cast him out and have ignored him in their future plans.
Some years ago the professional medical edu- cators gave up on keeping that train running on the tracks that produced kinds such as ourselves. They never really offered incentives for such production. Recently, some severe and chilly winds have been blowing at the Ivory Towrers. A series of national studies, one of the most im- portant of which was underwritten by the AMA and was dubbed the “Millis Report” espoused and promoted the term “primary physician.”
Now, we have had additional reports and recommendations from health bureaucrats and politically active officials which have given us the euphorious term “health care delivery.”
Whether the term demands come from con- sumers, planners, politicians or the profession itself, it is quite apparent that things should be done to supply working-type doctors. From this has come the positive action to increase the size and number of medical schools. By natural selec- tion and inclination there may be still a few hardy souls who, upon meeting licensure re- quirements, paint a shingle, buy a black bag, and go to work. Such is the natural resiliency of youth and the adaptability of the public that things get along fairly well. With help from colleagues and a self-started planning program for continuing education, this neophyte becomes a journeyman doctor.
Now we have a new creation known as a specialist in family practice. In a few weeks, somewhat less than two thousand doctors will have a new diploma to add to their walls, at- testing to all beholders that the proprietor has had extra recognition. Those who are here that
12
SOUTH DAKOTA
16
had a lost weekend in February will agree that this will have been no minor achievement if they get that diploma.
Some very dedicated and thoughtful people worked for many years to create the Board of Family Practice. While its effect on making some of us hit the books this winter is credit- able, in my mind the only long-run worthwhile objective is in creating a comparable standing and stability for those future physicians who are now students. The effort will not be really worthwhile unless recruiting of new general practitioners is a result.
The future requirements for eligibility for this examination will require the serving of a resi- dency that has some fairly comprehensive de- tails. In addition to covering the same ground as other residents in the hospital, the family practice resident will be made responsible for the continuing total care of clearly identifiable bodies of patients, usually in family units. So he will have not only horizontal patients, but ver- tical ones as well.
Now, all of these training programs are housed in the Ivory Towers of acute care. A given part of the training must be in extramural settings and the community supplies the laboratory.
Several of the schools have recognized the need for the latter in the training of students. Your own school has had lengthy experience with rural preceptorships. Each year a few more schools of the country do the same thing.
Let’s describe what we think are the elements of a graduate training program. First, let me show you what happens if we try to make fine, neat compartments.
SIX WISE MEN OF MEDICINE
There were six men of Medicine To learning much decided Who went to see an old GP Whom all had much derided That each by observation Might prove where he abided.
The first approached a busy ward And happening to see That Doc had tied a belly cord At once exclaimed with glee,
“God bless me! but the family man Does nothing but OB.”
The second seeing stethoscope
Applied to hairy chest
Cried, “I have the truth, I hope.
This man performs the very best Giving well the clientele Skills of an internist.”
The third approached our doctor friend While with a child he spoke Of an illness soon to end And cheered him with a joke.
“I see” quoth he “this old GP Has Pediatrics in his cloak.”
The fourth reached out an eager hand And felt about the table.
“What this wondrous creature is like To see it now I’m able.
It’s clear enough this fellow though Is a surgeon without a label.”
The fifth who chanced to spot a couch Said “Friends, here is a twist.
We’ve burned out fuel, observed as fools We can’t see through the mist.
It’s plain to me, this old GP Is a psychiatrist.”
The sixth no sooner did inquire About habits and intention When spying Tines, Paps, and smears Bloods and urines in convention Said “Brethren, I’m sure he has Great skills in ills’ prevention.”
And so these men of medicine Contended loud and strong That each observed his single truth With findings clear and strong Though each was partly in the right They all were in the wrong.
MORAL
So oft in scientific circles The observers one often sees Rail on in partial ignorance Of ships on medical seas,
And never appreciate the forests They only see the trees.
This binding substance or mortar should be obtained by the extra skills acquired by a trainee in the family practice unit. If he handles the diverse problems of carrying a diabetic through three years of additional management, a mother from pre-marital days through several pregnancies and in the rearing of those children from those pregnancies, and a father from ulcers to angina, he should then have a depth of con- fidence and ability that makes him a credit to our profession.
If you really let your mind explore the full meaning of the term “family medicine,” there are all kinds of implications. I just mentioned some nice, clear-cut clinical entities, but what about child-rearing, family finances, sex coun- seling, home safety, and what to buy at the grocery store? If the traditional family is to sur- vive this century, it will need a trusted and de- pendable friend.
Some Definitions
Lynn Carmichael, M.D.
While we feel there is a distinct difference between general practice and family medicine, frequently the terms are confused and used in- terchangeably. Perhaps the following def- initions will clarify this.
Family Medicine
Family Medicine is that branch of medical science that has as its responsibility the con- tinuing health maintenance of the family. As an academic discipline it has a distinct body of
FEBRUARY 1971
13
17
knowledge and is housed in the university. Others besides physicians are involved in the discipline.
General Practice
The general practice of medicine is a form of delivering medical care. It involves the episodic treatment of disease without regard to age, sex or organ system. The goal is service and there are cultural, political, geographic and economic aspects.
Comprehensive Care
Health concerns can be divided into demands, for which the patient seeks care, and needs, of which the individual or family is largely un- aware. The degree of “comprehensiveness” is the extent to which the needs as well as the demands are met.
Family Physician
The family health care specialist is a phys- ician who, through continuity of care, has de- veloped a tenured relationship with the family. He accepts the family as the unit of care and actively promotes its health. In the past one could become a family physician through ex- perience gained in the general practice of med- icine or pediatrics. While many general prac- titioners, internists and pediatricians have be- come good family doctors, none have been
specifically trained for this role.
So, in the training program leading to eligi- bility for certification, we are thinking of all these sorts of problems. In our own University we are talking to everybody that will listen and listening to everyone that will talk. Our train- ing program, briefly, envisions the management of a given number of families who, at the pres- ent time or at a future date, will become em- ployees of the University or the new Veterans Hospital. The resident will spend approximately 10 percent of his working week during the first year of his program, 20 percent of his second year, and 50 percent of his third year in the Family Practice Clinic. During certain demand- ing services in the first year, it is obviously a compromise between the needs of the in-hospital cases and the out of the hospital cases and so. at least while in the Department of Medicine he will have a full-time devotion to the Depart- ment of Medicine.
This is not the favoritism that you might think. All the studies that have been done so far as to differences in the quality of care, as performed by the general practitioner, revolve I about the skills exhibited by that doctor in the specialty of Internal Medicine. While I am not
(Continued on Page 19)
Noludar30
(methyprylon)
i one capsule k for the rest k of the night
Before prescribing, please consult complete product ^ information, a summary of which follows:
I INDICATION: Relief of insomnia of varied etiology.
CONTRAINDICATIONS: Patients with known hyper- jj., sensitivity to the drug.
WARNINGS: Caution patients about combined ef- Bp' ’ fects with alcohol and other CNS depressants.
I JH W Caution against hazardous occupations requir- I B ® ing complete mental alertness, such as op- J^W Mft erating machinery or driving a motor vehicle Km shortly after ingesting the drug.
Physicdl and Psychological Dependence: Physical and psychological dependence rarely re- ported. If withdrawal symptoms do occur they may resemble those associated with withdrawal of barbiturates and should be treated in the same fashion. Use caution in administering to individuals known to be addiction-prone or those whose history sug- gests they may increase the dosage on their own initiative. Repeat prescriptions should be IKf under adequate medical supervision.
WBi' Usage in Pregnancy: Weigh potential benefits in
|F pregnancy, during lactation, or in women of child-
bearing age against possible hazards to mother and child.
PRECAUTIONS: If sleeplessness is pain-related, an anal- gesic should also be prescribed. Perform periodic blood counts if used repeatedly or over prolonged periods. Total daily intake should not exceed 400 mg, as greater amounts do not i significantly increase hypnotic benefits.
| ADVERSE REACTIONS: At recommended dosages, there have f been rare occurrences of morning drowsiness, dizziness, mild to moderate gastric upset (including diarrhea, esopha- gitis, nausea and vomiting), headache, paradoxical excita- tion and skin rash. There have been a very few isolated reports of neutropenia and thrombocytopenia; however, the evidence does not establish that these reactions are re- lated to the drug.
