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Infective endocarditis in patients over age 60
Infective
endocarditis
in patients
over age 60
Mark M. Applefeld, M.D. Richard B. Hornick, M.D. Baltimore, Md.
Few diseases present greater insurmountable difiticulties in diagnosis than infective endocarditis. No less a student of the disease than William Osler stressed that fully one-half of the patients are detected postmortem.17 This diagnostic dilemma is particularly true in the older patient.‘s4J2J5 Recent reviewsl,2,7J3 have not specifically stressed the problems of detection and management in patients over age 60. This paper will attempt to re-emphasize pertinent aspects of infectious endocarditis in the elderly. Methods and materials
A retrospective analysis was made of the records of patients admitted to the University of Maryland Hospital between the years 1950 through 1970, with a diagnosis of bacterial endocarditis. A search was also undertaken of autopsy reports of patients with similar diagnoses during the same period. To be included for analysis, patients were required to manifest: (1) positive blood cultures, fever greater than 100” F., splenomegaly or signs of peripheral embolization, heart murmur, and hematuria; or (2) heart murmur, pyrexia over 100” F., hematuria and/or splenomegaly with signs of peripheral embolization, leukocytosis on admission greater than 12,000 per cubic millimeter, and hemoglobin less than 12 grams; or (3) negative blood cultures, fever greater than 100” F., heart murmur, hematuria, splenomegaly, and signs of embolization; or (4) a pathologically proved diagnosis of From the Division of Infectious Diwaees, Department of Medicine, University of Maryland School of Medicine, Baltimore, Md. 21201. Reprint requests should be addressed to Dr. Hornick. Received for publication Jan. 16, 19’74. * Currently Fellow in Cardiology, Georgetown Univereity Hospital, Washington, D. C.
90
infective endocarditis. One hundred and thirtysix case records fulfllled the above criteria; 29 (21 per cent) patients, 60 years or older, will be discussed Results Of the 29 patients, 20 (85 per cent) were 65 years or older; 15 (51 per cent) were over 70 years of age. Pyrexia of unknown etiology was the presenting complaint in 14 instances (48 per cent). Over one-third of the patients9 presented with neurologic signs, most commonly coma or hemiplegia of acute onset. If disorientation is included, the Sgure is increased to 45 per cent. The danger of incriminating an infectious process as the sole cause of alteration of sensorium in this age group is recognized. Despite neurologic changes, only three patients received diagnostic lumbar puncture. The predisposing causes of illness include: 10 (35 per cent) secondary to an operative procedure; 9 (31 per cent) related to dental manipulation or decubitus ulcers; and 8, cryptogenic (Table I). The vast majority of infections occurred in patients with known organic aortic valvular disease, primarily of a ““rheumatic” etiology. Eight patients (27 per cent) had aortic valvular insufficiency; 8, aortic stenosis; 2 (7 per cent), calcific aortic stenosis; 10 (34 per cent), mitral regurgitation; and in 10, no murmur was detected. New regurgitant murmurs were noted in 4 instances (14 per cent); aortic in 3 instances, and mitral in 1 instance. Organisms of the staphylococcal or streptococcal group were the causative agents in 20 cases (69 per cent) (Table II). Endocarditis caused by fungae or rickettsiae was not noted. Twenty-one patients (72 per cent) had two or more positive blood cultures for the infecting agent while 9 of
July, 1974, Vol. 88, No. 1, pp. 90-94
Infective endocarditis
group (31 per cent) had received antibiotic therapy prior to taking blood for culture. Sixteen C55 per cent) of the group had a fever of 100” F. or greater on admission, while 8 (27 per cent) experienced septic fluctuations during their hospital courses. Sixty-two per cent had a leukocytosis of greater than 12,000 per cubic millimeter; a similar number demonstrated hemoglobin of less than 12 grams. Splenomegaly and splinter hemorrhages were uncommon findings, being detected in 17 per cent and 34 per cent of the instances, respectively. Roth’s spots, Osler’s nodes, and Janeway’s lesions were not noted. There were slight differences in clinical manifestations among patients su8pected to have bacterial endocarditis and those detected postmortem (Fig. 1). The presence of petechiae and splenomegaly was greater antemortem, whereas neurologic signs and the degree of leukocytosis were