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Isolated pericardial empyema secondary to Staphylococcus aureus
European Journal of Internal Medicine 12 (2001) 377–379 www.elsevier.com / locate / ejim
Brief report
Isolated pericardial empyema secondary to Staphylococcus aureus P. Rachael James* Cardiac Department, Royal Sussex County Hospital, Eastern Road, Brighton BN2 5 BE, UK Received 25 April 2000; received in revised form 18 January 2001; accepted 30 January 2001
Abstract Pericardial empyema, or purulent pericarditis, is a condition uncommonly encountered in routine medical practice but one which is rapidly fatal if left untreated. Early diagnosis is paramount if the patient is to survive. This case report highlights the covert nature of presentation which may occur, hindering early diagnosis, and reviews the current literature. 2001 Elsevier Science B.V. All rights reserved. Keywords: Pericardial effusion; Pericardiocentesis; Staphylococcus aureus
1. Introduction A 77-year-old man presented with cardiac failure but failed to respond to conventional anti-failure treatment. He developed a neutrophilia, but there was no pyrexia or localising signs to suggest a septic focus. When a pericardial effusion subsequently developed, pericardiocentesis was undertaken because of the lack of response to antifailure treatment. Quite unexpectedly, however, drainage yielded thick pus which grew Staphylococcus aureus. Despite aggressive antibiotic therapy, the patient died. A post-mortem examination confirmed the sepsis was isolated to the pericardium.
2. Case report A 77-year-old man with longstanding cardiac failure was admitted with a 4-week history of worsening dyspnoea. He had been taking perindopril 8 mg, digoxin 250 mg and frusemide 40 mg daily. Examination confirmed biventricular failure and he was commenced on intravenous frusemide and glyceryl trinitrate along with *Tel.: 144-1273-696-955; fax: 144-1273-684-554. E-mail address: [email protected] (P.R. James).
oral spironolactone. After 5 days of treatment, the patient had not responded. He remained oedematous and dyspnoeic with signs of a left pleural effusion, subsequently confirmed on chest X-ray. The intravenous diuretics were increased and metolazone was added. Over the ensuing 6 days, the patient’s weight decreased and he appeared to be making a modest response to the antifailure treatment, although he had become anorexic. Over the next few days the patient developed a low-grade neutrophilia (WCC 12.1310 9 / l) but was afebrile. He was not toxic and there were no localising signs. Blood cultures were taken which were subsequently sterile. He had an indwelling urinary catheter in situ and a urinary tract infection was suspected and trimethoprim commenced. A repeat chest X-ray revealed a globular heart suggestive of a pericardial effusion. A transthoracic echocardiogram confirmed an effusion with no signs of tamponade and impaired left ventricular function. In view of the continued poor condition of the patient, pericardiocentesis under local anaesthesia with fluoroscopy guidance was arranged. A transudate had been expected; however, 1.5 l of thick pus was aspirated and a drain was left in situ which yielded a further 300 ml. The pus grew S. aureus. Intravenous cefuroxime had been initially commenced following microbiology advice, but this was changed to flucloxacillin following the culture results. An ultrasound-
0953-6205 / 01 / $ – see front matter 2001 Elsevier Science B.V. All rights reserved. PII: S0953-6205( 01 )00130-3
378
P.R. James / European Journal of Internal Medicine 12 (2001) 377 – 379
guided left pleural aspirate obtained 300 ml of strawcoloured fluid. Despite these measures the patient continued to deteriorate and 6 days post-pericardiocentesis he became febrile (388C) and tachycardic. S. aureus was isolated in the urine. The pericardial drain remained in situ but was no longer draining. Incomplete drainage was suspected secondary to loculation and the patient was reviewed by the cardiothoracic team with a view to surgical drainage. He was felt to be unfit for the procedure and subsequently died. At no time was there evidence of constrictive pericarditis. A post-mortem examination confirmed Staphylococcal empyema and 150 ml of pus remained within the pericardial cavity. The visceral pericardium was markedly thickened by fibrosis and inflammatory reaction. The left ventricle was enlarged and hypertrophied with calcific coronary disease and a calcified aortic valve. There was no evidence of infection involving the heart valves or lungs, and a loculated left pleural effusion was not infected. There was no evidence of sepsis elsewhere in the body, particularly in the urinary tract.
