Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens, Part 92

Author: Jacob Anthony Kimmell
Publication date: 1910
Publisher:
Number of Pages: 1189

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ERYTHEMA MULTIFORME IRIS DURING THE COURSE OF TYPHOID FEVER. By H. P. PARKER, M. D., Professor of Medicine in Howard University, Washington, D. C.

AND

H. H. HAZEN, M. D.,

Clinical Professor of Dermatology in Howard University, Washington, D. C.

re the time of Willan, the various forms of erythema, te exanthemata, and inflammations of the skin were I together, as was exemplified by the writings of Plenck 1783. In 1808 Robert Willan (2) separated the a multiforme group from the acute exanthemata on hand, and from the inflammations due to external irri-

tants on the other. It is interesting to note that in the same volume under the heading of purpura he described what was probably a case of erythema multiforme associated with vomit- ing, abdominal pain, arthritic pains, and an anasarcous swelling.

In 1835 Rayer (3) cited several cases of Bonnet's to show

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that the various forms of erythema might coexist, and in 1854 Hebra (4) showed that the several types of erythema multi- forme were forms of one and the same malady. In 1876 Lewin (5) stated that some cases had a fatal termination, and ran the course of an acute infection, though he considered the cutaneous symptoms to be reflex in origin and frequently due to urethral irritation.

In 1895 Osler (6) first published a series of cases in which urticaria, angioneurotic œdema, erythema multiforme and pur- pura occurred successively or together in the same individual, and in association with a large array of visceral manifestations. Osler supplemented this article by two others, and many other writers, notably Mackenzie (7), Chenoweth (8), Neisser (9), Bulkley (10), Galloway (11) and Sachs (12) have extended this work until we know that the skin lesions of the erythema multiforme symptom complex include urticaria, angioneurotic œdema, purpura, erythema multiforme and nodosum, and if we are to believe Galloway and Macleod (13) certain cases of lupus erythematosus as well. In the minds of the writers it is questionable whether certain other diseases, notably erythema scarlatinoides and dermatitis herpetiformis should not be in- cluded.

Visceral Symptoms .- Any one of the following visceral symptoms may occur; sometimes there are no manifest skin lesions.

Acute tonsillitis, otitis media, laryngitis, phlyctenular conjunctivitis.

Ulceration of the lips and tongue.

Temporary delirium, aphasia, hemiplegia, meningitis.

Gastro-intestinal crises with colic, vomiting, and diarrhea.

Appendicitis, degeneration of the liver, jaundice.

Enlargement of the liver and spleen.

Bronchitis, pneumonia, pleurisy with effusion.

Endocarditis and pericarditis, anemia.

Hemorrhages from the nose, intestines, stomach, lungs, and kidneys.

Arthritis and infiltration of the synovial sheaths and periarticular structures.

Nephritis and ulceration of the cervix uteri.

Fever, usually irregular and of short duration, but often high.

Etiology .- As regards etiology there have been many theories. In 1835 Gibert (14) wrote that some cases of erythema were symptomatic due to derangements of the in- ternal viscera. In 1850 Bulkley (15) stated that it was es- pecially associated with digestive disturbances and gout. In 1864 Köbner (16) said that it was an angioneurosis due to vasomotor disturbances. In 1876 Lewin mentioned reflex causes, frequently urethral. 'Chaisse (17), Legendre (18), and Galloway (19) thought that it was due to autointoxication. Finger (20) thought that the local effect of bacteria upon the tissues caused some cases. Many writers, as Singer (21) and Howard (22) found bacteria in the blood, but in the majority of cases the technique of the blood-culture was not above criticism, and Koch's postulates were never fulfilled. As Cor-

lett's (23) case well illustrates some at least were undoubted': due to streptococcus infections.

