- Email: [email protected]
Diagnosis and management of pericardial abscess in trauma patients
Diagnosis and Management of Pericardial Abscess in Trauma Patients Thomas T. Sato, MD, Randolph L. Geary, MD, David G. Ashbaugh, MD, Gregory J. Jurkovich, MD, Seattle,Washington
Pericardial infection is an unconunon clinical entity after traumatic injury. Although invasive intervention is rarely necessary for mild pericardial inflammation, pericardial abscess can be life-threatening. The charts of 27 patients with pericarditis requiring management in the intensive care unit and/or invasive intervention at Harborview Medical Center during a lO-year period were reviewed. Six cases of trauma-related pericarditis were identified, including three cases of perieardial abscess following torso trauma without initial cardiac or pericardial injury. Pericardial abscess following trauma was associated with the sepsis syndrome and multiple system organ failure (MSOF) in all patients. Computed tomography and pericardiocentesis were useful diagnostic adjuncts. All patients required thoracotomy for pericardial drainage and pericardiectomy. Successful surgical management of pericardial abscess contributed to the resolution of sepsis, multiple end-organ dysfunction and, ultimately, patient survival in all cases. We conclude that perieardial abscess, although rare, should be considered a potential occult site of sepsis capable of driving MSOF in trauma patients. Expedient diagnosis and surgical drainage are essential for successful patient outcome.
rauma continues to be the leading cause of death T among Americans between 1 and 44 years of age [I]. Trauma victims who survive the initial hours after injury are vulnerable to a third mortality peak in the trimodal death distribution, specifically, late deaths occurring days or weeks after injury [2]. Post-traumatic late deaths are frequently attributable to infection, with subsequent development and progression of the sepsis syndrome and, ultimately, multiple system organ failure (MSOF). Infection is considered an etiologic factor in at least 50% of patients who develop MSOF, and approximately 30% of patients who die of MSOF are found to have untreated infections [3]. Therefore, the identification and treatment of occult septic loci in the trauma patient with progressive sepsis syndrome or MSOF remains an essential surgical principle. Acute pericarditis is believed to be a common but often subclinical entity [4]. In distinct contrast, purulent pericarditis or pericardial abscess is an infrequently encountered disease, with an estimated incidence of 0.26% derived from autopsy reports [5]. Pericardial abscess is typically observed as a secondary complication of a coexisting illness or iatrogenic procedure, with pericardial involvement reflecting extension of hematologic, pulmonary, cardiac, or subdiaphragmatic infectious foci [4-7]. The difficulty encountered in the clinical recognition of this disease is demonstrated by the dismal 18% antemortem diagnosis rate [5] and the rapidly fatal course if left untreated. Thus, successful management and outcome of patients with pericardial abscess require expedient diagnosis and appropriate surgical intervention. Recently, the first reported case of purulent pericarditis following blunt trauma was reported [8]. Because of the diagnostic difficulty associated with this uncommon disease and the failure to consider the pericardial space as a potential site of infection, pericardial abscess may occur as an unrecognized but salvageable complication in the trauma patient. Herein, we review and describe our institution's experience with pericardial abscess following trauma during the last decade. We report that pericardial abscess, although rare, should be considered as a potential occult source of sepsis capable of producing endorgan dysfunction and progressive MSOF in trauma patients.
PATIENTS AND METHODS We retrospectively reviewed the records of 54 patients Fromthe DepartmentOfSurgery,HarborviewMedicalCenter,Universityof WashingtonSchoolof Medicine,Seattle,Washington. with the discharge diagnosis of acute or infective pericarRequestsfor reprintsshouldbe addressedto GregoryJ. Jurkovich. ditis (ICD-9-CM codes 420.90 and 420.99) hospitalized MD, DepartmentofSurgery,ZA-16,HarborviewMedicalCenter,325 between March 1982 and March 1992 at Harborview Ninth Avenue,Seattle,Washington98104. Presentedat the 79th AnnualMeetingof the North PacificSurgi- Medical Center, the level I regional trauma center for the cal Association,Tacoma,Washington,November13-14, 1992. Pacific Northwest. Patients with post-pericardotomy THE AMERICANJOURNAL OF SURGERY VOLUME165 MAY 1993 637
SATO ET AL
TABLE I
Clinical Symptoms and Signs No. of Patients
(%) WBC count > 105 cells/mm 3 Dyspnea Chest pain Fever Tachycardia > 120/rain SBP <90 mm Hg CVP > 10 cm H20 Decreased heart sounds Friction rub Pulsus paradoxus Cough
16 (59) 14 (52) 12 (44) 10 (37) 9 (33) 7 (26) 7 (26) 6 (22) 6 (22) 6 (22) 3 (11)
WBC = white blood cell; SBP = systolicblood pressure; CVP = centralvenous pressure.
