Journal of the Royal Society of Medicine Volume 85 May 1992

Infective endocarditis in


district general hospital

M Manford MRcp J Matharu K Farrington MD MRCP King George Hospital, Eastern Avenue, Ilford, Essex

Department of Medicine,

Keywords: infective endocarditis; district general hospital; audit

Summary Thirty-three cases of infective endocarditis presenting during a 6.5 year period to a district general hospital were analysed retrospectively. The annual incidence was 22 cases per million population. Twenty-two cases had pre-existing cardiac disease, mainly valvular disease - usually rheumatic (nine cases) and prosthetic valves (10 cases). Recognizable precipitants such as recent surgery were uncommon. Two cas'es presented after deliberate drug overdose possibly due to depression exacerbated by systemic disease. Symptoms were usually non-specific. All but two cases had murmurs and most were pyrexial. Splinter haemorrhages and clubbing were seen in about 20% of cases. Viridans-type streptococci were the commonest infecting organisms (14 cases). Staphylococcal infection (six cases) was confined to intravenous drug abusers and patients with prosthetic valves. Five cases were culture negative. Cerdiac failure was present in 13 cases at presentation and developed in seven others during treatient. Acute valve replacement was necessary in eight cases, and late replacement in three. Renal impairment (plasma urea > 8 mmol/l and/or plasma creatinine > 120 unmol/l) occurred in 19 cases during the course of their illness. Embolic phenomena occurred in 12 patients and mostly involved the central nervous system. In the 8 fatal cases, the cause of death was cardiac failure in six, cerebrovascular accident in one, and myocardial infarction in one. Four of the six patients who subsequently died of cardiac failure had been referred for surgery. Both those who were not referred had coexisting medical problems. Factors associated with increased mortality were age, male sex, cardiac failure (P8 mmol/l and/or plasma creatinine > 120 pmol/l) was seen in 19 cases (58%) during the course of their illness.

Imaging Echocardiography was performed in 12 cases. It was diagnoticofIR(vegetations)in five cases, equivocal in five, and negative in two.



Journal -of the Royal Society of Medicine Volume 85 May 1992

Table 2. Signs and symptoms in 33 consecutive infective endocarditis




Present Absent Unrecorded

Malaise Fatigue Fever Weight loss Anorexia Sweats Breathlessness Cough Arthralgia Chest pain Palpitations Chills Documented pyrexia Murmurs (static) Murmurs (changing) Tachycardia Cardiac failure (clinical) Cardiac failure (radiological) Hypotension Splinters Clubbing

28 20 17 15 14 14

Splenomegaly Rash Lymphadenopathy Osler's nodes Roth spots

1 6 11 14 13 11 18 21 15 22 23 18 8 2 0 16 18 15 20 14 25 25 18 22 13 12

12 9 7 7 4 3 21 22 9 17 13

12 8 6 6 5 4 4 1 0

4 7 54 6 6 3 3 11 4 6 12 3 0 0 0 2 6 5 13 2 3 11 7 19 21

Site of infection Mitral valve involvement predominated especially in native valve infection (Table 5). Treatment In 6 cases penicillin-sensitive organisms were treated with intravenous penicillin alone for 2 weeks and then oral amoxycillin for a further 4 weeks. All survived. Remaining patients with penicillin-sensitive organisms, and most cases of enterococcal infection were treated with -an amino-

glycoside, usually gentamicin, and intravenous penicillin for 2-4 weeks, and then oral amoxycillin. One patient who had severe renal failure and combined infection with enterococci and micrococci was treated with ampicillin and vancomycin. Staphylococcal infections were treated with an aminoglycoside and intrav-enous fluclox4cillin for 2 weeks and then oral flucloxacillin and fucidin. One patient with severe renal impairment received vancomycin instead of gentamicin. Treatment was titrated against laboratory measures of minimum inhibitory concentration in all culture positive cases. Culture negative cases were treated with penicillin and gentamicin except -n case 29 in which a previous pseudomonas urinary tract infection dictated a combination of ceftazidime and amikacin.