Erythema multiforme is also known to occur with sat definite infections as typhoid fever, diphtheria, syphilis, goncr- rhœa, tuberculosis, cholera, pneumonia, leprosy, malaria, tp- panosomiasis, and with suppurative processes in any portix of the body, and may also occur with nephritis and diabetes Various drugs and antitoxins, and some articles of food also give erythematous, papular, and bullous eruptions that har: the same clinical picture as the erythema multiforme group.

Erythema multiforme is frequently spoken of as occurring in typhoid, but we have been able to find only two instance: where the eruption occurred during the course of the fever, the cases of Lauffer (24) and Goldstein (25), while Peter's (2% case developed the lesions during his convalescence. Man: writers, of whom DaCosta (27), and Hutinel and de Gimar? (28) may be taken as fair samples, speak of measley and c. scarlatinoid eruptions. Schamberg's (29) article gives an ex- cellent summary of these conditions. In a study of 1500 case: of typhoid at the Johns Hopkins Hospital McCrae (30) note: erythema as occurring 15 times, urticaria twice, purpura 3: times and a pemphigoid eruption once. Thus it will be seen that true cases of erythema multiforme in the course of typhoid are very few.

J. B., a school boy, 14 years of age, a mulatto, was admitted to Freedmen's Hospital on November 5, 1909, complaining of a buri- ing feeling in his eyes, severe headache, great weakness, bleeding from his nose, and a slight cough.

His family history was unimportant, his father, mother and two brothers having died of unknown causes, and his remaining brothers and sisters being in good health.

The patient had suffered from measles, mumps, malaria, and rheumatism, but from no other complaints, though he had had some vague indigestion, and some abdominal pain at night. He was accustomed to drink coffee and a little beer and whiskey, but otherwise his habits were good.

The present illness began two days before admission with a severe headache, which disappeared shortly to be replaced by : burning sensation about his eyes. He was so weak that he had to take to his bed at once. On the following day he had a severe chill, and in the evening nose-bleed. There was some slight cough.

On admission to the hospital the following notes were made:

" The patient is a well-built, well-nourished boy; the facial ex- pression is dull and heavy; the pupils are equal and react to light and accommodation. The tongue is covered with a heavy fur; the pulse is 108 to the minute, regular in force and rythm. of good volume and tension. The chest is well formed and syn- metrical; the breathing costo-abdominal in type, 28 to the minute. On percussion and auscultation both lungs are clear throughout. The heart is not enlarged to either the right or the left. The heart sounds are clear and forcible. The abdomen is not dis- tended, it is everywhere soft and tympanitic, the liver is not en- larged, but the edge of the spleen is felt two fingers' breadth be low the costal margin. The knee jerks are present."

On admission the temperature was 103º F., and during the illness ran between 100.8° and 103.8º F., the pulse from 80 to 115, and the respirations from 25 to 30. Typhoid was suspected because of the history and initial symptoms, the continued high fever, and the facies. The patient was given an initial purge, and was put on six ounces of milk every four hours, alternating with albumin every four hours. An ice cap was put to the head

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ur He was sponged every three hours when the temperature rose 102.5° F., or higher. An enema was given every second day. x ounces of water were given every two hours. Typhoid isola- in was carried out.

Two days after admission the following note was made: "The tient shows over the back of his right hand and extensor sur- ces of forearms a number of roughly circular, bluish patches out 1/2 cm. in diameter. Careful examination shows no rash on y part of the body with the exception of a few small rose- lored patches on abdomen and lower chest that disappear on essure." Later in the day the following special note on the skin adition was made: "On the hands and forearms, both sur- ces, extending half way to the elbow, the fingers, the dorsal rfaces of the feet and the shins there are two varieties of tions, one of which is macular, ill-defined and varying in size om 1/2 to 3 cm. in diameter. The other lesion is distinctly an- lar, from 1/2 to 2 cm. in diameter, the center is red and the riphery is whitish. The edge is very well defined. On the tensor surfaces of both forearms there are scattered areas or ots that are free from pigment but having a hyperpigmented eola. The proximal finger joints seem slightly swollen, and are ight red in color, the general appearance being similar to the ¿thematous areas on the arms and legs." It was later found at the patient had suffered every spring for the last four years m an eruption that he described as being similar to the pres- t one save that the lesions became vesicular and burst, leaving ese white scars.