TABLE II
Etiology of Pericarditis (n = 27 ) No. of Patients
(%) Autoimmune disease Idiopathic Malignancy Myocardial infarction Tuberculosis/pneumonia Trauma Other
2 9 2 2 3 6 3
(7) (35) (7) (7) (11 ) (22) (11)
syndrome or mediastinitis resulting from descending head/neck infections, cardiothoracic surgical procedures, or extension of infective endocardial/valvular lesions were excluded from this analysis. Patients with pericardial abscess fulfilled at least one of the following criteria: (1) pericarditis with purulent pericardial fluid; (2) bacteria by stain of pericardial fluid; or (3) bacteria identified by culture of pericardial fluid or tissue. The records were reviewed for patient demographics, presenting clinical symptoms and signs, diagnostic procedures performed, hospital course, and pathologic operative findings. Nonparametric statistical analysis was performed using the Mann-Whitney U test with significance set at p <0.05. RESULTS In the 10-year period from March 1982 to March !992, 27 patients with either acute or infective pericarditie requiring admission to the intensive care unit and/or invasive intervention at Harborview Medical Center were identified. The average patient age was 38 years (range: 20 to 79 years), with 17 men and 10 women. Clinical findings in these patients are delineated in Table L Table II summarizes the etiologies of pericarditis in all patients. Three patients in this series had nontraumatic, infective pericarditis due to either tuberculosis or bacterial pneumonia. Six trauma patients (22%) were diagnosed with pericarditis without initial cardiac or pericardial 638
THE AMERICAN JOURNAL OF SURGERY
injury. Three of the trauma patients developed pericardial abscesses in association with the characteristic metabolic and hemodynamic abnormalities of the sepsis syndrome [9-12] and, ultimately, multiple organ failure. Mechanisms of injury in this group included a pelvic/lower extremity crush injury, blunt motor vehicle accident trauma, and penetrating gunshot wounds to the right chest and abdomen. Two-dimensional echocardiographywas performed in 25 patients (93%). Abnormal echocardiographic findings supporting the diagnosis of pericarditis or pericardial abscess included the detection of pericardial effusion in 17 patients. Due to the presence of subcutaneous emphysema or chest wall edema, echocardiographic images were uninformative in two patients with nontraumatic pericarditis and one trauma patient with pericardial abscess. However, computed tomographic (CT) scanning in two of these patients demonstrated massive pericardial effusions. Among the 17 patients with pericardial effusions, 10 were found to have a small volume of effusion (less than 100 mL), 1 had a moderate volume (100 mL to 300 mL), and 6 had large volumes (more than 300 mL). At least three patients with small effusions and three patients with large effusions fulfilled the clinical criteria for cardiac tamponade using Beck's triad (decreased arterial pressure, increased central venous pressure, muffled heart sounds) [13]. Of note, all trauma patients with pericardial abscess demonstrated clinical cardiac tamponade. Admission characteristics common to the three male trauma patients (mean age: 30 years) who developed pericardial abscesses after injury include Revised Trauma Scores [14] of less than 9, endotracheal intubation either in the field or the emergency trauma center, and intravenous fluid infusion of greater than 4 L of crystalloid solution during the first hour of resuscitation. Two patients were taken emergently to the operating room for ongoing hemorrhage. All patients in this group underwent operation, including exploratory laparotomy, for injuries unrelated to the heart or pericardium within 72 hours after admission. Additionally, two of the patients underwent open reduction and internal fixation of multiple orthopedic injuries of the pelvis and lower extremities within 3 to 8 days after admission. A combined total of 35 surgical procedures were performed in these 3 critically ill patients. Rapid development of respiratory failure and the adult respiratory distress syndrome occurred in all posttraumatic patients with pericardial abscess. Each patient manifested progression of the sepsis syndrome and at least six criteria for either end-organ dysfunction or advanced MSOF [3,15] preceding or coexistent with the diagnosis of pericardial abscess. In addition to pulmonary and cardiovascular system failure, all patients met the criteria for hepatic, renal, intestinal, and central nervous system dysfunction; two patients also manifested fulminant hepatic and renal failure. The diagnosis of pericardial abscess in patients after trauma was made 51 4- 18 days (mean 4- SE) after admission, compared with 4 4- 2 days after admission for
VOLUME 165
MAY 1993
PERICARDIAL ABSCESS
patients with nontraumatic pericarditis. In comparison with the 21 nontrauma patients, the development of pericardial abscess following trauma was associated with statistically and clinically significant prolongation of the stay in the intensive care unit (ICU), as well as in the overall length of hospitalization (Table HI). In addition to cardiac tamponade, clinical manifestations of pericardial abscess common to these three patients included fever greater than 38.5~ absolute leukocytosis greater than 105 cells/mm3, abnormal electrocardiographic findings (sinus tachycardia, diffuse ST-wave elevation, and persistently low QRS voltage), and an abnormal cardiac silhouette on the chest roentgenograph. CT scanning revealed pericardial effusions in all three patients without other obvious sources of infectious intra-abdominal lesions. Pericardiocentesis was performed in all patients, either in the ICU or in the operating room. A definitive microbiologic diagnosis was made preoperatively in two patients on the basis of staining and culturing of pericardial fluid. These cultures identified Staphylococcus epidermidis in one patient and Pseudomonas aeruginosa with enterococci in the other patient; concomitantly, these patients had positive blood cultures from both central and peripheral intravenous sites. Upon diagnosis, each patient received broad-spectrum antibiotics for a minimum of 14 days (range: 14 to 28 days). The third patient was receiving broad-spectrum antibiotics at the time of diagnosis, and, despite purulent pericardial fluid at operation, no organisms were recovered by stain or culture. Operations for pericardial abscess following trauma were performed within 24 hours of the definitive diagnosis. Left anterior or anterolateral thoracotomy, drbridement, and partial pericardiectomy with preservation of the left phrenic nerve was uniformly performed. Left pleural chest tubes were placed in each patient, and additional closed suction drains were placed in one patient to drain the posterior pericardial space. Purulent pericardial effusions (greater than 90% polymorphonuclear cells) ranged in volume from 800 mL to 1,400 mL and were associated with fibrinous exudate extending from the epicardiurn to the pericardium. The pericardium was noted to be grossly thickened in all patients, with histologic evidence of acute and subacute inflammatory cell infiltration. There were no operative deaths in thisgroup and no complications related to the pericardial drainage procedures. In each case, operative drainage of the pericardial abscess led to abatement of clinical sepsis and gradual resolution of MSOF. Despite stormy postoperative courses, all patients survived and were subsequently discharged from the hospital without signs of cardiac compromise. COMMENTS Pericardial inflammatory conditions represent a diverse spectrum of disease, extending from acute, subclinical pericarditis to fulminant, life-threatening pericardial abscess. The actual incidence of pericarditis remains unknown, because many self-limited subclinical cases remain undetected [4]. Of note, the severity of the pericar-
TABLE III
Duration of ICU Stay a n d O v e r a l l Hospitalization (days [mean _+ S E M ] ) Condition Acute nontraumatic pericarditis Post-traumatic pericardial abscess
ICU Stay 2 _+ 0.4 (n = 15)* 129 +- 40 (n = 3)t
Hospitalization 8 -+ 2 (n = 21) 136 -+ 38 (n = 3)t
ICU = intensive care unit. *Six patients were monitored in a cardiac telemetry unit. tp <0.001 by Mann-Whitney U test.