more common in the group detected at autopsy. The average splenic weight in the latter group was 286 grams. Taken in context, these findings substantiate the similarity between these two groups and stress the importance of adequacy and thoroughness of physical examination. Strikingly, 14 (48 per cent) of the total group received inappropriate antibiotic therapy and 21 (72 per cent) of the 29 patients in the older age group died. There was no significant correlation between duration of illness from onset of hospitalization until time of death or discharge and the degree of fever or leukocytosis. The etiologic agent, likewise, was unrelated to the degree of pyrexia, leukocytosis, or morbidity. Of six patients infected with coagulase-positive staphylococcus, three died within one to two weeks of hospitalization; three within four to eight weeks. Length of clinical course until death in patients with endocarditis caused by streptococcal viridans and alpha-streptococci was similar. Specific anatomic correlations were not possible in all cases in this series. However, of the total number of cases examined postmortem, 19, only a single instance of acute chordal rupture, and four with acute cusp rupture (2 aortic, 2 mitral) were recorded. There were two instances each of myocardial abscess, “suppurative” myocarditis, and left atria1 extension of infective vegetation;
this
American
Heart Journal
Table I. Presumed
predisposing
in patients
over 60
causes in 29 pa-
tients Cause Decubitw UbXF.’ Dental CUFk?S: Denfal manipulation: Puruknt colyunctivitis: Aplastic anemia: Operative pFOWdUFe: Repeated urethral catheterizations Postoperative transurethral resection Prostatic biopsy with Perineal absceae Infected Beny button Herniorrhaphy Ureteroileostomy with enterocutaneous fistula Colectomy with ileocutaneous fistula Gastric resection with wound abscess Small bowel resection Bleeding kg ulcer with tight urosheath and penile necrosis: Unknown: *One
4 4* 1* 1 1 2 1
1
8
patient appears in both categories.
Table II. Bacteriologic
isolates in 29 cases
Organism
j
Staphylocvcci: Coagulase (+) Coagulase (-) Streptococci: Viridans Pyogenes P-Hemolytic Enterococcus D. pneumvniae: E. coli: Unknown:
and single examples of mitral ring abscess and aortic arch endarteritis. Occlusion of mediumsize blood vessels, predominantly intra-abdominal, was noted in 17 per cent of the cases.
In a recently reported series,1-8 the incidence of infective endocarditis in patients older than 60 years varies between 12 and 45 per cent. The present figure of 21 per cent is within this range. Although the precise nature of underlying heart disease is uncertain in most of our cases, postmortem examination confirmed a rheumatic
91
Applefeld
and Hornick
DISCOVERED 0
SUSPECTED
POSTMORTEM CLINICALLY
DENOMINATOR-TOTAL NUMERATOR-
woo
F,
Fig. 1.
klepm
npb)
WBC l12r103/mm31
BEMATITURIA l>2/HPf)
Findings detected antemortem
etiology in 4 (14 per cent) and calcific aortic stenosis in 2 (7 per cent). No organic valvular lesion was noted in 14 (48 per cent) cases. Robinson,“?n a study of pathologic specimens, reported an incidence of rheumatic heart disease in 31 per cent and calcific aortic stenosis in 10 per cent, the remainder occurred in apparently normal Buchbinderz3 noted hearts. Roberts and anatomically normal valves in 53 per cent of their patients. This contrasts with Lerner and Weinstein’s series’ in which 50 per cent of the vegetations in bacterial endocarditis involving this age group occurred on rheumatic valves; 30 per cent on normal valves. These figures reemphasize the spectrum of this disease and its propensity to affect undamaged cardiac valves. A relative minority (30 per cent) of the infecting agents were of low virulence; the remainder, either unidentified or pathogenic bacteria such as coagulase-positive staphylococci, enterococcus, Diplococcus pneumoniae, and Escherichia coli (Table II). In other studies,4-7 isolation of usually low-virulence organisms occurs with simThe role of antecedent ilar frequency. staphylococcal infections has also been noted previously.1-s Twenty-seven per cent of our total number of cases of staphylococcal endocarditis appeared in the older age group; in 71 per cent of these patients, underlying valvular heart disease was not previously known to exist. In Wilson’s and Hamburger’s study9 of patients surviving staphylococcal septicemia and presumed to have infective endocarditis, 43 per cent apparently
92
NUMBER NUMBER
WITH
IN
EACH
PARTICULAR
NEUROLOGIC SISNS
GROUP MANFESTAT,ON
PETECHIAE
SPLENOMEGALY
and at necropsy.