/rochTs Roche
\ / LABORATORIES
Division of Hoffmann-La Roche Inc.
Nutley, New Jersey 07110
lie night shift of depression, insomnia
Depression is a 24-hour-a-day problem. And insomnia is often its nocturnal expression. In fact, insomnia may be a key symptom in establishing the diagnosis of depression.
ELAVIL HCI (Amitriptyline HCI, MSD) may prove quite helpful when you have arrived at such a diagnosis. Unlike psychic energizers or agents that merely elevate mood, ELAVIL HCI embodies a mild antianxiety action which manifests itself even before the fundamental antidepressant activity of the drug becomes evident. Daytime drowsiness occurs in some patients, usually within the first few days of therapy.
NOTE: Not recommended during the acute recovery phase following myocardial infarction. Patients with cardiovascular disorders should be watched closely; arrhythmias, sinus tachycardia, and prolongation of the conduction time have been reported, particularly with high doses; myocardial infarction and stroke have been reported with drugs of this class. Close supervision is required for hyperthyroid patients or those receiving thyroid medication. Concurrent electroshock therapy may increase the hazards of therapy; such treatment should be limited to patients for whom it is essential. Discontinue the drug several days before elective surgery if possible.
Contraindications: Known hypersensitivity. Should not be given concomitantly with or within at least 14 days following the discontinuance of a monoamine oxidase inhibitor. Then initiate dosage of amitriptyline HCI cautiously with gradual increase in dosage until optimum response is achieved. Not recommended during the acute recovery phase following myocardial infarction or for patients under 12 years of age.
Warnings: May block the antihypertensive action of guanethidine or similarly acting compounds. Should be used with caution in patients with a history of seizures or urinary retention, or with narrow-angle glaucoma or increased intraocular pressure. Patients with cardiovascular disorders should be waiched closely; arrhythmias, sinus tachycardia, and prolongation of the conduction time have been reported, particularly with high doses; myocardial infarction and stroke have been reported with drugs of this class. Close supervision is required for hyperthyroid patients or those receiving thyroid medication. May impair mental and/or physical abilities required for performance of hazardous tasks, such as operating machinery or driving a motor vehicle. Safe use during pregnancy and lactation has not been established; in pregnant patients, nursing mothers, or women who may become pregnant, weigh possible benefits against possible hazards to mother and child.
Precautions: When used to treat the depressive component of schizophrenia, psychotic symptoms may be aggravated; in manic-depressive psychosis, depressed patients may experience a shift toward the manic phase, and paranoid delusions, with or without associated hostility, may be exaggerated; in any of these circumstances, it may be advisable to reduce the dose of amitriptyline HCI, or to use a major tranquilizing drug, such as perphenazine, concurrently.
When given with anticholinergic agents or sympathomimetic drugs, close supervision and careful adjustment of dosages are required. May enhance the response to alcohol and the effects of barbiturates and other CNS depressants. The possibility of suicide in depressed patients remains during treatment and until significant remission occurs; this type of patient should not have easy access to large quantities of the drug. Concurrent electroshock therapy may increase the hazards of therapy; such treatment should be limited to patients for whom it is essential. Discontinue the drug several days before elective surgery if possible.
Adverse Reactions: Note: Included in this listing are a few adverse reactions not reported with this specific drug. However, pharmacological similarities among the tricyclic antidepressant drugs require that each reaction be considered when amitriptyline is administered.
Cardiovascular: Hypotension, hypertension, tachycardia, palpitation, myocardial infarction, arrhythmias, heart block, stroke. CNS and Neuromuscular: Confusional states; disturbed concentration; disorientation; delusions; hallucinations; excitement; anxiety; restlessness; insomnia; nightmares; numbness, tingling, and paresthesias of the extremities; peripheral neuropathy; incoordination; ataxia; tremors; seizures; alteration in EEG patterns; extrapyramidal symptoms. Anticholinergic: Dry mouth, blurred vision, disturbance of accommodation, constipation, paralytic ileus, urinary retention, dilatation of urinary tract. Allergic: Skin rash, urticaria, photosensitization, edema of face and tongue. Hematologic: Bone marrow depression including agranulocytosis, eosinophilia, purpura, thrombocytopenia. Gastrointestinal: Nausea, epigastric distress, vomiting, anorexia, stomatitis, peculiar taste, diarrhea, parotid swelling. Endocrine: Testicular swelling and gynecomastia in the male, breast enlargement and galactorrhea in the female, increased or decreased libido. Other: Dizziness, weakness, fatigue, headache, weight gain or loss, increased perspiration, urinary frequency, mydriasis, drowsiness, jaundice. Withdrawal Symptoms: Abrupt cessation of treatment after prolonged administration may produce nausea, headache, and malaise; these are not indicative of addiction.
How Supplied: Tablets containing 10 mg and 25 mg amitriptyline HCI, in single-unit packages of 100 and bottles of 100, 1000, and 5000; tablets containing 50 mg amitriptyline HCI, in single-unit packages of 100 and bottles of 100 and 1000; for intramuscular use, in 10-cc vials containing per cc: 10 mg amitriptyline HCI, 44 mg dextrose, and 1.5 mg methylparaben and 0.2 mg propylparaben as preservatives.
For more detailed information, consult your MSD representative or see the Direction Circular. Merck Sharp & Dohme, Division of Merck & Co., Inc., West Point, Pa. 19486
when the diagnosis is depression
ELAVIL1*1
(AMITRIPTYLINE HCI I MSD)
MSD MERCK SHARP & DOHME
I have been asked why the increase in AMA dues? What do I get for my AMA dues?
The AMA is operating at a deficit at this time. For the past two years it has kept narrowly in balance. The cost of operation has increased due to inflation, new programs, unprecedented activ- ity of government in health affairs, the possibility that federal tax will be levied on income derived from advertising in the AMA Journal, plus many other factors.
The cost of operation is estimated to be $34,000,000 this year. The expenses are broken down as follows: programs — $25,647,000; occupancy — $1,526,000; administrative — $6,791,000. There are over 1,000 employees. The funds will come from the following sources: membership dues — 33.7%; advertising — 36% (later cut to 33.7%); subscriptions — 9%; investments — 2%; books, pamphlets and royalties — 14%.
The AMA is involved in many facets of medicine. It sets professional standards and profes- sional ethics throughout the United States. It helps set hospital standards through the Joint Com- mission. It sets medical school standards as well as internship and residency requirements.
The AMA aids in continued education, through the AMA Journal, plus the ten other specialty journals, the scientific sessions, through its library, scientific also socio-economic (one of the finest in the world) yet how many of you have ever used it? It acts as an information center on a mul- titude of subjects just by your asking. There are motion pictures, audio visual aids, speech ma- terials, also booklets.
The AMA through the Education Research Foundation (ERF) supports medical schools and med- ical education.
I think the words of our president, Dr. Walter C. Bornemeier, summarizes the AMA very well.
“The AMA is not an organization in some distant city. It is not a building, or a staff, or a budget. The AMA is you. It is your colleagues in practice, on the hospital staff, in education, in research. It is your fellow physicians throughout the United States. With support from you and more than 200,000 ethers like you, the AMA provides a wide variety of useful and valuable services to you and other physicians. It speaks to the government and to the public as the voice of American med- icine. It maintains the standards of qualification, performance and ethics of the entire medical pro- fession, all for the benefit of the people and the nation. The AMA and the medical profession are one and the same. The medical profession is you.”
22
J. A. Muggly, President
SOUTH DAKOTA
CLINICOPATHOLOGICAL CONFERENCE
From the Intern and Resident Teaching Conferences at the Sioux Valley Hospital, conducted by the Department of Pathology of the Hospital and of the School of Medicine of the University of South Dakota
EVERETT W. SANDERSON, M.D., FACP*
Internist - Discusser
JOHN F. BARLOW,
Pathologist - Editor
SIXTY-SIX YEAR OLD CAUCASIAN FEMALE WITH PROGRESSIVE SOMNOLENCE
CASE NO. A-69-63 (M488887)
This 66-year old Caucasian married female entered Sioux Valley Hospital because of pro- gressive somnolence of approximately six months duration.