dial inflammation does not necessarily improve the diagnostic accuracy; consequently, the diagnosis of pericardial abscess presupposes a high index of clinical suspicion. Previous investigations have emphasized the difficulty in achieving the clinical diagnosis of purulent pericarditis, with antemortem diagnostic rates of only 18% to 69% [5,7]. Recent anecdotal reports of suppurative pericardial infections suggest that more cases are occurring in immunologically compromised patients [16-18]. Groups at high risk for pericardial abscess indude postoperative cardiothoracic surgery patients, patients with impaired host defenses such as individuals receiving immunosuppressive agents or who have malignancies, and patients with severe debilitating disease [19]. Trauma patients with multiple injuries should also be considered at high risk for infectious complications such as pericardial abscess, since these patients manifest significant, global immunologic disability and alteration of the metabolic response to injury. Our experience with acute and infective pericarditis at Harborview Medical Center suggests that the "classic" findings of fever, substernal chest pain, and a friction rub occur in less than half of the patients with pericardial inflammation. Other reported experiences have also observed a lack of consistently present diagnostic symptoms and signs [4]. With respect to patients with pericardial abscess, however, some distinguishing diagnostic features emerge. In a review of the 68 cases of purulent pericarditis reported in the literature from 1945 to 1989, Hall [6] noted that symptoms and signs common to these patients included fever (88%), dyspnea (61%), chest pain (57%), pulsus paradoxus (65%), hepatomegaly (59%), and elevated central venous pressure (58%). Additionally, leukocytosis, tachycardia, and pericardial effusions noted by echocardiography occurred with 100% frequency. Similarly, all of our trauma patients with pericardial abscess had fever, leukocytosis, and tachycardia. Our patients also uniformly had abnormalities on their electrocardiograms and chest roentgenograms, as well as evidence of cardiac tamponade. We believe that this clinical scenario necessitates urgent diagnostic and therapeutic manuevers to either definitively rule out or treat pericardial abscess. Recognition and diagnosis of purulent pericarditis by both chest radiography [20] and echocardiography [21]
THE AMERICAN JOURNAL OF SURGERY
VOLUME 165
MAY 1993
639
SATOET AL
Figure 1. Computed tomographic scan of the chest shows large effusion that was subsequently demonstrated to be a pericardial abscess. Note that the soft tissue edema of the chest wall precluded echocardiography.
due to intrapericardial gas-forming organisms has been previously reported. Echocardiography has been considered the most sensitive technique for detecting pericardial effusion [4,22]. CT has also been demonstrated to be a sensitive technique for imaging pericardial thickening and effusion [23]. We found echocardiography useful and diagnostic of pericardial effusion in two trauma patients with pericardial abscess. Although echocardiography was attempted in the third patient, his impressive chest wall edema prevented adequate imaging of the heart and pericardium. CT was accurate in diagnosing pericardial effusion in all of our trauma patients. Furthermore, CT helped to exclude the abdomen as a potential source of infection. We believe that there is a small number of patients with clinically suspected pericardial abscess in whom echocardiography does not provide technically adequate data; we recommend that these patients undergo CT examination (Figure 1). The etiology of infecting organisms causing purulent pericarditis has evolved over the past century. Prior to 1944, Streptococcus pneumoniae was the predominant bacterial isolate; since the clinical introduction of penicillin in 1944, the most common infecting organism has been Staphylococcus aureus [5-7]. With technologic advances including ventilator support, broad-spectrum antibiotics, aggressive cancer chemotherapy, and transplant immunosuppression, more unusual, opportunistic infections are becoming clinically apparent. The causative organisms in our small series suggest that these nosocomial infections occurred in trauma patients with an altered immunologic status. The increase of gram-negative [6] and fungal organisms [19,24] causing purulent pericarditis reflects a generalized trend that has been observed in contemporary medicine [25]. Pericardial abscess in our study was associated with clinical sepsis and progressive multiple organ failure. Pericardial effusion, presumably due to uremia, was noted in two of our patients with renal failure prior to the development of sepsis and cardiac tamponade. The pre640