had no previous valvular heart disease. In those who died, essentially the same figure pertains. Thus, the potential seriousness of staphylococcal bacteremia is again recognized and we concur with the current recommendationl~sof treatment with appropriate agents for a minimum of six weeks. Until 1972, there are only nine well-documented cases of fungal endocarditis reported in the English literature in persons over 60.18-22The organisms identified were: Candida, three cases; Histoplasma capsulatum, two cases; and single examples of Blastomyces dermatitides, Mucor, Aspergillus fumagatum , and Torulopsis glubrata. Clinical signs of endocarditis were detected premortem in two patients, each caused by the genus Candida. At necropsy, valvular vegetations were noted in five instances; the remaining lesions involved either the atria1 and/or ventricular endocardium. Only three patients over age 60 have been reported with endocarditis caused by Rickettsia burneti.24-25 Two patients survived their illness; one required aortic valve replacement. To our knowledge, none have been reported from the United States. The lack of a febrile response has been commented upon.1,*o*17 In Jackson and Allison’s series,lO although no figure is specifically mentioned, pyrexia was noted on admission in 44 per cent but was consistently absent in 25 per cent of their patients. In our study, 55 per cent had fever of at least 100.5” F. during their hospitalization; 27 per cent demonstrated a septic-type curve
July, 1974, Vol. 88, No. 1
infective
during their illness. However, the number of patients remaining entirely afebrile re-emphasizes the potentially occult nature of this disease. Only three patients showed neither fever or leukocytosis, negative findings stressed by Gleckler.“” Twenty per cent of patients had either sterile blood cultures or no specimens taken. If all of these are considered to be instances of abacteremia, an unlikely assumption, our figure approaches that of others .1,2,5,71n fact, this appears to be an overestimate and suggests that the majority of patients will indeed manifest bacteremia. Seventy-six per cent in our series showed two to ten positive cultures; 50 per cent, between two and four positive cultures. This substantiates earlier work.lla 23 Thus, pyrexia, leukocytosis, and positive blood cultures remain useful markers of the presence of this disease. Our incidence of splenomegaly, 17 per cent probably spuriously low, is strikingly less than that of others,‘, 5,lo, 12.14while that of splinter hemorrhages, 34 per cent, is within the reported range.1.5.12110 Osler’s nodes, Roth’s spots, and Janeway’s lesions were not detected in this series. Obviously, the presence or absence of these physical signs is dependent upon the care with which they are sought. &men and Slegal’s admonitiorP “ . . . it is obvious that, when the possibility of endocarditis is unsuspected, little time will be given to looking for skin lesions (and splenomegaly)” merits emphasis. Our mortality rate of 72 per cent simulates other data.2~4~7,10~12 The reasons for our large number of treatment failures are uncertain. Illness was fulminant in some causing an early death. However, other instances represented patients in whom bacteriologic isolates were apparently known and yet therapy not instituted or inadequate dosage regimens used. The reasons were probably related to variation in clinical competence among the responsible physicians and in their more cautious attitude toward handling geriatric patients. Of those patients treated appropriately, 60 per cent survived. In conclusion, this series demonstrates that infective endocarditis is not necessarily an uncommon disease with unusual manifestations in patients over age 60. In the appropriate clinical setting, i.e., fever and/or leukocytosis, with or without a cardiac murmur, it needs to be carefully ex-
American
Heart
Journal
endocarditis
in patients
over 60
cluded. Dramatic clinical differences do not appear to be present between patients being treated appropriately and those who are not. Blood cultures will yield the infecting agent in the majority of instances. Abacteremic cases do occur albeit infrequently. Antibiotic regimens should be judiciously selected with treatment in proper dosage of adequate periods. Only in this manner can the excessive mortality from this disease be decreased. REFERENCES 1. 2.
