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Bacterial endocarditis: a rare complication following orthotopic cardiac transplantation
CASE REPORTS
Bacterial Endocarditis: A Rare Complication Following Orthotopic Cardiac Transplantation Heinke Kunst, MB, MRCP, Pratap K. Paruchuru, FRCS(Edin), Brendan Madden, MD, MSc, FRCPI, FRCP We describe a 46-year-old man who developed infective endocarditis, meningitis, sternal abscess, and infective cerebral emboli after cardiac transplantation. Staphylococcus aureus was the infective organism. We successfully managed the patient with flucloxacillin and fusidic acid to treat infection, and with prostacyclin for systemic embolization. J Heart Lung Transplant 2001;20:483–485.
CASE REPORT A 46-year-old man underwent orthotopic cardiac transplantation for ischemic heart disease. We immunosuppressed the patient with cyclosporine (trough whole-blood level of 500 ng/ml for the first post-operative month and 150 to 250 ng/ml for the remainder of the first post-operative year) and azathioprine (2 mg/kg/day). Although immediate post-operative recovery was good, a routine endomyocardial biopsy 5 weeks after his transplant showed histologic evidence of International Society for Heart and Lung transplantation Grade 3A rejection. We treated him with intravenous methylprednisolone, 1 g daily for 3 consecutive days, followed by oral prednisolone, 60 mg daily, reducing by 5 mg per day to zero. One week after he completed intravenous steroid therapy, another endomyocardial biopsy still showed Grade 3A rejection. He was treated with intravenous human antithymocyte globulin (HATG), 1 g daily for 3 From the Department of Cardio-Thoracic Surgery, St. George’s Hospital, London, United Kingdom. Submitted June 14, 2000; accepted July 24, 2000. Reprint requests: Brendan Madden, MD, Consultant CardioThoracic and Transplant Physician, St. George’s Hospital, London SW17 0QT, United Kingdom. Telephone: ⫹44-181725-1094. Fax: ⫹44-181-725-2049. Copyright © 2001 by the International Society for Heart and Lung Transplantation. 1053-2498/01/$–see front matter PII S1053-2498(00)00184-4
consecutive days. Subsequent endomyocardial biopsy 1 week later showed only Grade 1 changes, and he remained asymptomatic. Two weeks after receiving HATG, he presented with a 24-hour history of chest pain, pyrexia, vomiting, and confusion. Physical examination revealed pyrexia of 39.2° C and an inflamed and unstable sternotomy wound, with purulent discharge. Chest and cardiovascular examination were normal. We noted no audible heart murmurs. Neurologic examination showed a Glasgow Coma Scale of 12/15, and we observed signs of meningism, but no focal neurologic signs. We found evidence of ischemia in the right big toe and fingers of the left hand (Figure 1). Investigations showed leukocytosis (white cell count, 14.6 ⫻ 109/liter) and raised C-reactive protein at 629 mg/liter (normal range ⬍ 10 mg/liter). Computerized tomography of the brain was normal. Cerebrospinal fluid examination showed glucose of 5.6 mmol/liter (plasma, 10.6 mmol/liter), protein of 1.4 g/liter, and white cell count of 1180/mm3 with 100% polymorphs, but gram stain of the fluid did not reveal any organisms. Transesophageal echocardiography showed a mass in the left ventricle attached to the posterior papillary muscle (Figure 2) and good left ventricular function. We obtained blood, pus from the sternal wound, and cerebrospinal fluid for microbial culture. A fully sensitive Staphylococcus aureus was subsequently isolated from blood, pus, and cerebrospinal fluid samples. 483
484
Kunst et al.
The Journal of Heart and Lung Transplantation April 2001
FIGURE 1 Right big toe (A) and fingers of the left hand (B) showing ischemic changes. While awaiting culture results, we made a provisional diagnosis of infective endocarditis and began intravenous flucloxacillin 2 g once daily and oral fusidic acid 500 mg 3 times a day. We incised and drained the sternal wound abscess.
One week after initial presentation, the patient developed focal neurologic signs, and magnetic resonance imaging of the brain showed multiple lowdensity lesions consistent with septic cerebral emboli (Figure 3). In view of an open sternotomy wound, we opted not to anti-coagulate this patient, and because of septic cerebral and systemic embolization, gave him intravenous prostacyclin 5 ng/kg/ min for 5 days. His pyrexia settled, and he had an uneventful recovery with no residual neurologic deficit. The sternal wound healed well. Repeat echocardiography at hospital discharge 6 weeks after initial presentation showed persistence of the left ventricular mass, and he started low-dose aspirin. At outpatient follow-up 2 months later, echocardiography revealed no evidence of the left ventricular mass.
DISCUSSION
FIGURE 2 Transesophageal echocardiography showing a mass in the left ventricle. The mass was attached to the posterior papillary muscle.
Our case highlights a very uncommon diagnosis after heart transplantation (sternal abscess, infective endocarditis, meningitis, and infective cerebral emboli). Infective endocarditis in heart transplant recipients carries a high mortality1 because of the
The Journal of Heart and Lung Transplantation Volume 20, Number 4
Kunst et al.