cise moment at which these pericardial effusions became infected, and the relationship between pericardial infection and the onset of MSOF, is unknown. The dramatic clinical improvement and resolution of multiple organ failure we observed after definitive treatment suggests that pericardial abscess contributed to the maintenance of end-organ dysfunction in our patients. We speculate that, in the constellation of MSOF following severe mechanical or thermal injury, the immune system also fails, leading to an increased incidence of infection. Subsequently, the addition of infectious foci in this scenario increasingly contributes to uncontrollable, overwhelming inflammation. Loss of inflammatory regulation fueled by sepsis-induced mediators is thought to play an important role in progressive end-organ injury and MSOF [26]. Prominent factors contributing to acute death in purulent pericarditis include sepsis and cardiac tamponade. As such, initial measures such as intravascular volume expansion with intravenous fluids alone or in combination with therapeutic pericardocentesis can be life-saving [4]. Untreated, pericardial abscess has a mortality rate of 100% [27]. With the use of antibiotics alone, the mortality rate is between 66% and 82% [28]. Recent series combining surgical treatment with medical therapy suggest the mortality rate should be less than 20% [29,30]. In the absence of MSOF, successful percutaneous catheter drainage of purulent pericarditis has been reported [31,32]. However, we do not advocate this approach in septic, critically ill trauma patients with advancing multiple organ failure. We and others [29,30,33] believe that, once the initial diagnosis of pericardial abscess has been made, operative drainage is mandatory. We have uniformly used either a left anterior or anterolateral thoracotomy with partial pericardiectomy for drainage of pericardial pus. This approach offers immediate resolution of tamponade and rapid elimination of the septic foci. Additionally, operative drainage combined with pericardiectomy via thoracotomy allows for the removal of fibrin clots and loculi within the pericardial space, reducing the
THE AMERICANJOURNALOFSURGERY VOLUME165 MAY 1993
PERICARDIAL ABSCESS
likelihood of pus re-accumulation or late pericardial constriction [29,30]. Subxiphoid tube drainage has also been described as an effective, less invasive treatment for pericardial abscess [34-36]; this approach is somewhat limited by the inability to perform extensive pericardial drbridement and pericardiectomy. In conclusion, we report three cases of pericardial abscess following noncardiac trauma associated with sepsis and MSOF. The diagnostic difficulty encountered with this disease is amplified in trauma patients undergoing multiple operative procedures for other injuries. Findings such as evidence for infection (fever, leukocytosis, tachycardia) associated with an abnormal electrocardiogram, a cardiac silhouette on the chest radiograph, pericardial effusion, or cardiac tamponade demand further clinical investigation. Pericardiocentesis has both diagnostic and therapeutic roles, and, after the diagnosis of pericardial abscess, we recommend appropriate antimicrobial therapy combined with operative drainage via thoracotomy, pericardial drbridement, and pericardiectomv. REFERENCES 1. Baker CC, Oppenheimer L, Lewis FR, Trunkey DD. Epidemiology of trauma deaths. Am J Surg 1980; 140: 144-50. 2. Trunkey DD, BlaisdeU FW. Epidemiology of trauma. In: Wilmore DW, Brennan MF, Harken AH, Holcroft JW, Meakins JL, editors. Care of the surgical patient. New York: Scientific American, Inc., 1992: Chapter 6: 1-7. 3. Deitch EA. Multiple organ failure. Ann Surg 1992; 216:117-34. 4. Sternbach GL. Pericarditis. Ann Emerg Med 1988; 17: 214-20. 5. Klaesmann PG, Bulkley BH, Hutchins GM. The changed spectrum of purulent pericarditis. Am J Med 1977; 63: 666-73. 6. Hall IP. Purulent pericarditis. Postgrad Med J 1989; 65: 444-8. 7. Rubin RH, Moellering RC Jr. Clinical, microbiologic,and therapeutic aspects of purulent pericarditis. Am J Med 1975; 59: 68-78. 8. Van Vooren JP, Thys JP, Vanderhoeft P. Purulent pericarditis resulting from blunt chest trauma. J Thorac Cardiovasc Surg 1990; 100: 932-4. 9. Douglas RG, Shaw JHF. Metabolic response to sepsis and trauma. Br J Surg 1989; 76: 115-22. 10. Trunkey DD. The treatment of sepsis and other complications in the trauma patient. Clin Ther 1990; 12 (Suppl B): 21-33. 11. Mileski WJ. Sepsis. Surg Clin North Am 1991; 71: 749-64. 12. Hotchkiss RS, Karl IE. Reevaluation of the role of cellular hypoxia and bioenergetic failure in sepsis. JAMA 1992; 267: 1503-10. 13. Beck CS. Two cardiac compression triads. JAMA 1935; 104: 714-6. 14. Champion HR, Copes WS, Sacco W J, Flanagan ME. Injury severity scoring. In: Moore EE, editor. Early care of the injured patient. Philadelphia: BC Decker, Inc., 1990: 12-26. 15. Henao FR, Daes JE, Dennis RJ. Risk factors for muttiorgan
failure: a case-control study. J Trauma 1991; 31: 74-80. 16. Demey HE, Eycken M, Vandermast M, Bossaert LL. Purulent pericarditis due to methicillin-resistant Staphylococcus aureus. Acta Cardiol 1991; 46: 485-91. 17. Kumar VV, Herzog C. Purulent pericarditis caused by group G streptococcus. JAMA 1990; 264: 34-5. 18. Law EJ, Orlet HK, Still JM, Catalano PW, Mucha E. Purulent pericarditis in an adult burn patient treated with survival. Burns 1991; 17: 254-6. 19. Kraus WE, Valenstein PN, Corey GR. Purulent pericarditis caused by Candidtz'report of three cases and identification of highrisk populations as an aid to early diagnosis. Rev Infect Dis 1988; 10: 34-41. 20. Chow WH, Chow LTC, Suen HC. Purulent pericarditis: recognition from the chest radiograph. Int J Cardiol 1991; 30: 229-30. 21. Ku CS, Hsiung MC, Hsu TL, Ding YA, Shieh SH. Spontaneous contrast in the pericardial sac caused by gas-forming organisms. J Am Soc Echocardiogr 1991; 4: 67-8. 22. Horowitz MS, Schultz CS, Stinson EB, Harrison DC, Popp RL. Sensitivity and specificity of echocardiographic diagnosis of pericardial effusion. Circulation 1974; 50: 239-47. 