3.
4.
5.
10. 11.
12. 13.
14. 15. 16. 17. 18.
19.
20.
Lerner, P. I., and Weinstein, L.: Infective endocarditis in the antibiotic era, N. Engl. J. Med. 274199, 1966. Shinebourne, E. A., et al.: Bacterial endocarditis 1950-1956: analysis of clinical features and treatment in relation to prognosis and mortality, Br. Heart J. 31:536, 1969. Wallach, J. B., Glass, M., Lukash, L., and Angrist, A. A.: Bacterial endocarditis in the aged, Ann. Intern. Med. 42:1206, 1955. Cummings, V., Furman, S., and Dunst, M.: Subacute bacterial endocarditis in the older age group, J.A.M.A. 172:137, 1960. Cherubin, C. S., and Neu, H. C.: Infective endocarditis at the Presbyterian Hospital in New York City from 19361967. Am. J. Med. 51:83. 1971. Hughes, P.: Bacterial endocarditis: a changing disease, Q. J. Med. U&511, 1966. Blount, J. G.: Bacterial endocarditis. Am. J. Cardiol. 38:909, 1965. Robinson, M. J.: Infective endocarditis at autopsy: 1965-1969, Am. J. Med. 52492, 1972. Wilson, R., and Hamburger, M.: Fifteen years’ experience with staphylococcus septicemia in a large city hospital, Am. J. Med. 22437, 1957. Jackson, J. F., and Allison, F.: Bacterial endocarditis, South. Med. J. 54~1331, 1961. Belli, J., and Wastren, B. A.: Number of blood cultures necessary to diagnose most cases of bacterial endocarditis, Am. J. Med. Sci. 238:264, 1956. Anderson, H. T., and Staffurth. J. J.: Subacute bacterial endocarditis in the elderly, Lancet 1:1055, 1955. Rabinovich, S., Evans, J., Smith, I. M.. and January, L. E.: A long-term view of bacterial endocarditis, Ann. Intern. Med. 63185, 1965. Wedgewood, J.: Early diagnosis of subacute bacterial endocarditis, Lancet 21058. 1955. Zemen, F. D., and Slegal, S.: Acute bacterial endocarditisin the aged, AM. HEART J. 29:597,1972. Robinson, M. J.: Infective endocarditis at autopsy: 1965-1969, Am. J. Med. 52:492, 1972. Osler, W.: Malignant endocarditis. Lancet 1:415, 459, 505, 1885. Merchant, R. K., Lourice, D. B., Geisier, P. H., Edgcomb, J. H.. and Utz, J. P.: Fungal endocarditis: review of the literature and report of three cases, Ann. Intern. Med. 48~242, 1958. Solera-Bechara, J., Soscia, J. L., Kennedy, R. J., and Grace, W. J.: Candida endocarditis. Am. J. Cardiol. 13:820, 1964. Andriole, V. T., Knaretz, H. M., Roberts, W. C., and Utz, J. P.: Candida endocarditis, Am. J. Med. 32:251, 1962.
93
Applefeld
and Hornick
21. Hair&on, P., and Lee, W. H.: Mycotic endocarditis after cardiovascular surgery, Am. Surg. 36:136,1969. 22. Lees, A. W., Rao, S. S., Garret, J. A., and Boot, P. A.: Endocarditis due to Torulopaisglabrata, Lancet 1:943, 1971. 23. Roberts, W. C., and Buchbinder, N. A.: Left-sided valvular active infective endocarditis, Am. J. Med. 53~26, 1972.
94
24. Kristinason, A., and Bentall, H. H.: Medical and surgical treatment of Q-fever endocarditis, Lancet 2:693, 1967. 25. Evans, A. D., Powell, D. E. B., and Burrell, C. D.: Fatal endocarditis associated with Q-fever, Lancet 1:864, 1959. 26. Gleckler, W. J.: Diagnostic aspects of subacute bacterial endocarditis in the elderly, Arch. Intern. Med. 102:761, 1959.
July, 1974, Vol. 88, No. 1
endocarditis
in patients
over age 60
Mark M. Applefeld, M.D. Richard B. Hornick, M.D. Baltimore, Md.