Five months prior to admission her children had noted she was more sleepy than usual and wanted to be in bed most of the time. She was admitted to another hospital for a 30-day period. She was diagnosed as having a “stroke” and was placed on anticoagulation with Coumadin. Her somnolence improved and she was discharged. She did well after discharge except for inter- mittent periods of lethargy. Her prothrombin time was 31 seconds with a control of 13 seconds. During the two weeks prior to admission she be- came more somnolent than usual with increased periods of sleepiness but would then wake up, be in contact with her enviroment, answer ques- tions, and be quite rational. For two days prior to admission she had become unresponsive. The patient’s children stated that she had always been anemic, tired and had high blood pressure. There was a history of gallbladder surgery years previously but no other hospitalizations for major disease.
Physical examination revealed a very de- hydrated elderly female who was somnolent with sunken eyes and dry skin. The complexion was sallow and pasty and there was loss of skin turgor. Pulse was slow and regular at 72/ minute, respirations 16/minute, temperature 103°F. rectally, blood pressure 70 systolic and 52 diastolic. The patient responded to painful stim- uli but not to voice commands. The neck was
* Specialist in Internal Medicine, Sioux Valley Hos- pital, Clinical Assistant Professor of Medicine, School of Medicine, University of South Dakota. **Pathologist, Sioux Valley Hospital, Professor of Clinical Pathology, School of Medicine, University of South Dakota.
Supported in part by Clinical Cancer Training Grant T12 CA 08032 from the National Cancer Institute of the National In- stitutes of Health, U. S. Public Health Service.
fairly supple. The only abnormalities of the head and neck were mild arteriosclerotic fundal changes and dryness of the oral mucosa. The thyroid was unremarkable. The chest had an in- crease in A-P diameter with some hyper-reson- ance to percussion. She appeared to be hypo- ventilating. There were a few rhonchi scattered throughout the chest. The heart was not en- larged to percussion and there was a normal sinus rhythm with good heart tones and no mur- murs. The abdomen was soft with tenderness in the right upper quadrant to deep palpation. A vague mass was present. The liver edge was palp- able but the liver was not enlarged. The spleen was not palpable. The pelvic examination was negative. The deep tendon reflexes were respon- sive and symmetrical. The plantar reflexes were flexor. The pupils were midpoint and slightly irregular but equal. They reacted to light very sluggishly. Corneal reflexes were hypoactive. The conjunctivae were suffused. The optic nerve heads were flat. There were no retinal hemor- rhages. The patient would not move her eyes to either side. The remainder of the cranial nerves appeared intact.
Clinical pathology data: Urinalysis - yellow, clear, specific gravity 1.012, pH 5.0, negative for protein, glucose, ketone bodies, hemoglobin; sediment — 1-2 leukocytes/high power field. Hemoglobin 16.3 gm%, red count 4.14 million/ mm,3 hematocrit 46 Vol.%, mean corpuscular hemoglobin 34 micromicrograms, mean corpus- cular volume 97 cubic micra, mean corpus- cular hemoglobin concentration 36%. Total leu- kocyte count 5.000/mm,3 with 40% neutrophils, 7% neutrophilic bands, 1% eosinophils, 1% basophils, 50% lymphocytes, 1% monocytes. The red cells were normochromic with moderate anisocytosis. The platelets appeared increased. There were mild toxic changes in the neutro- phils. Carbon dioxide content was 24 meq/L.,
FEBRUARY 1971
27
chloride 98 meq/L., fasting blood sugar 118 mgs/ 100 ml., blood urea nitrogen 37 mgs/100 ml., pro- thrombin time 16.5 seconds with a 12.0 second control. Total protein was 5.2 gms/100 ml., al- bumin 2.3 gms/100 ml., alpha 1 globulin 0.3 gms/ 100 ml., alpha 2 globulin 0.8 gms/100 ml., beta globulin 0.7 gms/100 ml., gamma globulin 1.1 gms/100 ml., serum glutamic oxaloacetic trans- aminase 32 R-F units, bilirubin-total 0.3 mgs/100 ml., indirect 0.1 mgs/100 ml., direct 0.2 mgs/100 ml., alkaline phosphatase 1.3 sigma units. Creat- inine 0.7 mgs/ 100 ml. Triiodothyronine resin uptake (T-3) was 28%. PBI was 12.4 micro- grams/100 ml. A spinal tap revealed an opening pressure of 110 mm of H20. The fluid was xan- thochromic but clear. There were 5 red cells and 6 leukocytes/mm.3 All leukocytes were polynuclear. The cerebrospinal fluid protein was 325 mgs/ 100 ml. The cerebrospinal fluid sugar 52 mgs/100 ml., the cerebrospinal fluid creatine phosphokinase was 5 units. The spinal fluid serology was nonreactive. Culture of spinal fluid was negative for mycobacteria, fungi, and other pathogens. A tuberculin skin test (PPD inter- mediate) was negative at 48 hrs. Urine 17-keto- steroids were 2 mgs/day (normal 5-15 mgs/ day). 17 ketogenic steroids 4 mgs/day (8.3-15.5 mgs/ day normal). Creatinine on this sample was 0.45 gms/24 hours (normal 0. 7-2.0 gms/24 hrs.) Repeat showed 17 ketosteroids to be 6.7 mgs/24 hrs. and 17-hydroxy steroids to be 1.4 mgs/24 hrs. creat- inine 0.6 gms/24 hrs. A Schilling test showed 4.4% excretion (normal 8% excretion or over). Repeat electrolytes 3 days later revealed carbon dioxide 33 meq/L., sodium 148 meq/L., potas- sium 4.5 meq/L., chloride 89 meq/L. Three blood cultures were negative. Electrocardiogram was abnormal with low QRS voltage and there was diffuse ST and T wave changes and sinus tachy- cardia. Her fever returned to normal slowly. Chest film was unremarkable except for linear atelectasis in the left base. Skull films showed generalized demineralization of the bones and an impacted left maxillary anterior tooth. A percutaneous arteriogram showed findings con- sistent with a subdural hematoma on the left with a possible associated neoplasm in the pos- terior parietal region superiorly. A brain scan using Technetium-99 showed mottled areas in the left and right lateral views in temporal re- gions.
A left parietal craniectomy and evacuation of intracerebral cyst was performed on the ninth hospital day. There was no evidence of subdural hematoma. Fluid from the cyst cavity was sterile and revealed blood clot on microscopic
examination. The fluid was grossly bloody with 41,000 red cells and xanthochromic after cen- trifugation. The protein was 2.1 gms/100 ml. During hospitalization she continued to run a low grade fever. After surgery she became less responsive and the left pupil became dilated and fixed to light. Cold water calorics revealed a tonic deviation of the eyes toward the side irrigated. This was interpreted as indicating an intact brain stem with bilateral deep cerebral lesions. After surgery the sodium became pro- gressively elevated to a level of 160 meq/L., with a potassium of 2.4 meq/L., chloride of 108 meq/L., carbon dioxide content 28 meq/L. The blood urea nitrogen climbed to 98 mgs/100 ml. The patient was receiving intravenous fluids during this time. The patient developed periodic breathing and died on the sixteenth hospital day.
DR. SANDERSON: Dr. Lang, will you review the brain scan?
*DR. LANG: The brain scan was definitely ab- normal. The right and left lateral views show irregular mottling which could be due to dam- age to the capillaries from any number of causes such as infarction, tumor, etc. This was in- terpreted as a deep cerebral lesion.
DR. SANDERSON: Thank you. Dr. Chipman, would you help us look at some of the x-rays particularly the carotid arteriograms.
**DR. CHIPMAN: The right carotid arteriogram is unremarkable. On the left you see an in- creased space between the vessels and the skull which is a finding often seen in a subdural hematoma as suggested in the protocol. I see no other diagnostic changes.
***DR. WALTER K. SOSSEY: Was there ever evidence of localization of neurologic findings in this case?
DR. CHIPMAN: No.
DR. SANDERSON: I have some difficulty in- terpreting all the data. Unfortunately, there was no localization of the neurologic findings. In this case we have a woman who was somnolent for several months and came to the hospital de- hydrated with a blood pressure of 70/50. This depleted condition makes one wonder about a metabolic disturbance. This lady had an ele- vated carbon dioxide content, but unfortunately blood gas studies were not reported. Nor were
^Pathologist, Sioux Valley Hospital, Assistant Pro- fessor of Pathology, School of Medicine, University of South Dakota.