485
FIGURE 3 Magnetic resonance imaging of the brain showing multiple low-density lesions, consistent with septic cerebral emboli.
presence of sepsis in an immunosuppressed patient. Not surprisingly, a previous fatal case report of sternal abscess and infective endocarditis was described,2 but fortunately our patient survived. A case of infective endocarditis and a ventricular mass associated with staphylococcus in a transplanted heart has been reported, and as in our patient, over time the mass regressed with successful treatment.3 The mass in this case however was on the right side of the heart. The reasons why our patient developed left-sided endocarditis at this particular site are not clear. We were concerned about anti-coagulation in our patient because of the presence of septic cerebral infarcts and an open sternal wound. We chose to use anti-platelet agents. Interestingly, these agents have been shown to reduce vegetation weight in experimental Staphylococcus aureus endocarditis.4,5 Our case is unique in that our patient responded well to this treatment. The methods used in case reports do not permit us to scientifically establish an association between intervention and outcome6 because chance alone could cause the outcome in a single case. However, case reports exert powerful influence on clinical behavior7 because they give clinicians useful reminders, helping them
to more effectively manage similar patients in the future. REFERENCES 1. Uip DE, Amato Neto V, Varejao Strabelli TM, Alcides Bocchi E. Infections caused by virus in 100 patients submitted to heart transplantation. Arq Bras Cardiol 1996;66(4):199 –203. 2. Khoo DE, Zebro TJ, English TA. Bacterial endocarditis in a transplanted heart. Pathol Res Pract 1989;185(4):445–7. 3. Stewart MJ, Huwez F, Richens D, Naik S, Wheatley DJ. Infective endocarditis of the tricuspid valve in an orthotopic heart transplant recipient. J Heart Lung Transplant 1996; 15(6):646 –9. 4. Nicolau DP, Tessier PR, Nightingale CH, Quintiliani R. Influence of adjunctive ticlopidine on the treatment of experimental Staphylococcus aureus endocarditis. Int J Antimicrob Agents 1998;9(4):227–9. 5. Kupferwasser LI, Yeaman MR, Shapiro SM, et al. Acetylsalicylic acid reduces vegetation bacterial density, hematogenous bacterial dissemination, and frequency of embolic events in experimental Staphylococcus aureus endocarditis through antiplatelet and antibacterial effects. Circulation 1999;99(21): 2791–7. 6. Haynes RB. Loose connections between peer-reviewed clinical journals and clinical practice. Ann Intern Med 1990;113: 724 – 8. 7. Enkin MW, Jadad AR. Using anecdotal information in evidence-based health care: heresy or necessity? Ann Oncol 1998;9:963– 6.
Bacterial Endocarditis: A Rare Complication Following Orthotopic Cardiac Transplantation Heinke Kunst, MB, MRCP, Pratap K. Paruchuru, FRCS(Edin), Brendan Madden, MD, MSc, FRCPI, FRCP We describe a 46-year-old man who developed infective endocarditis, meningitis, sternal abscess, and infective cerebral emboli after cardiac transplantation. Staphylococcus aureus was the infective organism. We successfully managed the patient with flucloxacillin and fusidic acid to treat infection, and with prostacyclin for systemic embolization. J Heart Lung Transplant 2001;20:483–485.
CASE REPORT A 46-year-old man underwent orthotopic cardiac transplantation for ischemic heart disease. We immunosuppressed the patient with cyclosporine (trough whole-blood level of 500 ng/ml for the first post-operative month and 150 to 250 ng/ml for the remainder of the first post-operative year) and azathioprine (2 mg/kg/day). Although immediate post-operative recovery was good, a routine endomyocardial biopsy 5 weeks after his transplant showed histologic evidence of International Society for Heart and Lung transplantation Grade 3A rejection. We treated him with intravenous methylprednisolone, 1 g daily for 3 consecutive days, followed by oral prednisolone, 60 mg daily, reducing by 5 mg per day to zero. One week after he completed intravenous steroid therapy, another endomyocardial biopsy still showed Grade 3A rejection. He was treated with intravenous human antithymocyte globulin (HATG), 1 g daily for 3 From the Department of Cardio-Thoracic Surgery, St. George’s Hospital, London, United Kingdom. Submitted June 14, 2000; accepted July 24, 2000. Reprint requests: Brendan Madden, MD, Consultant CardioThoracic and Transplant Physician, St. George’s Hospital, London SW17 0QT, United Kingdom. Telephone: ⫹44-181725-1094. Fax: ⫹44-181-725-2049. Copyright © 2001 by the International Society for Heart and Lung Transplantation. 1053-2498/01/$–see front matter PII S1053-2498(00)00184-4
consecutive days. Subsequent endomyocardial biopsy 1 week later showed only Grade 1 changes, and he remained asymptomatic. Two weeks after receiving HATG, he presented with a 24-hour history of chest pain, pyrexia, vomiting, and confusion. Physical examination revealed pyrexia of 39.2° C and an inflamed and unstable sternotomy wound, with purulent discharge. Chest and cardiovascular examination were normal. We noted no audible heart murmurs. Neurologic examination showed a Glasgow Coma Scale of 12/15, and we observed signs of meningism, but no focal neurologic signs. We found evidence of ischemia in the right big toe and fingers of the left hand (Figure 1). Investigations showed leukocytosis (white cell count, 14.6 ⫻ 109/liter) and raised C-reactive protein at 629 mg/liter (normal range ⬍ 10 mg/liter). Computerized tomography of the brain was normal. Cerebrospinal fluid examination showed glucose of 5.6 mmol/liter (plasma, 10.6 mmol/liter), protein of 1.4 g/liter, and white cell count of 1180/mm3 with 100% polymorphs, but gram stain of the fluid did not reveal any organisms. Transesophageal echocardiography showed a mass in the left ventricle attached to the posterior papillary muscle (Figure 2) and good left ventricular function. We obtained blood, pus from the sternal wound, and cerebrospinal fluid for microbial culture. A fully sensitive Staphylococcus aureus was subsequently isolated from blood, pus, and cerebrospinal fluid samples. 483
484
Kunst et al.