The urine had a specific gravity of 1026, and showed a trace of oumin but no casts nor red blood cells. The leucocytes num- red 4400, and a differential count of 500 cells gave:

Polymorphonuclears

66.6%

Eosinophiles

0.4%

Large mononuclears 1.0%

Small mononuclears 29.6%

Transitionals 2.4%

No mastcells or myelocytes.

The Gruber-Widal reaction, 1 to 50 for one hour, was negative. e blood pressure was 110.

In the 9th, two days after the last note, the carpo-phalangeal ats of both hands were red and swollen, and there were a few dish macules on the proximal phalanges: the annular lesions 1 persisted on the forearms and backs of the hands and on the

In the 19th there remained only a few annular lesions on both ds and feet. The temperature had now been normal for five 8. He left the hospital on the 30th, with the same annular ons still persisting. Blood cultures and cultures taken from annular lesions were alike sterile. A Widal reaction, tried before he left, was noted as suggestive.

wing to the short duration of the fever, the absence of the al reaction, and the marked cutaneous symptoms it was tionable whether the patient was suffering from typhoid r complicated by erythema multiforme, or from one of the re forms of erythema with enlargement of the spleen, joint ptoms and continued high fever. In favor of typhoid were continued high fever, the mental dulness, the coated tongue, the low leucocyte count. Against typhoid spoke the abrupt ', and the short duration of the fever, the absence of the reaction and the negative blood culture, although the lat- vas taken rather late. The other symptoms and physical including the differential count, could have occurred with disease. A definite diagnosis was not made.

December 6, one week after his discharge, the patient was admitted to the hospital. His temperature was 103.6º F., 110, and respiration 30. On the 7th the following note was " The patient looks dull and heavy, he complains of head-

ache and pain in his eyes, there is slight discharge from the nose; the patient is not disposed to look at the light. The upper lip is somewhat swollen. The tongue is furred and there is injection of the throat. The chest is negative with the exception of numer- ous sonorous râles heard during inspiration; these clear up quickly after coughing and are probably transmitted from the larger tubes. The heart sounds are clear. The spleen is easily palpable. There is a marked redness of the palms of the hands and of the heels. A few small rose-colored papules are visible over the various portions of the body. Wherever the patient makes pressure with any part of the body there is a marked erythema. The patient is coughing, and spitting up grayish, frothy, mucopurulent material."

The blood coagulation time, taken by Wright's tubes, was six minutes.

On the 8th the temperature was 104.8º F., pulse 110, and respira- tion 33. The Widal reaction at one to fifty for one hour was sug- gestive. A blood culture was taken and an organism found whose cultural characteristics agreed with those of the typhoid bacillus, and which was definitely agglutinated by the serum from a known case of typhoid fever. This made the diagnosis of typhoid fever certain.

On the 10th the leucocyte count was 5700, the red blood cells 4,104,000 and the hæmoglobin 62%. A differential count of 500 cells gave the following results:

Polymorphonuclears 65.2%

Eosinophiles

0.6%

Large mononuclears .6%

Small mononuclears 25.8%

Transitionals

3.4%

Mastcells

0.0%

Myelocytes 0.4%

The urine showed a large amount of albumin; no casts or red blood cells were noted.

The course of this attack was much more severe, the tempera- ture running as high as 105° F. The treatment was the same as during the first attack with the addition of a mild expectorant for the cough. On the 9th it was noted that the patient was having bloody expectoration. On the 18th he had a rather free epistaxis in the morning and also coughed up a considerable amount of blood, which might of course have come from the nose. On per- cussion the lungs were clear throughout, but on auscultation there were numerous sibilant râles at the bases, both front and back. Over the chest, abdomen and back there were some pinkish macules about 1 mm. in diameter, and a few other papules that resembled acne lesions. There were no new lesions of erythema multiforme, but the old annular lesions still persisted.