23. Isner JM, Carter BL, Bankoff MS, Konstam MA, Salem DN. Computerized tomography in the diagnosis of pericardial heart disease Ann Intern Med 1982; 97: 473-9. 24. FifeTD, Finegold SM, Grennan T. Pericardial actinomyeosis: case report and review. Rev Infect Dis 1991; 13: 120-6. 25. Finland M. Changing ecology of bacterial infections as related to antibacterial therapy. J Infect Dis 1970; 122: 419-31. 26. Maier RV. Critical care and metabolism. Bulletin of the American College of Surgeons 1992; 77: 22-6. 27. Okoromora EO, Perry LW, Scott LR. Acute bacterial pericarditis in children: report of 25 cases. Am Heart J 1975; 90: 709-13. 28. Berk SL, Rice PA, Reyholds CA, Finland M. Pneumococcal pericarditis: a persistent problem in comtemporary diagnosis.Am J Med 1981; 70: 247-51. 29. Sethi GK, Nelson RM, Jenson CB. Surgical management of acute septic pericarditis. Chest 1973; 63: 732-5. 30. Majid AA, Omar A. Diagnosis and management of purulent pericarditis. J Thorac Cardiovasc Surg 1991; 102: 413-7. 31. Bouwels L, Jansen E, Janssen J, et al. Successful long-term catheter drainage in an immunocompromisedpatient with purulent pericarditis. Am J Med 1987; 83: 581-3. 32. Houghton JL, Becherer PR. Haemophilus influenzae pericarditis successfullytreated by catheter drainage. South Med J 1987; 80: 766-8. 33. Cameron EWJ. Surgical management of staphylococcal pericarditis. Thorax 1975; 30: 678-81. 34. Adebo OA, Adebonojo SA. Purulent pericarditis in children. J Thorac Cardiovasc Surg 1984; 88: 312-3. 35. Hardy CC, Raza SN, Isalska B, Barber PV. Atraumatic suppurative mediastinitis and purulent pericarditis due to Eikenella corrodens. Thorax 1988; 43: 494-5. 36. Palatanos GM, Thurer R J, Kaiser GA. Comparison of effectiveness and safety of operations on the pericardium. Chest 1988; 88: 30-3.
THE AMERICAN JOURNAL OF SURGERY VOLUME 165 MAY 1993 641
Pericardial infection is an unconunon clinical entity after traumatic injury. Although invasive intervention is rarely necessary for mild pericardial inflammation, pericardial abscess can be life-threatening. The charts of 27 patients with pericarditis requiring management in the intensive care unit and/or invasive intervention at Harborview Medical Center during a lO-year period were reviewed. Six cases of trauma-related pericarditis were identified, including three cases of perieardial abscess following torso trauma without initial cardiac or pericardial injury. Pericardial abscess following trauma was associated with the sepsis syndrome and multiple system organ failure (MSOF) in all patients. Computed tomography and pericardiocentesis were useful diagnostic adjuncts. All patients required thoracotomy for pericardial drainage and pericardiectomy. Successful surgical management of pericardial abscess contributed to the resolution of sepsis, multiple end-organ dysfunction and, ultimately, patient survival in all cases. We conclude that perieardial abscess, although rare, should be considered a potential occult site of sepsis capable of driving MSOF in trauma patients. Expedient diagnosis and surgical drainage are essential for successful patient outcome.
rauma continues to be the leading cause of death T among Americans between 1 and 44 years of age [I]. Trauma victims who survive the initial hours after injury are vulnerable to a third mortality peak in the trimodal death distribution, specifically, late deaths occurring days or weeks after injury [2]. Post-traumatic late deaths are frequently attributable to infection, with subsequent development and progression of the sepsis syndrome and, ultimately, multiple system organ failure (MSOF). Infection is considered an etiologic factor in at least 50% of patients who develop MSOF, and approximately 30% of patients who die of MSOF are found to have untreated infections [3]. Therefore, the identification and treatment of occult septic loci in the trauma patient with progressive sepsis syndrome or MSOF remains an essential surgical principle. Acute pericarditis is believed to be a common but often subclinical entity [4]. In distinct contrast, purulent pericarditis or pericardial abscess is an infrequently encountered disease, with an estimated incidence of 0.26% derived from autopsy reports [5]. Pericardial abscess is typically observed as a secondary complication of a coexisting illness or iatrogenic procedure, with pericardial involvement reflecting extension of hematologic, pulmonary, cardiac, or subdiaphragmatic infectious foci [4-7]. The difficulty encountered in the clinical recognition of this disease is demonstrated by the dismal 18% antemortem diagnosis rate [5] and the rapidly fatal course if left untreated. Thus, successful management and outcome of patients with pericardial abscess require expedient diagnosis and appropriate surgical intervention. Recently, the first reported case of purulent pericarditis following blunt trauma was reported [8]. Because of the diagnostic difficulty associated with this uncommon disease and the failure to consider the pericardial space as a potential site of infection, pericardial abscess may occur as an unrecognized but salvageable complication in the trauma patient. Herein, we review and describe our institution's experience with pericardial abscess following trauma during the last decade. We report that pericardial abscess, although rare, should be considered as a potential occult source of sepsis capable of producing endorgan dysfunction and progressive MSOF in trauma patients.