Table 3. Laboratory investigations in patients with infective endocarditis

ESR range

Haemoglobin (gldl)

Patient numbers


1 9 13 10


(mm/h) < 20

20-50 >50 U

Patient numbers

Plasma urea range

(mmol/l) 17


Patient number

14 9 4 6


Protein present 9 absent 15 U 9

10 17 6

ESR: erythrocyte sedimentation rate; U: unrecorded in case record Table 4. Details of 19 patients wiih infective endocrditis who had renal imparmwent at presention or developed it during btabnent

Case 1 2

7 8 10 12 15 18 19 20 21b 22 23 24 25 26 27 29 30

Renal function Initial Final

U8.7 C118 U5.4 U8.3 U8.4 U14.1 U11.3 CC25 C232 C402 U24.0 U8.0 C198 C134 U17.7 U7.6 C152 U43.0 U18.0

U7.6 C161 U9.2 U15.3 U30.0 U6.8 U7.9 C436 C319 U8.8 U5.5 C112 U13.0 U9.0 C53 U47.0 U14.2

Urinalysis Drugs



h, p, w



P+N P P+G P+G P+G A+G A+Vancomycin A+N

CF, MI CF. CF CF CF, septic arthritis


h, w

h, p h, w, c

c, w h, p


h, w

F+G F+G F+Fucidin Vancomycin



h, c



(UTI) .

P+G-G Cetasidime/Amikacii. P+G



U: plasma urea (mmoIl), C: plasma creatinine (jimol/l), CC: creatizine clearance (mi/m)n), c: casts, h: haematuria, G: entami N: ntilmicin,-P: penicilli. For other abbreviations p: proteinuria; w: pyuria, A: ampicillin, F: flucGoilin, see legend to Table 1

Journal of the Royal Society of Medicine Volume 85 May 1992 265 > 120 jmol/l) was seen in 19 patients (Table 4) during the course of their admission, and was significantly associated with increased mortality, (P< 0.05). Three patients (cases 19, 20 and 29), had known pre-existing Prosthetic Native chronic renal failure, and--to of these died. Renal ___________________________________ function deteriorated (>20% increment in plasma urea and/or creatinine) during admission in five 4* 64 Aortic 14 4* ,patients, two of whom died. It improved in nine Mitral patients (>20% fall in these parameters), three of 11 defect eptal deet 00 Ventricular septal 0 whom died. All five patients with deteriorating renal -1 Unknown function had heart failure and four had received -___________-___________ -_____ aminoglycosides. Of the nine-patients whose renal *One patient had both mitral and aortic valve replacement function improved, three-had coeing heart failure and aminoglycoside exposure. None of these patients had toxic drug levels. Table 6. Complications arising in 33 episodes of infective

Table 5. Site of infection in 33 episodes of infective endocarditis in 31 patients


endocarditis in 31 patients


13 Eight of the 33 episodes of IE resulted in death, a Cardiac failure at presentation 7 mortality of 24%. Deaths were due to heart failure Cardiac failure during treatment 12 (six patients), cerebrovascular accident (one patient), Atrial fibrillation 12 Embolic phenomena and myocardial infarction (one patient). The mean age 1 Meningitis/CVA Ofsurvivors was 55.8 years and ofthose who died was CVA 4 66.9 years. There were no deaths among the nine Amaurosis fugax 1 patients in the 20-44 year age group, two in the six Septic arthritis 1 patients aged 45-64 years, and six in the 18 patients Pulmonary embolism over 65 years. A higher proportion of males (6 out of 2 Multiple lung abscesses 1 18) tha females (2 out of 13) died. The major factors Splenic infarction (requiring splenectomy) associated with increasedimortality were hBart failure Myocardial infarction (P< 0.01), renal impairment (P< 0.05), and the Renal impairment at presentation or during treaitment 19 1 Aminoglycoside ototoxicity occurrence of.embolic phenomena (P8 mmol/I and/or plasma creatinine


In many respects our data are similar to those from previous studies from regional centres. There are similarities in incidence"6'7, sex- ratio5 and predisposing factors2'8'9, though we are not aware of previous reports of IE presenting with deliberate self-poisoning, as in two of our patients. Conceivably IE may precipitate or exacerbate depression. Characteristically, presenting symptoms were non-specifilc, murmurs and pyrexia almost universal, and the classical stigmata of IE uncommon4"10. The bacteriological spectrum was typical5'8"10, and the incidence of culture negative disease also similar to previous reportsZ8,11-13, particularly to those excluding cultures of material obtained at surgery or autopsy. As in other studies penicillin-resistant infection carried a higher mortality than penicillin-sensitive infection'4-'6. The mortality of 24%, and increasing death rate with increasing age correspond with other studies5. Complications of IE were the major factors predictive of increased mortality, particularly heart failure, renal impairment, and embolic phenomena, as previously established4"19. Heart failure was the most important complication. All but two of our patients who subsequently died of cardiac failure had been transferred for valve replacement. These two were considered unsuitable because of their poor general condition. Echocardiography was not available to most of our patients in the early years of the study period. Its more ready availability then may well have influenced the selection of patients for transfer for surgery, and the timing of such transfer, and perhaps reduced mortality. It would clearly be desirable in all patients with suspected IE. Renal impairment was common and our data suggest that the combination