The Journal of Heart and Lung Transplantation April 2001
FIGURE 1 Right big toe (A) and fingers of the left hand (B) showing ischemic changes. While awaiting culture results, we made a provisional diagnosis of infective endocarditis and began intravenous flucloxacillin 2 g once daily and oral fusidic acid 500 mg 3 times a day. We incised and drained the sternal wound abscess.
One week after initial presentation, the patient developed focal neurologic signs, and magnetic resonance imaging of the brain showed multiple lowdensity lesions consistent with septic cerebral emboli (Figure 3). In view of an open sternotomy wound, we opted not to anti-coagulate this patient, and because of septic cerebral and systemic embolization, gave him intravenous prostacyclin 5 ng/kg/ min for 5 days. His pyrexia settled, and he had an uneventful recovery with no residual neurologic deficit. The sternal wound healed well. Repeat echocardiography at hospital discharge 6 weeks after initial presentation showed persistence of the left ventricular mass, and he started low-dose aspirin. At outpatient follow-up 2 months later, echocardiography revealed no evidence of the left ventricular mass.
DISCUSSION
FIGURE 2 Transesophageal echocardiography showing a mass in the left ventricle. The mass was attached to the posterior papillary muscle.
Our case highlights a very uncommon diagnosis after heart transplantation (sternal abscess, infective endocarditis, meningitis, and infective cerebral emboli). Infective endocarditis in heart transplant recipients carries a high mortality1 because of the
The Journal of Heart and Lung Transplantation Volume 20, Number 4
Kunst et al.
485
FIGURE 3 Magnetic resonance imaging of the brain showing multiple low-density lesions, consistent with septic cerebral emboli.
presence of sepsis in an immunosuppressed patient. Not surprisingly, a previous fatal case report of sternal abscess and infective endocarditis was described,2 but fortunately our patient survived. A case of infective endocarditis and a ventricular mass associated with staphylococcus in a transplanted heart has been reported, and as in our patient, over time the mass regressed with successful treatment.3 The mass in this case however was on the right side of the heart. The reasons why our patient developed left-sided endocarditis at this particular site are not clear. We were concerned about anti-coagulation in our patient because of the presence of septic cerebral infarcts and an open sternal wound. We chose to use anti-platelet agents. Interestingly, these agents have been shown to reduce vegetation weight in experimental Staphylococcus aureus endocarditis.4,5 Our case is unique in that our patient responded well to this treatment. The methods used in case reports do not permit us to scientifically establish an association between intervention and outcome6 because chance alone could cause the outcome in a single case. However, case reports exert powerful influence on clinical behavior7 because they give clinicians useful reminders, helping them
to more effectively manage similar patients in the future. REFERENCES 1. Uip DE, Amato Neto V, Varejao Strabelli TM, Alcides Bocchi E. Infections caused by virus in 100 patients submitted to heart transplantation. Arq Bras Cardiol 1996;66(4):199 –203. 2. Khoo DE, Zebro TJ, English TA. Bacterial endocarditis in a transplanted heart. Pathol Res Pract 1989;185(4):445–7. 3. Stewart MJ, Huwez F, Richens D, Naik S, Wheatley DJ. Infective endocarditis of the tricuspid valve in an orthotopic heart transplant recipient. J Heart Lung Transplant 1996; 15(6):646 –9. 4. Nicolau DP, Tessier PR, Nightingale CH, Quintiliani R. Influence of adjunctive ticlopidine on the treatment of experimental Staphylococcus aureus endocarditis. Int J Antimicrob Agents 1998;9(4):227–9. 5. Kupferwasser LI, Yeaman MR, Shapiro SM, et al. Acetylsalicylic acid reduces vegetation bacterial density, hematogenous bacterial dissemination, and frequency of embolic events in experimental Staphylococcus aureus endocarditis through antiplatelet and antibacterial effects. Circulation 1999;99(21): 2791–7. 6. Haynes RB. Loose connections between peer-reviewed clinical journals and clinical practice. Ann Intern Med 1990;113: 724 – 8. 7. Enkin MW, Jadad AR. Using anecdotal information in evidence-based health care: heresy or necessity? Ann Oncol 1998;9:963– 6.