**Neurologist, Sioux Valley Hospital, Clinical Faculty, School of Medicine, University of South Dakota.
***Intern, Sioux Valley Hospital.
28
SOUTH DAKOTA
the results of multiphasic screening on the auto- analyzer available.
DR. BARLOW: This is an old case and predated both the arterial blood gas and multiphasic test- ing era.
DR. SANDERSON: There was a questionable mass in the right upper quadrant, but there were no further studies other than the liver function studies. The depressed total protein and albumin are consistent with her debilitated condition. The T3 was normal, but the protein bound iodine was elevated. We have seen a few elevated PBI’s in the last few months and per- haps this was due to some previous X-ray or medication. I do not think she was on estrogen therapy which would elevate the PBI. I am going to disregard the PBI as being a contam- inant. I think the significant findings in the spinal tap were the high protein and the fact that there are five polynuclear cells. The reports of urinary steroids are interesting. The crea- tinine is low which would indicate a less than 24 hour volume suggesting maybe that some of the urine was thrown out. I do not know whether she had a catheter in. The 17 ketosteroids are borderline low. Particularly disconcerting was the 17 hydroxy value on the second determina- tion which was extremely low as compared to the first value. These steroid values would cer- tainly go along with adrenal insufficiency or Addison’s disease. This would correlate with her dehydration and low blood pressure. However, the normal electrolytes deter me from making the diagnosis of adrenal insufficiency. I would expect the sodium to be lower and potassium to be higher. Fever is usually not seen in Ad- dison’s disease. The electrocardiographic find- ings are consistent with adrenal insufficiency.
I think I might mention some of the things which could cause somnolence and coma. Intra- cranial lesions which can give a decreased level of consciousness include infarction from throm- bosis or embolism, hemorrhage including not only intracerebral hematomas, but also sub- dural hematomas and subarachroid hemorrhage, brain neoplasms — primary or metastatic; and brain abscess. I do not believe the patient had a subdural hematoma as I would have expected her to have had headaches and a history of trauma. At operation she did not have a sub- dural hematoma. A patient with a brain abscess may or may not have fever. The polymorpho- nuclear cells from the spinal fluid may point to this diagnosis.
Among the metabolic diseases as a cause of coma are profound anemia, hypoxia, decreased
arterial blood flow due to arteriosclerosis or hy- potension (which the patient had), hypergly- cemia with acidosis in diabetes mellitus and hy- poglycemia from pancreatic adenoma. Uremia, myxedema, and liver failure can cause coma. The patient had a normal T-3 and no good evi- dence for advanced renal or hepatic disease. Hy- percalcemia due to hyperparathyroidism can cause coma. We did not have a calcium deter- mination on this lady. Acute and chronic menin- gitis can cause coma. There is no evidence of acute meningitis in this lady, but one of the forms of chronic meningitis may have been present. Tuberculous meningitis, cryptococcal meningitis, or toxoplasmic meningitis are possibilities. Any one of the viral ence- phalitidies might have given this picture. Parasites such as echinococcus from dog tapeworm or cysticercosis from the pork tape- worm, taenia solium, can cause coma. Lym- phomas involving the base of the brain might have produced this picture. Lymphoma is un- likely because the patient had no enlarged lymph nodes except for a questionable mass in the abdomen.
I want to come back to my diagnosis of brain abscess. Brain abscesses are usually associated with osteomyelitis of the skull secondary to mastoid or sinus infection or trauma to the skull. These were not present in this case. However, brain abscesses can occur from a n infection elsewhere in the body such as in the lungs. Metastatic abscesses may occur in the brain often associated with chronic bronchitis or bron- chiectasis. Bacterial endocarditis can also give rise to brain abscess. Brain abscesses may ap- pear secondary to a fracture of the skull which she did not have. Patients with brain abscess usually have an elevated cerebrospinal fluid pressure which the patient did not have. The protein is usually elevated, but the cell count may or may not be elevated depending on how well the abscess is encapsulated. Again I am going to grasp at the polys in the spinal fluid.
Post-operatively the patient had a very high sodium and a moderately low potassium. This suggests hyperaldosteronism. Since I have al- ready suggested Addison’s disease, it is hard to make the diagnosis of hyperaldosteronism and Addison’s in the same patient.
DR. BARLOW: Unfortunately, I left out that there was marked output of urine in the week prior to death when the patient was developing her marked hypernatremia. Outputs of 4500, 3800, 3500 all exceeding intake were found.
FEBRUARY 1971
29
DR. SOSSEY: Do you know the specific gravity on those urines?
DR. BARLOW: No, I don’t.
DR. SANDERSON: I suspect that the process was diabetes insipidus due to a central lesion in the thalamus or hypothalamus producing dia- betes insipidus.
DR. SANDERSON'S DIAGNOSIS
1. CEREBRAL ABSCESS OR TUMOR IN REGION OF HYPOTHALAMUS WITH
A. ? ADRENAL INSUFFICIENCY
B. ? DIABETES INSIPIDUS
DR. SOSSEY: I think it should be pointed out that this lady was very dehydrated when she came in and still only had a urine specific grav- ity of 1.012 which indicates she had some dia- betes insipidus early.
DR. CHIPMAN: I think one of the things you have to explain in this case is why was there hemorrhage. Was this hemorrhage into a neo- plasm? Certainly spontaneous hemorrhage in this region is rare.
*DR. GREGORY NAUGHTON: I think patients whom we put on anticoagulants have bleeding phenomenon. There is often a cause for that bleeding. If a patient has sudden bleeding from the gastrointestinal or urinary tract often there is a tumor or other lesion that can be picked up if there is investigation. Certainly, in this case there could have been bleeding into a prim- ary or secondary tumor. I am very suspicious of this mass that was present in the abdomen and not carefully followed up. I wonder if secondary tumor in the brain is not a likely possibility in this case. I certainly think that the patient had the classic signs of diabetes insipidus, probably due to hypothalamic involvement with very high sodium and low potassium.
DR. BARLOW: Dr. Rossing, you managed this patient, would you like to comment on her? **DR. WILLIAM ROSSING: I think that we knew this patient had adrenal insufficiency. Even if the steroid values had been 100% wrong, they still would have been low and we took this as good evidence of adrenal hypofunction. Whether this was primary or secondary, we were not sure. It was hard to explain her in- creasing somnolence.
DR. NAUGHTON: How much steroid did you give her?
DR. ROSSING: It amounted to about 150 of so- lumedrol daily.
* Specialist in Internal Medicine, Sioux Valley Hos- pital, Clinical Assistant Professor of Pathology, School of Medicine, University of South Dakota. **Intemist, Sioux Valley Hospital, Clinical Faculty, School of Medicine, University of South Dakota.
DR. SANDERSON: I think that the urinary values could have been correct and this was ad- renal insufficiency. However, the Schilling test was also only 4% with a normal of 8% and some degree of renal insufficiency may explain the low urinary values for the Schilling and steroids.
DR. NAUGHTON: Why was the Schilling test done?
DR. CHIPMAN: A rare cause of somnolence and coma is vitamin B-12 deficiency.
PATHOLOGIC FINDINGS DR. BARLOW: The pathologic findings in this case were extraordinary. The first picture shows a massive hemorrhage in the region of the brain stem and basal ganglion. Here is another section of the brain stem to show the extensiveness of the hemorrhage. (Fig. I & II) This is an unusual
Figure I.
Massive hemorrhage involving thalamus and hypo- thalamus.
Figure II.
Extension of hemorrhage into brain stem.
place for spontaneous hemorrhage. This photo- micrograph shows that there is a cellular area
30
SOUTH DAKOTA
near the hemorrhage. On higher power there were multiple hyperchromatic tumor cells with marked polymorphism. (Fig. Ill & IV) These cells tend to cluster around vessels and are prob- ably either glial in character or represent so- called microgliomatosis or so-called reticulum
Figure III.
Poorly circumscribed invasive cellular tumor on left of picture invading normal hypothalamus on right.
Figure IV.