PATIENTS AND METHODS We retrospectively reviewed the records of 54 patients Fromthe DepartmentOfSurgery,HarborviewMedicalCenter,Universityof WashingtonSchoolof Medicine,Seattle,Washington. with the discharge diagnosis of acute or infective pericarRequestsfor reprintsshouldbe addressedto GregoryJ. Jurkovich. ditis (ICD-9-CM codes 420.90 and 420.99) hospitalized MD, DepartmentofSurgery,ZA-16,HarborviewMedicalCenter,325 between March 1982 and March 1992 at Harborview Ninth Avenue,Seattle,Washington98104. Presentedat the 79th AnnualMeetingof the North PacificSurgi- Medical Center, the level I regional trauma center for the cal Association,Tacoma,Washington,November13-14, 1992. Pacific Northwest. Patients with post-pericardotomy THE AMERICANJOURNAL OF SURGERY VOLUME165 MAY 1993 637
SATO ET AL
TABLE I
Clinical Symptoms and Signs No. of Patients
(%) WBC count > 105 cells/mm 3 Dyspnea Chest pain Fever Tachycardia > 120/rain SBP <90 mm Hg CVP > 10 cm H20 Decreased heart sounds Friction rub Pulsus paradoxus Cough
16 (59) 14 (52) 12 (44) 10 (37) 9 (33) 7 (26) 7 (26) 6 (22) 6 (22) 6 (22) 3 (11)
WBC = white blood cell; SBP = systolicblood pressure; CVP = centralvenous pressure.
TABLE II
Etiology of Pericarditis (n = 27 ) No. of Patients
(%) Autoimmune disease Idiopathic Malignancy Myocardial infarction Tuberculosis/pneumonia Trauma Other
2 9 2 2 3 6 3
(7) (35) (7) (7) (11 ) (22) (11)
syndrome or mediastinitis resulting from descending head/neck infections, cardiothoracic surgical procedures, or extension of infective endocardial/valvular lesions were excluded from this analysis. Patients with pericardial abscess fulfilled at least one of the following criteria: (1) pericarditis with purulent pericardial fluid; (2) bacteria by stain of pericardial fluid; or (3) bacteria identified by culture of pericardial fluid or tissue. The records were reviewed for patient demographics, presenting clinical symptoms and signs, diagnostic procedures performed, hospital course, and pathologic operative findings. Nonparametric statistical analysis was performed using the Mann-Whitney U test with significance set at p <0.05. RESULTS In the 10-year period from March 1982 to March !992, 27 patients with either acute or infective pericarditie requiring admission to the intensive care unit and/or invasive intervention at Harborview Medical Center were identified. The average patient age was 38 years (range: 20 to 79 years), with 17 men and 10 women. Clinical findings in these patients are delineated in Table L Table II summarizes the etiologies of pericarditis in all patients. Three patients in this series had nontraumatic, infective pericarditis due to either tuberculosis or bacterial pneumonia. Six trauma patients (22%) were diagnosed with pericarditis without initial cardiac or pericardial 638
THE AMERICAN JOURNAL OF SURGERY
injury. Three of the trauma patients developed pericardial abscesses in association with the characteristic metabolic and hemodynamic abnormalities of the sepsis syndrome [9-12] and, ultimately, multiple organ failure. Mechanisms of injury in this group included a pelvic/lower extremity crush injury, blunt motor vehicle accident trauma, and penetrating gunshot wounds to the right chest and abdomen. Two-dimensional echocardiographywas performed in 25 patients (93%). Abnormal echocardiographic findings supporting the diagnosis of pericarditis or pericardial abscess included the detection of pericardial effusion in 17 patients. Due to the presence of subcutaneous emphysema or chest wall edema, echocardiographic images were uninformative in two patients with nontraumatic pericarditis and one trauma patient with pericardial abscess. However, computed tomographic (CT) scanning in two of these patients demonstrated massive pericardial effusions. Among the 17 patients with pericardial effusions, 10 were found to have a small volume of effusion (less than 100 mL), 1 had a moderate volume (100 mL to 300 mL), and 6 had large volumes (more than 300 mL). At least three patients with small effusions and three patients with large effusions fulfilled the clinical criteria for cardiac tamponade using Beck's triad (decreased arterial pressure, increased central venous pressure, muffled heart sounds) [13]. Of note, all trauma patients with pericardial abscess demonstrated clinical cardiac tamponade. Admission characteristics common to the three male trauma patients (mean age: 30 years) who developed pericardial abscesses after injury include Revised Trauma Scores [14] of less than 9, endotracheal intubation either in the field or the emergency trauma center, and intravenous fluid infusion of greater than 4 L of crystalloid solution during the first hour of resuscitation. Two patients were taken emergently to the operating room for ongoing hemorrhage. All patients in this group underwent operation, including exploratory laparotomy, for injuries unrelated to the heart or pericardium within 72 hours after admission. Additionally, two of the patients underwent open reduction and internal fixation of multiple orthopedic injuries of the pelvis and lower extremities within 3 to 8 days after admission. A combined total of 35 surgical procedures were performed in these 3 critically ill patients. Rapid development of respiratory failure and the adult respiratory distress syndrome occurred in all posttraumatic patients with pericardial abscess. Each patient manifested progression of the sepsis syndrome and at least six criteria for either end-organ dysfunction or advanced MSOF [3,15] preceding or coexistent with the diagnosis of pericardial abscess. In addition to pulmonary and cardiovascular system failure, all patients met the criteria for hepatic, renal, intestinal, and central nervous system dysfunction; two patients also manifested fulminant hepatic and renal failure. The diagnosis of pericardial abscess in patients after trauma was made 51 4- 18 days (mean 4- SE) after admission, compared with 4 4- 2 days after admission for
VOLUME 165
MAY 1993
PERICARDIAL ABSCESS