On the 22d of December it was noted that the patient had had a sudden rise of temperature, the temperature previously having fallen almost to normal. Examination showed dulness in the lower right axilla, and impairment of expansion over the same area. Over the right base in front, and over the whole back there were numerous sibilant rales at the end of inspiration. There was no alteration of the breath sounds. These physical signs were similar to those usually found in pneumonia accompanying typhoid.

On the following day the temperature again dropped, and after the 29th there was no fever. Three weeks later the patient was discharged. He still had the annular lesions on the hands and feet, but they were now fading. The same annular lesions per- sisted from the 7th of November to the 22d of January, 1910, an unusually long time for the annular lesions of erythema multi- forme.

It is certain that the patient had typhoid during his second stay in the hospital, and practically certain that he also was

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suffering from the same disease during his first admission. During the height of his first attack he had the following symptoms characteristic of the erythemas : annular and macu- lar skin lesions, and swelling and redness of the carpo-phalan- geal joints. During the height of his relapse he suffered from œdema of the upper lip (giant urticaria), erythema at points of pressure, and hemoptysis. The fact that these lesions occurred only when the infection was young and active would seem to indicate that the typhoid toxemia was responsible for them.

REFERENCES.

1. Plenck: " Doctrina de morbis cutaneis," 1780.

2. Willan: "On Cutaneous Diseases," 1808.

3. Rayer: "Traité théorique et pratique des maladies de la peau," 1826-7, I, 136, 265.

4. Hebra: "Diseases of the Skin " (New Sydenham Society, 1866-80, I, 285.

5. Lewin: Berl. klin. Wchnschr., 1876, XIII, 321.

6. Osler: Am. J. Med. Sc., 1895, CX, 629, 1904, CXXVII, 1; Brit. J. Derm., 1900, XII, 227.

7. Mackenzie: Brit. J. Derm. 1896, VIII, 116.

8. Chenoweth: Med. News, 1905, LXXXVI, 390.

9. Neisser and Jadassohn: Krankheiten der Haut, Handb. der prakt. Med., Stuttgart, 1901.

10. Bulkley: "Skin Diseases and Internal Disorders," New York, 1882, 106.

11. Galloway: Brit. J. Derm., 1903, XV, 235.

12. Sachs: Arch. f. Derm. u. Syphil., 1909, XCVIII, 35.

13. Galloway and Macleod: Brit. J. Derm., 1903, XV, 81; 1905, XX, 65.

14. Gibert: "Maladies spéciales de la peau," 1834, 89.

15. Bulkley: "Cazanave on the Skin," New York, 1852, 32, (footnote).

16. Köbner: "Klinische und Experimentale Mittheilung," 1864.

17. Chaisse: Quoted by Elliott, "Morrow's System," New York, 1894, vol. III, 114.

18. Legendre: Bull. et mem. Soc. med. d. hop. de Par., 1893, I 3d series, 216, 760.

19. Galloway: Loc. cit.

20. Finger: Arch. f. Derm. u. Syphil., 1893, XXV, 765.

21. Singer: Wien. klin. Wchnschr., 1897, X, 841.

22. Howard: J. Exper. Med., 1899, IV, 149.

23. Corlett: J. Cut. Dis., 1908, XXVI, 7.

24. Lauffer: Arch. f. Derm. u. Syphil., 1890, XXII, 379.

25. Goldstein: Internat. klin. Rundschau, Wien, 1890, IV, 1643.

26. Peter: Semaine méd., 1891, II, 281.

27. DaCosta: Am. J. Med. Sc., 1899, CXVIII, 1.

28. Hutinel et de Gimard: Med. Mod., Paris, 1890, I, 88, 101, 124.

29. Schamberg: "Diseases of the Skin and Eruptive Fevers," Phila., 1907, 500.

30. McCrae: "Osler's Modern Medicine," Phila., 1907, Vol. II, 117.

ACUTE TUBERCULOUS ENDAORTITIS .*

By PAUL G. WOOLLEY, M. D.,

Dean and Professor of Pathology, College of Medicine, University of Cincinnati, Cincinnati, Ohio.