Journal of the Royal Society of Medicine Volume 85 May 1992

of heart failure and aminoglycoside therapy maybe particularly detrimental to renal function even in the absence of toxic drug levels. The incidence of embolic complications often with neurological sequelae was comparable to that in other studies17"18. Tswo deaths in our series were probably due to embolic events, one due to cerebrovascular accident, and the other due to myocardial infarction.. These deaths must be regarded as potentially avoidable. We think that the similar outcome figures to those of studies originating in regional centres endorses the management of IE in the DGH setting, particularly in those with facilities for echocardiography, with transfer to regional centres for assesent for surgery when appropriate. It might be argued that the results from regional centres would be expected to be worse since they are referred the more severe cases. Our data suggest that there is an additional subgroup of patients, perhaps the sickest of all, who are not referred for surgery usually because of coexisting medical problems. The very poor prognosis of this subgroup may offset the effects on outcome figures of the other more obvious selection biases. There is no doubt though that optimal treatment of patients with IE depends on close cooperation between the DGH and the referral centre. Audit is an esential tool to ensure fine tuning of this interaction, and more studies from district general hospitals will be an important part of this process.

5 6 7

8 9


11 12 13 14


References 1 Skehan JD, Murray M, Mills PG. Infective endocarditis: incidence and mortality in the North East Thames region. Br Heart J 1988;59:62-8 2 Lien EA, Solberg CO, Kalager T. Infective endocarditis 1973-1984 at the Bergen University Hospital: clinical features, treatment and prognosis. Scand J Infect Dis

16 17 18

1988;29:239-46 3 Suryapranata H, Roelandt A, Haalebos M, Deneger J, Bos E, Hugenholtz P. Early cardiac valve replacement in infective endocarditis: a 10 year experience. Eur Heart J 1987;8:464-70 4 Hollanders E, De Scheerder I, De Buyzere M, Ingels G, Bogaert S, Clement DL. A six year review on 53 cases


of infective endocarditis: clinical microbiological and therapeutic features. Acta Cardiologica 1987;43:121-32 Young SEJ. Aetiology and epidemiology of infective endocarditis in England and Wales. J Antimicrob Chemother 1987;20(suppl A):7-14 Smith RH, Radford DJ, Clark RA. Julian DG. Infective endocarditis: a survey of cases in S.E. Scotland 1969-1972. Thorax 1976;31:373-9 Oakley CM. Infective endocarditis. Br J Hosp Med 1980,24:234-43 Baylias R, Clark C, Oakley CM, Somerville W, Whitfield AG, Young SEJ. Incidence, mortality and prevention of infective endocarditis. J R Coll Phys 1986;20:15-20 Arbulu A, Asfaw I. Management of infective endocarditis: a seventeen years experience. Ann Thorac Surg 1987;43:144-9 Bain RJ, Geddes AM, Littler WA, McKinley AW. The clinical and echocardiographic diagnosis of infective endocarditis. JAntimicrob Chemother 1987;20(suppl A): 17-24 Werner SA, Cobbs CG, Kaye D, Hook EW. Studies on the bacteraemia of bacterial endocarditis. JAMA 1967;202:199-203 Pesanti EL, Smith IM. Infective endocarditis with negative blood cultures: an analysis of 52 cases. Am J Med 1979;66:43-50 Washington DA. The microbiological diagnosis of infective endocarditis. J Antimicrob Chemother 1987; 20(suppl A): 29-36 McGivern D, Ispanhani P, Banks D. Factors influencing mortality from endocarditis in two district general hospitals. Postgrad Med J 1987;63:345-9 Woo KS, Lam YH, Kwok HT, Tse LK, Vallence-Owen J. Prognostic index in predicting mortality from infective endocarditis. Int J Cardiol 1989;24:47-54 Eykyn S. The treatment of staphylococcal endocarditis. J Antimicrob Chemother 1987;20(suppl A):161-7 Royden H. The neurological manifestations of infective endocarditis. Brain 1989;112:1295-315 Salgado AV, Furlan AJ, Keys TF, Nichols TR, Beck GJ. Neurological complications of endocarditis: a 12-year experience. Neurology 1989;39:173-8 Leporte C, Vilde JL, Bricaire F, et aL Fifty cases of late prostfhetic valve endocarditis: improvement in prognosis over a 15 year period. Br Heart J 1987;58:66-71

(Accepted 20 August 1991)

Infective endocarditis in a district general hospital.

Thirty-three cases of infective endocarditis presenting during a 6.5 year period to a district general hospital were analysed retrospectively. The ann...
884KB Sizes 0 Downloads 0 Views