Few diseases present greater insurmountable difiticulties in diagnosis than infective endocarditis. No less a student of the disease than William Osler stressed that fully one-half of the patients are detected postmortem.17 This diagnostic dilemma is particularly true in the older patient.‘s4J2J5 Recent reviewsl,2,7J3 have not specifically stressed the problems of detection and management in patients over age 60. This paper will attempt to re-emphasize pertinent aspects of infectious endocarditis in the elderly. Methods and materials
A retrospective analysis was made of the records of patients admitted to the University of Maryland Hospital between the years 1950 through 1970, with a diagnosis of bacterial endocarditis. A search was also undertaken of autopsy reports of patients with similar diagnoses during the same period. To be included for analysis, patients were required to manifest: (1) positive blood cultures, fever greater than 100” F., splenomegaly or signs of peripheral embolization, heart murmur, and hematuria; or (2) heart murmur, pyrexia over 100” F., hematuria and/or splenomegaly with signs of peripheral embolization, leukocytosis on admission greater than 12,000 per cubic millimeter, and hemoglobin less than 12 grams; or (3) negative blood cultures, fever greater than 100” F., heart murmur, hematuria, splenomegaly, and signs of embolization; or (4) a pathologically proved diagnosis of From the Division of Infectious Diwaees, Department of Medicine, University of Maryland School of Medicine, Baltimore, Md. 21201. Reprint requests should be addressed to Dr. Hornick. Received for publication Jan. 16, 19’74. * Currently Fellow in Cardiology, Georgetown Univereity Hospital, Washington, D. C.
90
infective endocarditis. One hundred and thirtysix case records fulfllled the above criteria; 29 (21 per cent) patients, 60 years or older, will be discussed Results Of the 29 patients, 20 (85 per cent) were 65 years or older; 15 (51 per cent) were over 70 years of age. Pyrexia of unknown etiology was the presenting complaint in 14 instances (48 per cent). Over one-third of the patients9 presented with neurologic signs, most commonly coma or hemiplegia of acute onset. If disorientation is included, the Sgure is increased to 45 per cent. The danger of incriminating an infectious process as the sole cause of alteration of sensorium in this age group is recognized. Despite neurologic changes, only three patients received diagnostic lumbar puncture. The predisposing causes of illness include: 10 (35 per cent) secondary to an operative procedure; 9 (31 per cent) related to dental manipulation or decubitus ulcers; and 8, cryptogenic (Table I). The vast majority of infections occurred in patients with known organic aortic valvular disease, primarily of a ““rheumatic” etiology. Eight patients (27 per cent) had aortic valvular insufficiency; 8, aortic stenosis; 2 (7 per cent), calcific aortic stenosis; 10 (34 per cent), mitral regurgitation; and in 10, no murmur was detected. New regurgitant murmurs were noted in 4 instances (14 per cent); aortic in 3 instances, and mitral in 1 instance. Organisms of the staphylococcal or streptococcal group were the causative agents in 20 cases (69 per cent) (Table II). Endocarditis caused by fungae or rickettsiae was not noted. Twenty-one patients (72 per cent) had two or more positive blood cultures for the infecting agent while 9 of
July, 1974, Vol. 88, No. 1, pp. 90-94
Infective endocarditis
group (31 per cent) had received antibiotic therapy prior to taking blood for culture. Sixteen C55 per cent) of the group had a fever of 100” F. or greater on admission, while 8 (27 per cent) experienced septic fluctuations during their hospital courses. Sixty-two per cent had a leukocytosis of greater than 12,000 per cubic millimeter; a similar number demonstrated hemoglobin of less than 12 grams. Splenomegaly and splinter hemorrhages were uncommon findings, being detected in 17 per cent and 34 per cent of the instances, respectively. Roth’s spots, Osler’s nodes, and Janeway’s lesions were not noted. There were slight differences in clinical manifestations among patients su8pected to have bacterial endocarditis and those detected postmortem (Fig. 1). The presence of petechiae and splenomegaly was greater antemortem, whereas neurologic signs and the degree of leukocytosis were more common in the group detected at autopsy. The average splenic weight in the latter group was 286 