High power of malignant primary brain tumor.
cell sarcoma of the brain. At any rate it is a highly malignant, poorly circumscribed tumor. Its location can certainly explain the terminal diabetes insipidus. The adrenals were atrophic and weighed 11 grams together. I think this sup- ports the clinical diagnosis and the laboratory data suggesting hypofunction of the adrenal glands. The thyroid weighed 15 grams and was slightly atrophic. There was severe left lower lobe and right lower lobe bronchopneumonia. Pancreatitis with focal fat necrosis was also present.
DR. NAUGHTON: Was there anything in the abdomen?
DR. BARLOW: No, there was no tumor, just
the focal pancreatitis. I might show a picture of the aorta which demonstrates an aorta com- pletely free of atherosclerosis. There was very little atherosclerosis in the coronary vessels or the vessels of the circle of Willis. We have had two brain tumors which showed hemorrhage after anticoagulation for “stroke.” Although both of these tumors were highly malignant and inoperable, I think one has to be careful before putting a patient on anticoagulation since brain tumor or brain hemorrhage must be ruled out first. I might also mention one of my favorite points. All people over the age of 50 do not have generalized atherosclerosis and all of their symptoms can not be attributed to this disease.
FINAL ANATOMIC DIAGNOSES
1. ASTROCYTOMA, GRADE III HYPOTHALAMIC REGION WITH MAS- SIVE HEMORRHAGE AND EXTENSION OF HEMORRHAGE INTO BRAIN STEM, CEREBELLUM AND BASAL GANGLION.
2. ATROPHY OF ADRENALS
3. ATROPHY OF THYROID
4. BRONCHOPNEUMONIA, LEFT LOWER LOBE, CONFLUENT AND RIGHT LOWER LOBE, FOCAL
5. DIVERTICULOSIS
6. PANCREATITIS WITH FOCAL FAT NECROSIS
7. DUODENITIS, CHRONIC, MODERATE DR. CHIPMAN: I think that the somnolence be- fore the patient had her massive hemorrhage certainly indicated something was wrong with the region of the hypothalamus and the vehi- cular core of the midbrain.
DR. NAUGHTON: Wouldn’t you think she would have some eye signs with all the mid- brain disturbance?
DR. CHIPMAN: I think that there was such massive destruction that the patient did not have any eye signs at all.
DR. BARLOW: I think the diabetes insipidus in this case was not much of a problem because she died of a tremendous hemorrhage, but post surgical diabetes insipidus can lead to massive dehydration with death especially in a comatose patient. Diabetes insipidus also evidently can be due to some new anesthetic agents such as methoxyflurane (penthrane).
DR. NAUGHTON: We have had a most interest- ing case with diabetes insipidus secondary to penthrane anesthesia. This was approximately four weeks ago in a man who had had two suc- ces:ive operations under penthrane anesthesia.
FEBRUARY 1971
31
The sodiums were up over 160 and the chlorides up over 130 meq/L. after surgery. The problem was obscured because he had many other comp- lications such as dehisence of the wound and gram negative septicemia. I had not heard of this entity and this man was losing water rapidly. We just kept giving him dextrose and water to the amount of 4-6 liters a day. At first we thought he was losing this fluid into his bowel, but we began to realize that he was losing it through his urinary tract only. After I had got- ten him out of the woods, I was informed about this problem with penthrane. I have had other problems with penthrane when I was in the service. The major problem then was the fact that I could not wake the patient up very well after surgery.
*DR. MAYER: This is self-limited, is it not?
DR. NAUGHTON: Yes, it is. All you have to do is give water replacement.
DR. SOSSEY: There seems to be a lot of prob- lems with penthrane and people are going more to the older anesthetic techniques such as cyclo- propane. There is evidently a problem with pre- cipitation of the crystals in the kidney when antibiotics and penthrane are used together. DR. SANDERSON: In patients with this type of diabetes insipidus is chlorthiazide helpful?
DR. NAUGHTON: I’m not sure. I think just water replacement is adequate because the dis- ease is self-limited.
* Intern, Sioux Valley Hospital.
BIBLIOGRAPHY
1. Nephrotoxicity associated with methoxyflurane anesthesia. W. B. Crandell, et al., Anesthesiology, Vol. 27, p. 591, 1966.
2. Nephropathy associated with methoxyflurane, Clin. -Alert No. 257, 1966, Clin.-Alert, No. 135, 1967.
3. Methoxyflurane, tetracycline and Renal Failure, Luzucu, Etem, YMD, JAMA, Vol. 211, pp. 1162, Feb. 16, 1970.
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SOUTH DAKOTA
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Vermillion, South Dakota 57069 December 12, 1970
Mr. Richard C. Erickson
Executive Secretary
South Dakota State Medical Association
711 North Lake Avenue
Sioux Falls, South Dakota 57104
Dear Mr. Erickson:
I would like to thank the South Dakota State Medical Association for their providing part of the funds for my travel expenses to the AMA Clinical Meeting in Boston. This was an in- valuable educational experience, which has greatly stimulated my interest in the AMA.
I find it very encouraging to see the phys- icians in our state recognizing the importance of acquainting the students with the operations of the AMA.
The hospitality shown Todd Biegler and me by the South Dakota Delegation was genuinely appreciated. I would also like to thank them for their support of the SAMA-MECO Resolution. Thank you.
Sincerely,
June Heilman
AVERAGE CITIZEN PAYS SMALLER PART OF HEALTH CARE TODAY
A smaller share of the private citizen’s per- sonal income is now being spent for medical costs than in 1965. According to a Social Secur- ity Administration report, “Public health pro- grams are, in fact, taking over some of the bur- den on consumers for financing the high costs of medical care and are leaving a greater propor- tion of the consumers’ income for other items.” The report showed that in 1929 the average con- sumer paid 3.5 percent of his disposable personal income for health purposes. By 1965 the figure rose to 6 percent, but by 1968 had dropped to 5.6 percent.
Dear Mr. Erickson,
Would you please convey my thanks to the State Medical Association for providing the money to finance my trip to Boston for the National AMA convention.
Holiday greetings,
Sincerely,
Todd Biegler
Student Representative
SAMA
U. of South Dakota
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36
SOUTH DAKOTA
REGIONAL MEDICAL LIBRARY - REGIONAL MEDICAL PROGRAM COOPERATION
by
E. N, Jyvaskyla, M.S.
Director, Medical Library The University of South Dakota Vermillion, South Dakota
James R. Nordstrom, MSPH Administrator, School of Medicine The University of South Dakota Vermillion, South Dakota
and
Henry M. Parrish, M.D., Dr. P.H.
Associate Dean, School of Medicine The University of South Dakota Vermillion, South Dakota
The Regional Medical Library (RML) system has divided the United States into ten regions, the Mid-Continent region being but one of these geographically-established regions. The Mid- Continent region (see figure one) is easily the largest geographically, yet represents the small- est population concentration, a total of 12,940,000 in a land area of 663,966 square miles with a population density of 19.5 persons per square mile. The majority of the population is in Mis- souri; Wyoming and South Dakota being the smallest and least densely populated; and Kan- sas, Nebraska, Colorado, and Utah in between.
As early as 1965, medical librarians in the greater St. Louis area were exploring the possi-
Fig. I: States included in the Mid-Continent Regional Medical Library
bilities of cooperative utilization of medical library resources. Although several meetings were held in the area, it was not until early in 1968 that twenty-two persons representing seven states’ medical libraries and schools of medicine met in St. Louis to seriously consider, and at- tempt to formulate, plans for the development of a regional medical library system. The out- come of this meeting was the formation of a loosely-knit consortium of university medical libraries given the task of formulating a work- able policy which was to underwrite the basis of an organization still in the neophytic stage. The consortium’s first concrete developments were the drafting of a set of governing by-laws and the draft of an application to the National Library of Medicine for funds to establish the region as an official entity in the amalgam of regional systems. This application was submitted to Washington in the latter part of 1969; the grant being awarded by the National Library of Medicine effective as of March 1, 1970. At this point the now-existent Mid-Continent Regional Medical Library system was born.