patients with nontraumatic pericarditis. In comparison with the 21 nontrauma patients, the development of pericardial abscess following trauma was associated with statistically and clinically significant prolongation of the stay in the intensive care unit (ICU), as well as in the overall length of hospitalization (Table HI). In addition to cardiac tamponade, clinical manifestations of pericardial abscess common to these three patients included fever greater than 38.5~ absolute leukocytosis greater than 105 cells/mm3, abnormal electrocardiographic findings (sinus tachycardia, diffuse ST-wave elevation, and persistently low QRS voltage), and an abnormal cardiac silhouette on the chest roentgenograph. CT scanning revealed pericardial effusions in all three patients without other obvious sources of infectious intra-abdominal lesions. Pericardiocentesis was performed in all patients, either in the ICU or in the operating room. A definitive microbiologic diagnosis was made preoperatively in two patients on the basis of staining and culturing of pericardial fluid. These cultures identified Staphylococcus epidermidis in one patient and Pseudomonas aeruginosa with enterococci in the other patient; concomitantly, these patients had positive blood cultures from both central and peripheral intravenous sites. Upon diagnosis, each patient received broad-spectrum antibiotics for a minimum of 14 days (range: 14 to 28 days). The third patient was receiving broad-spectrum antibiotics at the time of diagnosis, and, despite purulent pericardial fluid at operation, no organisms were recovered by stain or culture. Operations for pericardial abscess following trauma were performed within 24 hours of the definitive diagnosis. Left anterior or anterolateral thoracotomy, drbridement, and partial pericardiectomy with preservation of the left phrenic nerve was uniformly performed. Left pleural chest tubes were placed in each patient, and additional closed suction drains were placed in one patient to drain the posterior pericardial space. Purulent pericardial effusions (greater than 90% polymorphonuclear cells) ranged in volume from 800 mL to 1,400 mL and were associated with fibrinous exudate extending from the epicardiurn to the pericardium. The pericardium was noted to be grossly thickened in all patients, with histologic evidence of acute and subacute inflammatory cell infiltration. There were no operative deaths in thisgroup and no complications related to the pericardial drainage procedures. In each case, operative drainage of the pericardial abscess led to abatement of clinical sepsis and gradual resolution of MSOF. Despite stormy postoperative courses, all patients survived and were subsequently discharged from the hospital without signs of cardiac compromise. COMMENTS Pericardial inflammatory conditions represent a diverse spectrum of disease, extending from acute, subclinical pericarditis to fulminant, life-threatening pericardial abscess. The actual incidence of pericarditis remains unknown, because many self-limited subclinical cases remain undetected [4]. Of note, the severity of the pericar-
TABLE III
Duration of ICU Stay a n d O v e r a l l Hospitalization (days [mean _+ S E M ] ) Condition Acute nontraumatic pericarditis Post-traumatic pericardial abscess
ICU Stay 2 _+ 0.4 (n = 15)* 129 +- 40 (n = 3)t
Hospitalization 8 -+ 2 (n = 21) 136 -+ 38 (n = 3)t
ICU = intensive care unit. *Six patients were monitored in a cardiac telemetry unit. tp <0.001 by Mann-Whitney U test.
dial inflammation does not necessarily improve the diagnostic accuracy; consequently, the diagnosis of pericardial abscess presupposes a high index of clinical suspicion. Previous investigations have emphasized the difficulty in achieving the clinical diagnosis of purulent pericarditis, with antemortem diagnostic rates of only 18% to 69% [5,7]. Recent anecdotal reports of suppurative pericardial infections suggest that more cases are occurring in immunologically compromised patients [16-18]. Groups at high risk for pericardial abscess indude postoperative cardiothoracic surgery patients, patients with impaired host defenses such as individuals receiving immunosuppressive agents or who have malignancies, and patients with severe debilitating disease [19]. Trauma patients with multiple injuries should also be considered at high risk for infectious complications such as pericardial abscess, since these patients manifest significant, global immunologic disability and alteration of the metabolic response to injury. Our experience with acute and infective pericarditis at Harborview Medical Center suggests that the "classic" findings of fever, substernal chest pain, and a friction rub occur in less than half of the patients with pericardial inflammation. Other reported experiences have also observed a lack of consistently present diagnostic symptoms and signs [4]. With respect to patients with pericardial abscess, however, some distinguishing diagnostic features emerge. In a review of the 68 cases of purulent pericarditis reported in the literature from 1945 to 1989, Hall [6] noted that symptoms and signs common to these patients included fever (88%), dyspnea (61%), chest pain (57%), pulsus paradoxus (65%), hepatomegaly (59%), and elevated central venous pressure (58%). Additionally, leukocytosis, tachycardia, and pericardial effusions noted by echocardiography occurred with 100% frequency. Similarly, all of our trauma patients with pericardial abscess had fever, leukocytosis, and tachycardia. Our patients also uniformly had abnormalities on their electrocardiograms and chest roentgenograms, as well as evidence of cardiac tamponade. We believe that this clinical scenario necessitates urgent diagnostic and therapeutic manuevers to either definitively rule out or treat pericardial abscess. Recognition and diagnosis of purulent pericarditis by both chest radiography [20] and echocardiography [21]
THE AMERICAN JOURNAL OF SURGERY
VOLUME 165
MAY 1993
639
SATOET AL
Figure 1. Computed tomographic scan of the chest shows large effusion that was subsequently demonstrated to be a pericardial abscess. Note that the soft tissue edema of the chest wall precluded echocardiography.