grams. Taken in context, these findings substantiate the similarity between these two groups and stress the importance of adequacy and thoroughness of physical examination. Strikingly, 14 (48 per cent) of the total group received inappropriate antibiotic therapy and 21 (72 per cent) of the 29 patients in the older age group died. There was no significant correlation between duration of illness from onset of hospitalization until time of death or discharge and the degree of fever or leukocytosis. The etiologic agent, likewise, was unrelated to the degree of pyrexia, leukocytosis, or morbidity. Of six patients infected with coagulase-positive staphylococcus, three died within one to two weeks of hospitalization; three within four to eight weeks. Length of clinical course until death in patients with endocarditis caused by streptococcal viridans and alpha-streptococci was similar. Specific anatomic correlations were not possible in all cases in this series. However, of the total number of cases examined postmortem, 19, only a single instance of acute chordal rupture, and four with acute cusp rupture (2 aortic, 2 mitral) were recorded. There were two instances each of myocardial abscess, “suppurative” myocarditis, and left atria1 extension of infective vegetation;
this
American
Heart Journal
Table I. Presumed
predisposing
in patients
over 60
causes in 29 pa-
tients Cause Decubitw UbXF.’ Dental CUFk?S: Denfal manipulation: Puruknt colyunctivitis: Aplastic anemia: Operative pFOWdUFe: Repeated urethral catheterizations Postoperative transurethral resection Prostatic biopsy with Perineal absceae Infected Beny button Herniorrhaphy Ureteroileostomy with enterocutaneous fistula Colectomy with ileocutaneous fistula Gastric resection with wound abscess Small bowel resection Bleeding kg ulcer with tight urosheath and penile necrosis: Unknown: *One
4 4* 1* 1 1 2 1
1
8
patient appears in both categories.
Table II. Bacteriologic
isolates in 29 cases
Organism
j
Staphylocvcci: Coagulase (+) Coagulase (-) Streptococci: Viridans Pyogenes P-Hemolytic Enterococcus D. pneumvniae: E. coli: Unknown:
and single examples of mitral ring abscess and aortic arch endarteritis. Occlusion of mediumsize blood vessels, predominantly intra-abdominal, was noted in 17 per cent of the cases.
In a recently reported series,1-8 the incidence of infective endocarditis in patients older than 60 years varies between 12 and 45 per cent. The present figure of 21 per cent is within this range. Although the precise nature of underlying heart disease is uncertain in most of our cases, postmortem examination confirmed a rheumatic
91
Applefeld
and Hornick
DISCOVERED 0
SUSPECTED
POSTMORTEM CLINICALLY
DENOMINATOR-TOTAL NUMERATOR-
woo
F,
Fig. 1.
klepm
npb)
WBC l12r103/mm31
BEMATITURIA l>2/HPf)
Findings detected antemortem
etiology in 4 (14 per cent) and calcific aortic stenosis in 2 (7 per cent). No organic valvular lesion was noted in 14 (48 per cent) cases. Robinson,“?n a study of pathologic specimens, reported an incidence of rheumatic heart disease in 31 per cent and calcific aortic stenosis in 10 per cent, the remainder occurred in apparently normal Buchbinderz3 noted hearts. Roberts and anatomically normal valves in 53 per cent of their patients. This contrasts with Lerner and Weinstein’s series’ in which 50 per cent of the vegetations in bacterial endocarditis involving this age group occurred on rheumatic valves; 30 per cent on normal valves. These figures reemphasize the spectrum of this disease and its propensity to affect undamaged cardiac valves. A relative minority (30 per cent) of the infecting agents were of low virulence; the remainder, either unidentified or pathogenic bacteria such as coagulase-positive staphylococci, enterococcus, Diplococcus pneumoniae, and Escherichia coli (Table II). In other studies,4-7 isolation of usually low-virulence organisms occurs with simThe role of antecedent ilar frequency. staphylococcal infections has also been noted previously.1-s Twenty-seven per cent of our total number of cases of staphylococcal endocarditis appeared in the older age group; in 71 per cent of these patients, underlying valvular heart disease was not previously known to exist. In Wilson’s and Hamburger’s study9 of patients surviving staphylococcal septicemia and presumed to have infective endocarditis, 43 per cent apparently
92
NUMBER NUMBER
WITH
IN
EACH
PARTICULAR
NEUROLOGIC SISNS
GROUP MANFESTAT,ON
PETECHIAE
SPLENOMEGALY
and at necropsy.