3. Discussion The incidence of purulent pericarditis or pericardial empyema has declined since the era of broad-spectrum antibiotics [1], but it remains an important differential diagnosis since, untreated, the combination of tamponade and sepsis results in a mortality rate approaching 100% [2]. It can be a difficult diagnosis to make clinically and a high index of suspicion is required. Ultimately, the diagnosis rests on the aspiration of the pericardium, and it is not uncommon for the diagnosis to be made for the first time at post-mortem examination. Usually pericardial empyema occurs in association with sepsis elsewhere in the body, most commonly pneumonia (especially pneumococcal), although it has complicated oral cavity sepsis, osteomyelitis, genital tract infection following childbirth and infection associated with colonic carcinoma [3,4]. It is uncommon for a pericardial empyema to develop in isolation, as in this case [5]. A wide variety of bacteria and fungi have been isolated as causative agents although Streptococci and Staphylococci are most commonly isolated [6]. Pericardial empyema generally presents as an acute febrile illness, and patients invariably have a leucocytosis and often a tachycardia. However, localising signs are frequently absent. Some present with pericardial chest pain, but the classical ECG changes of pericarditis are uncommon [7] although ST elevation, T-wave inversion and atrial fibrillation have all been reported [3,8]. A large purulent collection may result in low amplitude QRS complexes [3]. Interestingly, the immediate resolution of ST elevation has been described following pericardiocentesis [9]. Patients with pericardial empyema need close observation since they are at high risk of developing cardiac tamponade (79% in one study) [3].
In addition, patients may go on to develop acute, and at times severe, constrictive pericarditis which may require emergency pericardectomy [3]. This case report is unusual in that the patient did not mount a pyrexia until after the evacuation of the majority of the purulent collection. The patient was not taking steroids but was uraemic. It is interesting to note that the patient did become febrile following drainage, and it is possible that the prior containment of pus within the pericardial sac contributed to the lack of fever. Blood cultures taken 4 days prior to the diagnosis were sterile, but S. aureus was subsequently isolated from a catheter specimen of urine following pericardiocentesis. There was no evidence of infection in any part of the urinary tract at post-mortem and asymptomatic bacteruria is a frequent concomitant of S. aureus bacteraemia [10]. It is likely that a bacteraemia followed the pericardiocentesis procedure, and during this time the patient did become febrile and tachycardic. The treatment of choice for pericardial empyema is intravenous antibiotics and drainage. There is evidence that management affects outcome: medical treatment alone will decrease the mortality rate to between 66 and 82%, but when coupled with pericardiocentesis, as in this case, the rate falls to 36% [7]. In some cases pericardial aspiration may be sufficient but surgical evacuation, with or without pericardectomy, is superior. Thick, purulent collections with extensive adhesions and areas of loculated collection are more responsive to the surgical approach, and with antibiotic therapy the mortality rate is in the order of 20% or less [7]. Clot evacuation and lysis of loculi can be achieved at operation with the installation of intrapericardial streptokinase, first described in the 1950s [11]. It is possible that the delay in seeking a surgical opinion, in this case, contributed to the death. When a surgeon was consulted, the patient’s condition was too poor for intervention. This case highlights the need for early surgical involvement.
Acknowledgements I am grateful to Dr C. Davidson, Consultant Cardiologist, Royal Sussex County Hospital, for his comments on the manuscript.
References [1] Klacsmann PG, Bulkley BH, Hutchins GM. The changed spectrum of purulent pericarditis. Am J Med 1977;63:666–73. [2] Mann-Segal DDM, Shanahan EA, Jones B, Ramasamy D. Purulent pericarditis: rediscovery of an old remedy. J Thorac Cardiovasc Surg 1996;111:487–8. [3] Sagrista-Sauleda J, Barrabes JA, Permanyer-Miralda G, Soler-Soler J. Purulent pericarditis: review of a 20-year experience in a general hospital. J Am Coll Cardiol 1993;22:1661–5. [4] Snyder RW, Braun TI. Purulent pericarditis with tamponade in a
P.R. James / European Journal of Internal Medicine 12 (2001) 377 – 379
[5] [6] [7]
[8]
postpartum patient due to group F Streptococcus. Chest 1999;115:1746–7. Boyle JD, Pearce ML, Guze LB. Purulent pericarditis: review of the literature and report of 11 cases. Medicine 1961;40:119–44. Brook I, Frazier EH. Microbiology of acute purulent pericarditis. Arch Intern Med 1996;156:1857–60. Majid AA, Omar A. Diagnosis and management of purulent pericarditis. Experience with pericardectomy. J Thorac Cardiovasc Surg 1991;102:413–7. Hall IP. Purulent pericarditis. Post Grad Med J 1989;65:444–8.
379
[9] Karim MA, Bach RG, Dressler F, Caracciolo E, Donohue TJ, Kern MJ. Purulent pericarditis caused by group B streptococcus with pericardial tamponade. Am Heart J 1993;126:727–30. [10] Lee BK, Crossley K, Gerding DN. The association between Staphylococcus aureus bacteremia and bacteruria. Am J Med 1978;65:303–6. [11] Wright LT, Smith DH, Rothman M, Metzger WI, Quash ET. Use of streptokinase-dornase in certain surgical conditions. J Int Coll Surg 1951;15:286–98.
