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Saudi Journal of Kidney Diseases and Transplantation
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LETTER TO EDITOR Table of Contents   
Year : 2001  |  Volume : 12  |  Issue : 4  |  Page : 550-552
Culture Negative Endocarditis After CAPD Peritonitis: True or Fortuitous Association?


1 Department of Nephrology, Dammam Central Hospital, Saudi Arabia
2 Department of Cardiology, Dammam Central Hospital, Saudi Arabia

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How to cite this article:
Youmbissi J T, Al Saif S, Malik T Q. Culture Negative Endocarditis After CAPD Peritonitis: True or Fortuitous Association?. Saudi J Kidney Dis Transpl 2001;12:550-2

How to cite this URL:
Youmbissi J T, Al Saif S, Malik T Q. Culture Negative Endocarditis After CAPD Peritonitis: True or Fortuitous Association?. Saudi J Kidney Dis Transpl [serial online] 2001 [cited 2019 Dec 14];12:550-2. Available from: http://www.sjkdt.org/text.asp?2001/12/4/550/33551
To the Editor:

Uremic patients on hemodialysis are more likely to develop endocarditis. Bacteremia in these patients is usually related to infections of vascular sites by Staphylococcus aureus or S. epidermidis. Bacterial endo­carditis causally associated to continuous ambulatory peritoneal dialysis (CAPD) peritonitis is not frequently reported. We report below an interesting case of a Saudi adolescent girl on peritoneal dialysis, who presented with typical echocardiographic features of endocarditis a few weeks after an episode of peritonitis, although we could not prove a causal relationship between the two diseases.

A 13-year-old Saudi girl with end-stage renal failure (ESRF) was started on CAPD in 1998. She had a congenital neurogenic bladder and had been suffering from recurrent urinary tract infections (UTIs) since childhood. Her CAPD treatment had been marred by several episodes of peritonitis. The last one occurred two months prior to the present admission. It was due to Staphylococcus epidermidis and was treated with cephradine. She had no past history of rheumatic heart disease and her previous cardiac evaluation was normal.

In March 2000, the patient developed pyrexia (38°C), dysuria and abdominal pain and was admitted for evaluation. She was commenced empirically on ceftriaxone and amikacin. Her peritoneal dialysis fluid (PDF) was sterile on admission but the cell count in the peritoneal fluid was moderately high (92/ml). Her urine culture on the other hand, yielded a group D Streptococcus that was sensitive to ampicillin. Treatment subsequently was continued with this sole antibiotic, Her ESR was 65 mm.

One week after admission, follow up examination of the patient revealed the presence of a pericardial friction rub. The patient was reviewed by a cardiologist who confirmed the diagnosis of pericarditis and the presence of a small pericardial effusion. The CAPD cycles were increased. Strikingly, echocardiographic findings also revealed: the existence of a large, shaggy, mobile, echogenic mass adherent to the anterior leaflet of the tricuspid valve. All leaflets were pliable and coapted well. Doppler and color flow mapping showed the presence of a moderate mitral regurgitation. Pulmonary venous flow showed a reverse ratio between the systolic waves with deep and broad waves (atrial reverse). There was mild tricuspid and pulmonary regurgitation.

Despite these echocardiographic findings, there were no peripheral signs of endo­carditis apart from the presence of the mitral and tricuspid regurgitation murmurs.

Six consecutive blood cultures were negative. The patient was considered to have a residual Staphylococcus epidermidis, peritonitis and a group D Streptococcus UTI, on a background of uremic immuno­suppression and intermittent bladder catheterization. Based on these assumptions, she was treated with vancomycin and gentamicin for the next six weeks. She became apyrexial two weeks after starting treatment. A repeat echocardiographic study one month later showed resolution of the vegetations and the pericardial effusion. The patient was discharged two weeks later. For the two months prior to reporting, the patient has had no abnormal findings on two cardiological evaluations. Her CAPD has also been uneventful.

It is well known that patients who undergo certain medical procedures in the oral cavity, the urinary tract or the gastro­intestinal tract may be exposed to the risk of developing bacterial endocarditis [1] and usually receive some form of antibiotic prophylaxis prior to these procedures. It is also known that in uremic patients on hemodialysis, infections of the vascular access may predispose these patients to bacterial endocarditis (2% to 6%) with at times a high mortality rate (up to 55%). [3]

However, infection of the peritoneal dialysis access has not often been linked to this kind of complication. But theoretically, any source of bacteremia may initiate a chain of events leading to bacterial endocarditis, and CAPD Peritonitis should be no exception. [4]

The diagnosis of bacterial endocarditis in our patient was based only on one major criterion (the echocardiographic findings) and three minor criteria (fever, high ESR and cardiac murmurs). [5] The patient was having a UTI that could also explain the fever and the high ESR. If the patient's bacterial endocarditis and her UTI were causally linked, the blood culture would have probably yielded the same organism as the one found in the urine. Our assumption is that the culture negative endocarditis was rather linked to the previous CAPD peritonitis and that antibiotic treatment, despite curing the peritonitis and suppressing the bacteremia, had failed to prevent the endocarditis. A non-bacterial thrombotic endocarditis was also considered but seems less likely. Nevertheless, the present sequence of clinical events may only have been fortuitous, but it should raise our awareness, and neph­rologists while managing CAPD associated peritonitis, should not forget the risk, however remote, of bacterial endocarditis.


   Acknowledgement Top


The authors wish to acknowledge the valuable contribution of Dr. Mona Al Subaily, Specialist Cardiologist/Echocardiographist for conducting the ultrasonographic studies.

 
   References Top

1.Everett ED, Hirschmann JV. Transient bacteremia and endocarditis prophylaxis: A review. Medicine 1997;56:61-7.  Back to cited text no. 1    
2.Durack DT. Prevention of infective endo carditis. N Engl J Med 1995;332:38-44.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]
3.Nsouli KA, Lazarus M, Schoenbaum SC, Gottlieb MN, Lowrie EG, Shocair M. Bacteremic infections in hemodialysis. Arch Intern Med 1979;139:1255-8.  Back to cited text no. 3  [PUBMED]  
4.Raad II, Bodey GP. Infectious complications of indwelling vascular catheters. Clin Infect Dis 1992;15:197-208.  Back to cited text no. 4  [PUBMED]  
5.Durack DT, Lukes AS, Bright DK. Dukes endocarditis service: New criteria for the diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Am JMed 1994;96:200-9.  Back to cited text no. 5    

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Correspondence Address:
J T Youmbissi
Consultant Nephrologist Dammam Central Hospital, P.O. Box 10388, Dammam 31443
Saudi Arabia
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PMID: 18209401

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