had no previous valvular heart disease. In those who died, essentially the same figure pertains. Thus, the potential seriousness of staphylococcal bacteremia is again recognized and we concur with the current recommendationl~sof treatment with appropriate agents for a minimum of six weeks. Until 1972, there are only nine well-documented cases of fungal endocarditis reported in the English literature in persons over 60.18-22The organisms identified were: Candida, three cases; Histoplasma capsulatum, two cases; and single examples of Blastomyces dermatitides, Mucor, Aspergillus fumagatum , and Torulopsis glubrata. Clinical signs of endocarditis were detected premortem in two patients, each caused by the genus Candida. At necropsy, valvular vegetations were noted in five instances; the remaining lesions involved either the atria1 and/or ventricular endocardium. Only three patients over age 60 have been reported with endocarditis caused by Rickettsia burneti.24-25 Two patients survived their illness; one required aortic valve replacement. To our knowledge, none have been reported from the United States. The lack of a febrile response has been commented upon.1,*o*17 In Jackson and Allison’s series,lO although no figure is specifically mentioned, pyrexia was noted on admission in 44 per cent but was consistently absent in 25 per cent of their patients. In our study, 55 per cent had fever of at least 100.5” F. during their hospitalization; 27 per cent demonstrated a septic-type curve
July, 1974, Vol. 88, No. 1
infective
during their illness. However, the number of patients remaining entirely afebrile re-emphasizes the potentially occult nature of this disease. Only three patients showed neither fever or leukocytosis, negative findings stressed by Gleckler.“” Twenty per cent of patients had either sterile blood cultures or no specimens taken. If all of these are considered to be instances of abacteremia, an unlikely assumption, our figure approaches that of others .1,2,5,71n fact, this appears to be an overestimate and suggests that the majority of patients will indeed manifest bacteremia. Seventy-six per cent in our series showed two to ten positive cultures; 50 per cent, between two and four positive cultures. This substantiates earlier work.lla 23 Thus, pyrexia, leukocytosis, and positive blood cultures remain useful markers of the presence of this disease. Our incidence of splenomegaly, 17 per cent probably spuriously low, is strikingly less than that of others,‘, 5,lo, 12.14while that of splinter hemorrhages, 34 per cent, is within the reported range.1.5.12110 Osler’s nodes, Roth’s spots, and Janeway’s lesions were not detected in this series. Obviously, the presence or absence of these physical signs is dependent upon the care with which they are sought. &men and Slegal’s admonitiorP “ . . . it is obvious that, when the possibility of endocarditis is unsuspected, little time will be given to looking for skin lesions (and splenomegaly)” merits emphasis. Our mortality rate of 72 per cent simulates other data.2~4~7,10~12 The reasons for our large number of treatment failures are uncertain. Illness was fulminant in some causing an early death. However, other instances represented patients in whom bacteriologic isolates were apparently known and yet therapy not instituted or inadequate dosage regimens used. The reasons were probably related to variation in clinical competence among the responsible physicians and in their more cautious attitude toward handling geriatric patients. Of those patients treated appropriately, 60 per cent survived. In conclusion, this series demonstrates that infective endocarditis is not necessarily an uncommon disease with unusual manifestations in patients over age 60. In the appropriate clinical setting, i.e., fever and/or leukocytosis, with or without a cardiac murmur, it needs to be carefully ex-
American
Heart
Journal
endocarditis
in patients
over 60
cluded. Dramatic clinical differences do not appear to be present between patients being treated appropriately and those who are not. Blood cultures will yield the infecting agent in the majority of instances. Abacteremic cases do occur albeit infrequently. Antibiotic regimens should be judiciously selected with treatment in proper dosage of adequate periods. Only in this manner can the excessive mortality from this disease be decreased. REFERENCES 1. 2.
3.
4.
5.
10. 11.
12. 13.
14. 15. 16. 17. 18.
19.
20.
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July, 1974, Vol. 88, No. 1