The present consensus of opinion is to the effect that tubercle bacilli cannot, except in the rarest instances, be ob- served in the circulating blood. Yet we know that they must be present there and often in large numbers. We have built up our ideas of the production of miliary tuberculosis upon the assumption that the organisms that cause the disease are distributed by the blood, to which they gain access in three ways; by rupture of a tuberculous focus in one or another organ into a blood vessel; by the invasion of the walls of blood vessels, especially veins, by the tuberculous process, with the production of a tuberculous lesion in the intima of the vessel from which bacilli are distributed; and by the in- volvement of the thoracic duct in a tuberculous process, from foci in which tubercle bacilli gain access to the venous blood.

Vascular involvement is frequent, and it is probable that a search in every case of miliary tuberculosis will be rewarded by finding a focus of extension, most frequently in the smaller pulmonary veins, or thoracic duct, less frequently in the renal or pulmonary arteries, aorta, or the vessels of one or another organ of the body.

Invasion per extensionem is the rule in small vessels. It is not so common in large ones, nor indeed is vascular involve- ment of any sort. This invasive process is the one that usually accounts for the production of a generalized tuber-

* Read before the Cincinnati Society of Medical Research, October 6, 1910.

culosis. It is the process by which the bacilli gain entrance to the blood stream, whence they are distributed. But there is a second process by which the secondary vascular lesions are produced. It may be assumed to occur generally as the result of thrombosis of, or endothelial phagocytosis in the capillaries of the tissues. As a result of either the vessel wall is involved from the side of the intima. This invasion from the lumen is frequent in small vessels but is infrequent in large ones for obvious reasons. It is least common in the aorta.

A review of the literature on tuberculosis reveals the fact that aortic lesions may be of the invasive or of the metastatic type, and that both are rare. The metastatic lesions may be acute or chronic in character.

In the cases of Dittrich and Kamen the aorta was involved from adherent tuberculous bronchial glands, and this wa followed by acute miliary tuberculosis and rupture of the aorta (Kamen). In Buttermilch's case the aortic involve- ment was secondary to a vertebral tuberculosis.

Schmorl mentions two cases of acute miliary tuberculosis which he conceives as being the result of the perforation of ª tuberculous lymph gland or of a pulmonary cavern into the aorta.

Examples of tuberculous aortitis by extension are the cases of Dittrich, Kamen, Schmorl, Hanau and Sigg, and Butter- milch. In the case of Hanau and Sigg an aneurism ruptured

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I'm we lang. It is entirely probable that the rta was weakened, its walls infiltrated and an aneurism ised thereby, after which rupture occured, for the edges of e torn wall of the aneurismal sac showed tuberculous vege- ions.

The chronic type of tuberculous endaortitis is illustrated the cases of Forssner, Benda, Aschoff, Longcope, Schmorl, ylord, Simnitsky and Luksch.