Member states include Missouri, Kansas, Ne- braska, South Dakota, Colorado, Wyoming and Utah. Member medical school libraries include:
FEBRUARY 1971
37
Washington University, St. Louis University, Kirksville College of Osteopathy, the University of Missouri, the University of Kansas, the Uni- versity of Nebraska, Creighton University, the University of Colorado, The University of South Dakota, and the University of Utah. Non- medical institutions represented are: Linda Hall Library (Science and Technology in Kansas City) and the University of Wyoming; Schools of Dentistry represented include, Washington University and the University of Colorado (due to open in 1971). Also represented are the Men- inger Clinic in Topeka and the Colorado State Veterinary School. The basic function of the Regional Medical Library network is to provide the physician and the allied health team with access to the literature in their respective fields with a minimum lapse of time.
Table one indicates the distribution of allied health professionals and the distribution of hos- pitals and nursing homes within the State of South Dakota. It is interesting to note that there are eleven out of sixty-seven counties that have neither M.D. or D.O. representation and twenty- five out of sixty-seven counties are without hos- pital facilities. The majority of the counties do not have recourse to adequate medical library facilities exclusive of individually-owned collec- tions maintained by individuals themselves.
The University of South Dakota Medical School Library’s integral function in this net- work is twofold. First to provide the health team within the State with ready access to the litera- ture; and, second, to upgrade the existent med- ical library service within the State by provid- ing seminars for persons serving as medical librarians on the local scene. The medical school librarian, when requested, will also serve as a consultant to other medical libraries or public libraries having medical collections within the State. The University of South Dakota Medical School Library is the only large medical library within the State and, therefore, must reflect and support all medical education and research en- deavors within South Dakota. Thus, in coopera- tion with the Regional Medical Program, the Medical Library and the School of Medicine, both located in Vermillion, are concerned with pro- viding the health care members of the commun- ity, both urban and rural, with the latest in- formation about heart diseases, cancer, stroke, and related diseases. The Medical School Li- brary staff are aware of the responsibility for filling the information needs of personnel in the medical as well as the allied health professions throughout the State, as well as all patrons,
actual and potential, who lack direct access to medical library services.
Methods through which the Medical Library of The University of South Dakota, in coopera- tion with the Regional Medical Program, intends to implement this function may include the answering of short reference questions; com- pilation of subject bibliographies; provision of inter-library loans to obtain materials not read- ily available locally; verification of manuscript bibliographies; and upon special request, trans- lations of articles not originally written in the English language. It is possible that in coopera- tion with the Regional Medical Program, a project grant might fund a survey of the State as recommended by the Regional Medical Library.
To implement inter-library loan services, a Union List of Biomedical Serials prepared by the Medical Library Center of New York is in prep- aration. This multi-volume work will list the serial (journal) holdings of eighteen major med- ical libraries in the region and will be available as of September 1, 1970. This will enable mem- ber state university resource medical libraries to ascertain instantly where a given journal title is located and to request it directly from the source. This ability will “speed up” inter-library loan services and allow rapid literature dissem- ination to the practicing physician and allied health professionals. With these improved facil- ities, it is hoped the Medical School Library will be able to provide information with twenty-four hour service from time of the request for service.
Another aspect of service is the establishment of a TWX or WATS line between the member university libraries that are tied in with the re- gional headquarters at the University of Ne- braska. Prior to trying the establishment of an inter-state TWX or WATS line will be the de- velopment of a similar line within South Da- kota. This line of communication will serve to link out-lying hospitals and communities with the Medical Library at USD’s School of Med- icine. This will further implement existing modes of communication.
Implementation of this program shall include a continuing education program for persons who are functioning in the capacity of medical li- brarians within South Dakota. This is to be con- ducted by the certified medical librarians or their representatives in each of the member states.
This is an effort to assist these persons to up- date their procedures and policies so as to pro-
38
SOUTH DAKOTA
Table 1
Distribution of Health Professionals and Facilities by Counties in South Dakota, 1970.
Categories of Health Professionals*
MT
|
j County |
MD |
DO |
RN |
LPN |
DDS |
RPh |
SE |
(ASCP) |
DVM |
Hosp |
NH |
|
Aurora |
1 |
0 |
15 |
0 |
1 |
3 |
0 |
0 |
1 |
0 |
1 |
|
Beadle |
20 |
1 |
126 |
13 |
10 |
16 |
0 |
2 |
7 |
1 |
3 |
|
Bennett |
2 |
0 |
8 |
5 |
1 |
2 |
0 |
0 |
1 |
1 |
0 |
|
Bon Homme |
5 |
1 |
31 |
9 |
4 |
5 |
0 |
0 |
3 |
1 |
2 |
|
Brookings |
14 |
0 |
109 |
13 |
10 |
33 |
3 |
1 |
8 |
1 |
3 |
|
Brown |
38 |
0 |
218 |
56 |
20 |
27 |
6 |
7 |
5 |
1 |
3 |
|
Brule |
3 |
1 |
34 |
9 |
2 |
5 |
0 |
0 |
3 |
1 |
2 |
|
Buffalo |
0 |
0 |
1 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
|
Butte |
6 |
0 |
28 |
3 |
4 |
11 |
1 |
1 |
3 |
1 |
4 |
|
Campbell |
1 |
0 |
4 |
0 |
0 |
2 |
0 |
0 |
1 |
0 |
n |
|
Charles Mix |
5 |
1 |
45 |
9 |
5 |
6 |
0 |
0 |
3 |
4 |
2 |
|
Clark |
1 |
0 |
14 |
1 |
1 |
6 |
0 |
0 |
3 |
4 |
1 |
|
Clay |
9 |
0 |
69 |
10 |
8 |
10 |
0 |
3 |
4 |
1 |
3 |
|
Codington |
24 |
1 |
105 |
38 |
16 |
16 |
1 |
1 |
9 |
2 |
6 |
|
Corson |
1 |
0 |
10 |
4 |
0 |
1 |
0 |
0 |
0 |
1 |
0 |
|
Custer |
3 |
1 |
15 |
1 |
1 |
4 |
0 |
0 |
0 |
1 |
0 |
|
Davison |
21 |
0 |
140 |
60 |
10 |
19 |
1 |
3 |
7 |
2 |
6 |
|
Day |
4 |
0 |
38 |
11 |
5 |
9 |
0 |
0 |
1 |
0 |
3 |
|
Deuel |
1 |
0 |
25 |
3 |
1 |
1 |
0 |
0 |
2 |
1 |
1 |
|
Dewey |
0 |
0 |
2 |
3 |
1 |
1 |
0 |
0 |
0 |
1 |
0 |
|
Douglas |
1 |
0 |
27 |
6 |
1 |
2 |
0 |
0 |
2 |
1 |
2 |
|
Edmunds |
2 |
0 |
15 |
5 |
2 |
2 |
0 |
0 |
2 |
1 |
2 |
|
Fall River |
10 |
0 |
52 |
13 |
5 |
10 |
0 |
0 |
3 |
2 |
2 |
|
Faulk |
2 |
0 |
19 |
11 |
2 |
4 |
0 |
0 |
2 |
0 |
1 |
|
Grant |
6 |
0 |
32 |
8 |
4 |
8 |
0 |
1 |
2 |
0 |
2 |
|
Gregory |
4 |
0 |
27 |
7 |
2 |
3 |
0 |
0 |
2 |
2 |
2 |
|
Haakon |
1 |
0 |
10 |
3 |
2 |
2 |
0 |
1 |
1 |
1 |
0 |
|
Hamlin |
3 |
0 |
24 |
9 |
3 |
6 |
0 |
0 |
3 |
0 |
2 |
|
Hand |
3 |
0 |
31 |
7 |
2 |
6 |
0 |
1 |
3 |
1 |
1 |
|
Hanson |