Brief report
Isolated pericardial empyema secondary to Staphylococcus aureus P. Rachael James* Cardiac Department, Royal Sussex County Hospital, Eastern Road, Brighton BN2 5 BE, UK Received 25 April 2000; received in revised form 18 January 2001; accepted 30 January 2001
Abstract Pericardial empyema, or purulent pericarditis, is a condition uncommonly encountered in routine medical practice but one which is rapidly fatal if left untreated. Early diagnosis is paramount if the patient is to survive. This case report highlights the covert nature of presentation which may occur, hindering early diagnosis, and reviews the current literature. 2001 Elsevier Science B.V. All rights reserved. Keywords: Pericardial effusion; Pericardiocentesis; Staphylococcus aureus
1. Introduction A 77-year-old man presented with cardiac failure but failed to respond to conventional anti-failure treatment. He developed a neutrophilia, but there was no pyrexia or localising signs to suggest a septic focus. When a pericardial effusion subsequently developed, pericardiocentesis was undertaken because of the lack of response to antifailure treatment. Quite unexpectedly, however, drainage yielded thick pus which grew Staphylococcus aureus. Despite aggressive antibiotic therapy, the patient died. A post-mortem examination confirmed the sepsis was isolated to the pericardium.
2. Case report A 77-year-old man with longstanding cardiac failure was admitted with a 4-week history of worsening dyspnoea. He had been taking perindopril 8 mg, digoxin 250 mg and frusemide 40 mg daily. Examination confirmed biventricular failure and he was commenced on intravenous frusemide and glyceryl trinitrate along with *Tel.: 144-1273-696-955; fax: 144-1273-684-554. E-mail address: [email protected] (P.R. James).
oral spironolactone. After 5 days of treatment, the patient had not responded. He remained oedematous and dyspnoeic with signs of a left pleural effusion, subsequently confirmed on chest X-ray. The intravenous diuretics were increased and metolazone was added. Over the ensuing 6 days, the patient’s weight decreased and he appeared to be making a modest response to the antifailure treatment, although he had become anorexic. Over the next few days the patient developed a low-grade neutrophilia (WCC 12.1310 9 / l) but was afebrile. He was not toxic and there were no localising signs. Blood cultures were taken which were subsequently sterile. He had an indwelling urinary catheter in situ and a urinary tract infection was suspected and trimethoprim commenced. A repeat chest X-ray revealed a globular heart suggestive of a pericardial effusion. A transthoracic echocardiogram confirmed an effusion with no signs of tamponade and impaired left ventricular function. In view of the continued poor condition of the patient, pericardiocentesis under local anaesthesia with fluoroscopy guidance was arranged. A transudate had been expected; however, 1.5 l of thick pus was aspirated and a drain was left in situ which yielded a further 300 ml. The pus grew S. aureus. Intravenous cefuroxime had been initially commenced following microbiology advice, but this was changed to flucloxacillin following the culture results. An ultrasound-
0953-6205 / 01 / $ – see front matter 2001 Elsevier Science B.V. All rights reserved. PII: S0953-6205( 01 )00130-3
378
P.R. James / European Journal of Internal Medicine 12 (2001) 377 – 379
guided left pleural aspirate obtained 300 ml of strawcoloured fluid. Despite these measures the patient continued to deteriorate and 6 days post-pericardiocentesis he became febrile (388C) and tachycardic. S. aureus was isolated in the urine. The pericardial drain remained in situ but was no longer draining. Incomplete drainage was suspected secondary to loculation and the patient was reviewed by the cardiothoracic team with a view to surgical drainage. He was felt to be unfit for the procedure and subsequently died. At no time was there evidence of constrictive pericarditis. A post-mortem examination confirmed Staphylococcal empyema and 150 ml of pus remained within the pericardial cavity. The visceral pericardium was markedly thickened by fibrosis and inflammatory reaction. The left ventricle was enlarged and hypertrophied with calcific coronary disease and a calcified aortic valve. There was no evidence of infection involving the heart valves or lungs, and a loculated left pleural effusion was not infected. There was no evidence of sepsis elsewhere in the body, particularly in the urinary tract.