In this series there has been, with few exceptions, a more or s severe arteritis or arteriosclerosis in association with the perculous changes, a coincidence that has lead to the as- nption that the specific lesions have been the result of in- tion of parietal thrombi by tubercle bacilli. In them the ocess has apparently shown no tendency to advance along : intima, so that the lesions have increased into the lumen ›ducing either flattened nodules or, more commonly, poly- d growths. In all the cases reported by Benda the lesions re polypoid. In two cases they were situated upon areas sclerosis, in a third upon an atheromatous ulcer. In ksch's case the lesions in the aorta, anonyma, and left sub- vian were upon an endarteritic basis. In Forssner's case re was no arteriosclerotic change, but it is possible that in s the lesion was primary in the media resulting from a mary involvement of one of the vasa vasorum. The in- ial tubercle measured 4 x 1 cm. Stroebes' case was one of hild in which there was a polypoid growth 7 mm. high and mm. thick, with no arteriosclerosis. Aschoff's case showed reme arteriosclerosis and a tuberculous mass the size of a n near the origin of the Ductus Botalli. The lesion de- ibed by Longcope was a polyp 3 cm. long, which was found the descending aorta of a child suffering from tuberculous disease. The report of Simnitsky, to which I have not had ess, save through Forssner's paper, concerned itself with a ? of chronic pulmonary and intestinal tuberculosis, and no iary tuberculosis. The aortic lesion was in one of the ises of Valsalva.

n all of Schmorl's five cases there was arteriosclerosis, and all the cases the tuberculous polypi were situated upon romatous ulcers.

ccordingly it appears that in this chronic group arterio- 'osis is more frequently present than is natural in tuber- sis, a disease in which the arterial tree is not as a rule rely affected, and it is therefore quite possible that the eption that the aortic lesions are the result of infection rural thrombi is correct in the majority of cases. Ten of teen of the reported cases showed the presence of arterio- osis. In two cases I have not been able to find a descrip- of the general aortic condition (Gaylord and Simnitsky) n two the patients were young individuals (Longcope and be). In this enumeration Forssner's case is excepted it is possibly in a class by itself.

e series of acute tuberculous endaortitis include the cases archand, Huber, Schuchardt, Hanot, Hanot and Levi, itsky, Blumer, Flexner and the one to be reported in aper. In all of these miliary tubercles were present in tima of the aorta.

The cases of Marchand and Huber were merely mentioned by Weigert who described them as showing the most exquisite structure, "giant cells, caseated center, etc." Schuchardt reported minute lesions situated near the junction of the thoracic and abdominal aorta. There was very little arterio- sclerosis. I have been unable to find the report of the cases of Hanot and Simnitsky. That of Hanot and Levy was one in which a tubercle was found in the superior portion of the thoracic aorta. The tubercle discovered by Flexner was situ- ated about 2.5 cm. below the left subclavian artery, and measured 2.5 x 1 mm. in diameter. The aorta was not scle- rotic. Flexner believed that this tubercle was secondary to an infective thrombus in the pulmonary artery.

In all of the cases, of either acute or chronic type, the lesions have been described as containing large numbers of tubercle bacilli, a fact that has an important bearing upon the manner of the production of the general miliary tubercu- losis that has been present in all except Simnitsky's first case, for many writers believe that the general lesions are the re- sult of the escape of bacilli from the aortic lesions. It would seem reasonable, however, to limit the production of secondary general disease to the chronic cases, for in the acute ones the aortic lesions seem rather to be a part than the cause of it.

The case that I wish to report falls in the category of acute tuberculous endaortitides.

CASE 152173 .- The patient, a man of 59 years, and a laborer, was admitted to the Cincinnati Hospital on November 11, 1909, complaining of "bladder trouble." In August, 1909, he had been admitted to a hospital for cystitis, which was improved by treat- ment with urotropin and irrigations. He had suffered with " bladder trouble " for some two years previously, that is to say, he had had pain on micturition, a symptom which was not con- stant, but which occurred in exacerbations, at the onset of each of which he passed some blood. At the time of his last admission he gave no evidence of pulmonary or cardio-vascular disease, ex- cept a slight roughening of the breath sounds during expiration. There was no splenic or hepatic enlargement. He suffered with involuntary urination accompanied by pain. The urine was dark red and contained blood clots.

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Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens, Part 92

Author: Jacob Anthony Kimmell Publication date: 1910 Publisher: Number of Pages: 1189

Author: Jacob Anthony Kimmell
Publication date: 1910
Publisher:
Number of Pages: 1189