0 |
0 |
23 |
7 |
1 |
1 |
0 |
0 |
4 |
0 |
0 |
|
Harding |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
|
Hughes |
18 |
1 |
75 |
46 |
5 |
11 |
5 |
1 |
8 |
1 |
2 |
|
Hutchinson |
8 |
1 |
28 |
21 |
5 |
7 |
0 |
1 |
6 |
2 |
5 |
|
Hyde |
0 |
0 |
8 |
3 |
1 |
2 |
0 |
0 |
2 |
0 |
1 |
|
Jackson |
2 |
0 |
7 |
5 |
0 |
1 |
0 |
0 |
0 |
0 |
1 |
|
Jerauld |
1 |
0 |
9 |
2 |
2 |
1 |
0 |
0 |
0 |
1 |
1 |
|
Jones |
1 |
0 |
5 |
1 |
1 |
1 |
0 |
0 |
0 |
0 |
0 |
|
Kingsbury |
3 |
0 |
21 |
12 |
6 |
7 |
0 |
0 |
5 |
2 |
3 |
|
Lake |
10 |
0 |
58 |
13 |
7 |
7 |
0 |
0 |
2 |
1 |
2 |
|
Lawrence |
15 |
1 |
85 |
21 |
13 |
11 |
2 |
5 |
1 |
3 |
8 |
|
Lincoln |
5 |
2 |
58 |
15 |
4 |
10 |
1 |
1 |
4 |
0 |
3 |
|
Lyman |
2 |
0 |
7 |
4 |
4 |
0 |
0 |
0 |
1 |
0 |
0 |
|
McCook |
1 |
0 |
22 |
8 |
2 |
6 |
0 |
0 |
5 |
0 |
2 |
|
McPherson |
1 |
0 |
31 |
0 |
2 |
4 |
0 |
0 |
1 |
2 |
1 |
|
Marshall |
4 |
0 |
18 |
2 |
1 |
8 |
1 |
0 |
2 |
0 |
1 |
|
Meade |
5 |
4 |
70 |
8 |
5 |
10 |
0 |
0 |
2 |
2 |
4 |
|
Mellette |
1 |
0 |
4 |
1 |
0 |
2 |
0 |
1 |
0 |
0 |
1 |
|
Miner |
1 |
0 |
22 |
4 |
3 |
2 |
0 |
0 |
2 |
0 |
1 |
|
Minnehaha |
120 |
2 |
672 |
270 |
53 |
74 |
4 |
25 |
28 |
4 |
12 |
|
Moody |
2 |
0 |
27 |
7 |
2 |
5 |
0 |
0 |
4 |
1 |
1 |
|
Pennington |
63 |
3 |
341 |
66 |
37 |
51 |
2 |
7 |
10 |
4 |
15 |
|
Perkins |
3 |
0 |
14 |
5 |
2 |
3 |
0 |
0 |
0 |
1 |
1 |
|
Potter |
3 |
0 |
23 |
11 |
3 |
3 |
0 |
1 |
2 |
1 |
1 |
|
Roberts |
4 |
0 |
40 |
14 |
4 |
6 |
0 |
0 |
1 |
2 |
3 |
|
Sanborn |
0 |
0 |
12 |
3 |
0 |
2 |
0 |
0 |
2 |
0 |
2 |
|
Shannon |
0 |
0 |
12 |
0 |
0 |
2 |
1 |
0 |
0 |
1 |
0 |
|
Spink |
8 |
0 |
54 |
8 |
3 |
r-7 i |
0 |
1 |
3 |
1 |
3 |
|
Stanley |
0 |
0 |
5 |
4 |
1 |
1 |
0 |
0 |
1 |
0 |
0 |
|
Sully |
1 |
0 |
6 |
4 |
0 |
21 |
0 |
0 |
0 |
0 |
0 |
|
Todd |
0 |
0 |
18 |
8 |
2 |
1 |
0 |
0 |
0 |
1 |
0 |
|
Tripp |
5 |
0 |
24 |
10 |
2 |
5 |
0 |
0 |
3 |
1 |
1 |
|
Turner |
7 |
0 |
36 |
9 |
6 |
7 |
0 |
0 |
7 |
1 |
4 |
|
Union |
1 |
1 |
18 |
6 |
5 |
7 |
0 |
0 |
6 |
0 |
2 |
|
Walworth |
7 |
0 |
32 |
7 |
4 |
8 |
1 |
0 |
3 |
1 |
2 |
|
Washabaugh |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
|
Yankton |
31 |
1 |
157 |
33 |
12 |
13 |
1 |
8 |
4 |
2 |
4 |
|
Ziebach |
0 |
0 |
2 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
Categories of Health Professionals:
MD — Doctor of Medicine DO — Doctor of Osteopathy RN — Registered Nurse LPN — Licensed Practical Nurse DDS — Doctor of Dentistry RPh — Registered Pharmacist
SE — Sanitary Engineer
MT(ASCP) — Registered Medical Technologist DVM — Doctor of Veterinary Medicine Hosp — Hospital NH — Licensed Nursing Home
FEBRUARY 1971
39
vide adequate and efficient service on the local level and to utilize local resources before turn- ing to the University for assistance. This is two- fold in its purpose: first, not to overburden the central source; and, second, not to undermine local resources.
When requests are made Xerox copies will be sent in lieu of the original volumes, as it is the concerted opinion of the executive and advisory committees of the Regional Medical Library that the original materials should be retained within the source library so as not to deprive its users of access to the materials. Xerox copies are to be furnished at 10 cents per page on the local or in-state level. Out-of-state requests will be provided on a pro-rated basis relative to the cost of the material which has been requested. Member university medical librarians are to sur- vey the medical library facilities within their re- spective states to determine the existing ser- vices and to upgrade or strengthen them where possible. This will be done by first surveying existent medical library holdings and providing, when requested, outlying medical libraries with supplemental materials (when available). Sec- ondly, the development of a Union List of med- ical periodical holdings and their locations with- in the State of South Dakota. And, thirdly, by
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conduction of continuing education seminars and workshops in cooperation with the Regional Medical Program for South Dakota’s medical librarians.
These services are expected to be fully opera- tional as of September 1, 1970, and members of the medical and the allied health professions are cordially invited to write or telephone the Med- ical Library at any time. The address and phone number of the Medical Library are:
Medical Library U.S.D. School of Medicine Vermillion, South Dakota 57069 Telephone: 1-605-677-5348
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SOUTH DAKOTA
MINUTES OF THE COUNCIL MEETING 11:30 A.M. Ramada Inn
Saturday, Jan. 9, 1971 Sioux Falls, South Dakota
The meeting was called to order by Dr. H. R. Lewis, chairman of the Council. Those present for roll call were Doctors J. A. Muggly, G. R. Bartron, W. R. Taylor, A. P. Reding, R. H. Quinn, J. J. Stransky, H. R. Lewis, David Seaman, G. E. Tracy, Bruce Lush- bough, C. L. Swanson, Fred Leigh, E. T. Lietzke, Duane Reaney, E. T. Ruud, M. R. Cosand, J. E. Ryan, J. B. Gregg and John F. Barlow. Also in attendance were Mr. Todd Biegler, student representative to the Council, Mr. Bob Warnick, AMA field service repre- sentative, Mr. Richard Erickson, Mr. Robert Johnson and Mr. Randall Tuffs.
Dr. Lietzke moved to dispense with the reading of the minutes of the last Council meeting inasmuch as they have been published. The motion was seconded by Dr. Tracy and carried.
The Council reviewed the report of the Commission on Legislation and Governmental Relations.
REPORT OF THE COMMISSION ON LEGISLATION AND GOVERNMENTAL RELATIONS
Submitted on December 4, 1970
There have been no formal meetings of the Com- mission since the last report to the Council. A meet- ing concerning the future development of the Medical School of the University of South Dakota is to be held and will be attended by the Chairman of this Commission on December 5. If any information pertinent to the Legislative Commission comes from this meeting, the Council will be informed at the meeting January 9.
J. B. Gregg, M.D.
Chairman
Commission on Legislation
and Governmental Relations
Mr. Erickson explained a bill which will be pro- posed by the Hospital Association concerning the requirement of a “Certificate of Need” prior to the building of a hospital or health care facility costing more than $100,000. Dr. Bartron moved that the Council take no position on this bill. The motion was seconded by Dr. Swanson and carried. Mr. Erick- son outlined a bill which will be proposed by the State Health Department allowing persons under twenty-one to give consent to physicians to make a diagnostic examination and render treatment for venereal diseases without the parents consent. Dr. Taylor moved that the Medical Association endorse this bill. The motion was seconded by Dr. Tracy and carried. The Council considered a bill which would create a four-state regional medical education board. Dr. Bartron moved that the State Medical Associa- tion endorse this legislation. The motion was sec- onded by Dr. Tracy and carried.
Mr. Erickson introduced Dr. David Seaman, new Councilor for the Aberdeen District, and Dr. Duane Reaney, new Councilor for the Yankton District.