3. Discussion The incidence of purulent pericarditis or pericardial empyema has declined since the era of broad-spectrum antibiotics [1], but it remains an important differential diagnosis since, untreated, the combination of tamponade and sepsis results in a mortality rate approaching 100% [2]. It can be a difficult diagnosis to make clinically and a high index of suspicion is required. Ultimately, the diagnosis rests on the aspiration of the pericardium, and it is not uncommon for the diagnosis to be made for the first time at post-mortem examination. Usually pericardial empyema occurs in association with sepsis elsewhere in the body, most commonly pneumonia (especially pneumococcal), although it has complicated oral cavity sepsis, osteomyelitis, genital tract infection following childbirth and infection associated with colonic carcinoma [3,4]. It is uncommon for a pericardial empyema to develop in isolation, as in this case [5]. A wide variety of bacteria and fungi have been isolated as causative agents although Streptococci and Staphylococci are most commonly isolated [6]. Pericardial empyema generally presents as an acute febrile illness, and patients invariably have a leucocytosis and often a tachycardia. However, localising signs are frequently absent. Some present with pericardial chest pain, but the classical ECG changes of pericarditis are uncommon [7] although ST elevation, T-wave inversion and atrial fibrillation have all been reported [3,8]. A large purulent collection may result in low amplitude QRS complexes [3]. Interestingly, the immediate resolution of ST elevation has been described following pericardiocentesis [9]. Patients with pericardial empyema need close observation since they are at high risk of developing cardiac tamponade (79% in one study) [3].
In addition, patients may go on to develop acute, and at times severe, constrictive pericarditis which may require emergency pericardectomy [3]. This case report is unusual in that the patient did not mount a pyrexia until after the evacuation of the majority of the purulent collection. The patient was not taking steroids but was uraemic. It is interesting to note that the patient did become febrile following drainage, and it is possible that the prior containment of pus within the pericardial sac contributed to the lack of fever. Blood cultures taken 4 days prior to the diagnosis were sterile, but S. aureus was subsequently isolated from a catheter specimen of urine following pericardiocentesis. There was no evidence of infection in any part of the urinary tract at post-mortem and asymptomatic bacteruria is a frequent concomitant of S. aureus bacteraemia [10]. It is likely that a bacteraemia followed the pericardiocentesis procedure, and during this time the patient did become febrile and tachycardic. The treatment of choice for pericardial empyema is intravenous antibiotics and drainage. There is evidence that management affects outcome: medical treatment alone will decrease the mortality rate to between 66 and 82%, but when coupled with pericardiocentesis, as in this case, the rate falls to 36% [7]. In some cases pericardial aspiration may be sufficient but surgical evacuation, with or without pericardectomy, is superior. Thick, purulent collections with extensive adhesions and areas of loculated collection are more responsive to the surgical approach, and with antibiotic therapy the mortality rate is in the order of 20% or less [7]. Clot evacuation and lysis of loculi can be achieved at operation with the installation of intrapericardial streptokinase, first described in the 1950s [11]. It is possible that the delay in seeking a surgical opinion, in this case, contributed to the death. When a surgeon was consulted, the patient’s condition was too poor for intervention. This case highlights the need for early surgical involvement.
Acknowledgements I am grateful to Dr C. Davidson, Consultant Cardiologist, Royal Sussex County Hospital, for his comments on the manuscript.
References [1] Klacsmann PG, Bulkley BH, Hutchins GM. The changed spectrum of purulent pericarditis. Am J Med 1977;63:666–73. [2] Mann-Segal DDM, Shanahan EA, Jones B, Ramasamy D. Purulent pericarditis: rediscovery of an old remedy. J Thorac Cardiovasc Surg 1996;111:487–8. [3] Sagrista-Sauleda J, Barrabes JA, Permanyer-Miralda G, Soler-Soler J. Purulent pericarditis: review of a 20-year experience in a general hospital. J Am Coll Cardiol 1993;22:1661–5. [4] Snyder RW, Braun TI. Purulent pericarditis with tamponade in a
P.R. James / European Journal of Internal Medicine 12 (2001) 377 – 379
[5] [6] [7]
[8]
postpartum patient due to group F Streptococcus. Chest 1999;115:1746–7. Boyle JD, Pearce ML, Guze LB. Purulent pericarditis: review of the literature and report of 11 cases. Medicine 1961;40:119–44. Brook I, Frazier EH. Microbiology of acute purulent pericarditis. Arch Intern Med 1996;156:1857–60. Majid AA, Omar A. Diagnosis and management of purulent pericarditis. Experience with pericardectomy. J Thorac Cardiovasc Surg 1991;102:413–7. Hall IP. Purulent pericarditis. Post Grad Med J 1989;65:444–8.
379
[9] Karim MA, Bach RG, Dressler F, Caracciolo E, Donohue TJ, Kern MJ. Purulent pericarditis caused by group B streptococcus with pericardial tamponade. Am Heart J 1993;126:727–30. [10] Lee BK, Crossley K, Gerding DN. The association between Staphylococcus aureus bacteremia and bacteruria. Am J Med 1978;65:303–6. [11] Wright LT, Smith DH, Rothman M, Metzger WI, Quash ET. Use of streptokinase-dornase in certain surgical conditions. J Int Coll Surg 1951;15:286–98.