The Council considered the report of the Commis- sion on Communications and Liaison and the request from the Bar Association to hold another medical- legal conference in conjunction with Medical School Recognition Days in 1971. Dr. Tracy moved that the Association plan a medical-legal conference for the fall of 1971 in conjunction with Medical School Recog- nition Days. The motion was seconded by Dr. Lush- bough and carried.
There was no report from the Commission on Medical Service or the Commission on Scientific Medicine.
The Council considered the proposed budget estab- lished by the Commission on Internal Affairs’ Budget and Audit Committee. Dr. Swanson moved that the Council accept the budget as proposed. The motion was seconded by Dr. Muggly and carried.
The Council considered a proposal from a Kentucky printing firm for the North Central states to have a 32 page common section in the Journal. Dr. Tracy
moved that the Association reaffirm its position that the Journal is a house organ for local news and scientific articles and that we are not interested in combining with the North Central states and printing a common scientific section. The motion was seconded by Dr. Lietzke and carried.
Mr. Erickson and Mr. Tuffs presented information pertaining to the physicians’ profiles by specialty for the Council’s information.
Mr. Warnick showed a film pointing out the facil- ities and information available to physicians through the American Medical Association for the Councilors’ information.
The Council considered a request from Indiana to join the North Central Conference. Dr. Tracy moved that the Council recommend that Indiana not be in- cluded in the North Central Conference. The motion was seconded by Dr. Cosand and carried.
Nominations were received for the Distinguished Service Award. A secret ballot was cast and the win- ner will be announced at the annual meeting awards’ banquet.
Nominations were received for the Community Service Award. A secret ballot was cast and the win- ner will be announced at the annual meeting awards’ banquet.
Mr. Erickson reported to the Council on the phys- ician donations to the Greater South Dakota Associa- tion for the Council’s information. Mr. Erickson was directed to contact the Greater South Dakota Associa- tion and request that health care be included in their list of industries.
The Council discussed the issue of charging for the completion of insurance claim forms. Dr. Tracy moved that the Association establish a policy stating that physicians should not charge for the initial com- pletion of the standard claim form for services rendered. Any additional forms may be billed at the discretion of the physician. The motion was seconded by Dr. Lushbough and carried.
The Council reviewed the recommendations of the State Utilization and Insurance Review Committee concerning post operative care. After lengthy dis- cussion Dr. Bartron moved that the Council recom- mend to the Utilization and Review Committee that they continue to use the present South Dakota Re- lative Value Study with more flexibility. The motion was seconded by Dr. Leigh and carried.
The Council considered the recommendation of the Blue Shield Board concerning the use of a five digit code for procedural terminology. Dr. Bartron moved that the Council recommend that the Associa- tion continue utilizing the four digit code system now in use. The motion was seconded by Dr. Tracy and carried.
A letter from the South Dakota Hospital Asso- ciation concerning their Association’s withdrawal from the South Dakota Research Institute was pre- sented for the Councilors’ information.
WANTED — General Practitioners in the “Heart of the Black Hills.” Well established community with a population of about 2,500, service area of about 6,500. A modern 16-bed general hospital constructed for easy expansion if necessary. At present we have one General Practitioner in town. Our 78-year-old doctor passed away re- cently. The staff will cooperate fully as desired. The State Hospital for the Severely Mentally Retarded is located 5 miles south of town. Large medical centers are only 45 minutes away. For more details contact: D. C. Kanwischer, Admin- istrator, Custer Community Hospital, Custer, South Dakota 57730.
FEBRUARY 1971
43
DOYLE, BIERLE & HAGERTY Attorneys and Counsellors Suite 4 Law Building Yankton, South Dakota 57078
November 13, 1970 John Zimmer, Esquire Attorney at Law Parker, South Dakota 57053
Dear Mr. Zimmer:
Presupposing that you are still the General Counsel of the South Dakota Health Research Institute we have been directed by the South Dakota Hospital Association to advise that formal action taken by the South Dakota Hospital Association at its annual meeting in Rapid City in September 1970, directed that said Association withdraw from participation in the activities of the Research Institute.
The action of the South Dakota Hospital Associa- tion further stated that no members thereof will be designated for participation on the Board of Directors of the Research Institute.
As General Counsel for the South Dakota Hospital Association we would like to cooperate with you in the changes which appear necessary to be made so that the South Dakota Hospital Association nor any of its members thereof remain affiliated with the Health Research Institute. As a matter of preliminary suggestion it would appear that the By-laws of the Research Institute should be amended with more specific attention directed to Article 3 thereof to eliminate the South Dakota Hospital Association therefrom. We shall also secure individual resig- nations of Mr. Schroeder and Sister Rosaria from the Board of Directors to be filed with the appropriate corporate office. However we did not wish to do this until communication had been made to you regarding the action of the South Dakota Hospital Association. Perhaps you may wish these people to remain as members of the Board until the By-laws can be ap- propriately amended. If you do not feel this way we feel confident these members shall wish to resign immediately.
Any suggestions you may have to immediately accomplish the withdrawal from participation from the corporate structure of the Research Institute by the South Dakota Hospital Association would be appreciated.
The Board of Trustees of the South Dakota Hos- pital Association will be meeting on November 18th and if at all possible we would like to hear from you by that time so that your ideas can be forwarded to this group.
Respectfully submitted,
DOYLE, BIERLE & HAGERTY
Don A. Bierle General Counsel
South Dakota Hospital Association DAB:ml
cc: James P. Steele, M.D.
Fred D. Leigh, M.D.
Myron C. Tank, M.D.
Eugene H. Stearns Sister M. Rosaria Kranz Lyle E. Schroeder Richard Erickson J. A. Muggly, M.D.
William T. Murphy
Dr. Swanson moved that the State Medical Asso- ciation withdraw from the South Dakota Research Institute. The motion was seconded by Dr. Leigh and carried.
Mr. Erickson explained a request from the Welfare Department for physicians’ approval of a report form G-41 (Revised) to be utilized for Title 19 pa- tients. Dr. Tracy moved that the Council accept the physician report form from the Welfare Department, and that physicians accept the fees set forth by the
Welfare Department for the completion of this form. The motion was seconded by Dr. Taylor and carried.
Mr. Erickson discussed the upcoming meeting with the Welfare Commission concerning the proposed cutting of physicians’ reimbursement for the care of Title 19 recipients. Dr. Cosand moved that the Asso- ciation go on record as objecting to the proposed de- crease in physician reimbursement and stating that it is the members opinion that physicians will not accept the Welfare Commissions proposal. The mo- tion was seconded by Dr. Lietzke and carried.
Mr. Erickson briefly discussed the annual meeting banquet. The Council determined that the awards should be presented at the banquet and that the banquet should be informal.
Dr. Tracy presented a resolution from the Water- town District Medical Society concerning the estab- lishment of guidelines for an abortion bill, should one be introduced in the 1971 legislature. Dr. Tracy moved that this resolution be adopted by the South Dakota State Medical Association. The motion was seconded by Dr. Cosand. Dr. Reaney moved that the residency requirement in the resolution be deleted. The motion was seconded by Dr. Lushbough. The amendment was defeated. A vote was then taken on the original resolution and this was defeated.
The Councilors heard a tape recording produced by the American Medical Association concerning phys- ician licensure and narcotics and incompetency.
The spring Council meeting was set for Saturday, April 24.
Dr. Lietzke moved that the meeting be adjourned. The motion was seconded by Dr. Leigh and carried.
CONTROLLING HEREDITY
Genetic transformation — the replacement of a gene or set of genes for another — is one way heredity can be controlled. Although geneticists cannot mold human progeny, they can control some aspects of bacterial heredity, according to molecular geneticist Arnold W. Ravin. Ravin, a professor of biology at the University of Chicago, can determine successfully the genetic fate of unborn bacteria by injecting normal bac- teria cell cultures with genetic material ex- tracted from bacteria which have acquired, by mutation, a resistance to antibiotics such as streptomycin and erythromycin.
DOCTOR AIDES EXPECTED TO IMPROVE MEDICAL CARE
Physician’s assistants, in training at Duke University School of Medicine, should event- ually improve both the quality and quantity of doctors’ efforts, two University faculty