due to intrapericardial gas-forming organisms has been previously reported. Echocardiography has been considered the most sensitive technique for detecting pericardial effusion [4,22]. CT has also been demonstrated to be a sensitive technique for imaging pericardial thickening and effusion [23]. We found echocardiography useful and diagnostic of pericardial effusion in two trauma patients with pericardial abscess. Although echocardiography was attempted in the third patient, his impressive chest wall edema prevented adequate imaging of the heart and pericardium. CT was accurate in diagnosing pericardial effusion in all of our trauma patients. Furthermore, CT helped to exclude the abdomen as a potential source of infection. We believe that there is a small number of patients with clinically suspected pericardial abscess in whom echocardiography does not provide technically adequate data; we recommend that these patients undergo CT examination (Figure 1). The etiology of infecting organisms causing purulent pericarditis has evolved over the past century. Prior to 1944, Streptococcus pneumoniae was the predominant bacterial isolate; since the clinical introduction of penicillin in 1944, the most common infecting organism has been Staphylococcus aureus [5-7]. With technologic advances including ventilator support, broad-spectrum antibiotics, aggressive cancer chemotherapy, and transplant immunosuppression, more unusual, opportunistic infections are becoming clinically apparent. The causative organisms in our small series suggest that these nosocomial infections occurred in trauma patients with an altered immunologic status. The increase of gram-negative [6] and fungal organisms [19,24] causing purulent pericarditis reflects a generalized trend that has been observed in contemporary medicine [25]. Pericardial abscess in our study was associated with clinical sepsis and progressive multiple organ failure. Pericardial effusion, presumably due to uremia, was noted in two of our patients with renal failure prior to the development of sepsis and cardiac tamponade. The pre640
cise moment at which these pericardial effusions became infected, and the relationship between pericardial infection and the onset of MSOF, is unknown. The dramatic clinical improvement and resolution of multiple organ failure we observed after definitive treatment suggests that pericardial abscess contributed to the maintenance of end-organ dysfunction in our patients. We speculate that, in the constellation of MSOF following severe mechanical or thermal injury, the immune system also fails, leading to an increased incidence of infection. Subsequently, the addition of infectious foci in this scenario increasingly contributes to uncontrollable, overwhelming inflammation. Loss of inflammatory regulation fueled by sepsis-induced mediators is thought to play an important role in progressive end-organ injury and MSOF [26]. Prominent factors contributing to acute death in purulent pericarditis include sepsis and cardiac tamponade. As such, initial measures such as intravascular volume expansion with intravenous fluids alone or in combination with therapeutic pericardocentesis can be life-saving [4]. Untreated, pericardial abscess has a mortality rate of 100% [27]. With the use of antibiotics alone, the mortality rate is between 66% and 82% [28]. Recent series combining surgical treatment with medical therapy suggest the mortality rate should be less than 20% [29,30]. In the absence of MSOF, successful percutaneous catheter drainage of purulent pericarditis has been reported [31,32]. However, we do not advocate this approach in septic, critically ill trauma patients with advancing multiple organ failure. We and others [29,30,33] believe that, once the initial diagnosis of pericardial abscess has been made, operative drainage is mandatory. We have uniformly used either a left anterior or anterolateral thoracotomy with partial pericardiectomy for drainage of pericardial pus. This approach offers immediate resolution of tamponade and rapid elimination of the septic foci. Additionally, operative drainage combined with pericardiectomy via thoracotomy allows for the removal of fibrin clots and loculi within the pericardial space, reducing the
THE AMERICANJOURNALOFSURGERY VOLUME165 MAY 1993
PERICARDIAL ABSCESS
likelihood of pus re-accumulation or late pericardial constriction [29,30]. Subxiphoid tube drainage has also been described as an effective, less invasive treatment for pericardial abscess [34-36]; this approach is somewhat limited by the inability to perform extensive pericardial drbridement and pericardiectomy. In conclusion, we report three cases of pericardial abscess following noncardiac trauma associated with sepsis and MSOF. The diagnostic difficulty encountered with this disease is amplified in trauma patients undergoing multiple operative procedures for other injuries. Findings such as evidence for infection (fever, leukocytosis, tachycardia) associated with an abnormal electrocardiogram, a cardiac silhouette on the chest radiograph, pericardial effusion, or cardiac tamponade demand further clinical investigation. Pericardiocentesis has both diagnostic and therapeutic roles, and, after the diagnosis of pericardial abscess, we recommend appropriate antimicrobial therapy combined with operative drainage via thoracotomy, pericardial drbridement, and pericardiectomv. REFERENCES 1. Baker CC, Oppenheimer L, Lewis FR, Trunkey DD. Epidemiology of trauma deaths. Am J Surg 1980; 140: 144-50. 2. Trunkey DD, BlaisdeU FW. Epidemiology of trauma. In: Wilmore DW, Brennan MF, Harken AH, Holcroft JW, Meakins JL, editors. Care of the surgical patient. New York: Scientific American, Inc., 1992: Chapter 6: 1-7. 3. Deitch EA. Multiple organ failure. Ann Surg 1992; 216:117-34. 4. Sternbach GL. Pericarditis. Ann Emerg Med 1988; 17: 214-20. 5. Klaesmann PG, Bulkley BH, Hutchins GM. The changed spectrum of purulent pericarditis. Am J Med 1977; 63: 666-73. 6. Hall IP. Purulent pericarditis. Postgrad Med J 1989; 65: 444-8. 7. Rubin RH, Moellering RC Jr. Clinical, microbiologic,and therapeutic aspects of purulent pericarditis. Am J Med 1975; 59: 68-78. 8. Van Vooren JP, Thys JP, Vanderhoeft P. Purulent pericarditis resulting from blunt chest trauma. J Thorac Cardiovasc Surg 1990; 100: 932-4. 9. Douglas RG, Shaw JHF. Metabolic response to sepsis and trauma. Br J Surg 1989; 76: 115-22. 10. Trunkey DD. The treatment of sepsis and other complications in the trauma patient. Clin Ther 1990; 12 (Suppl B): 21-33. 11. Mileski WJ. Sepsis. Surg Clin North Am 1991; 71: 749-64. 12. Hotchkiss RS, Karl IE. Reevaluation of the role of cellular hypoxia and bioenergetic failure in sepsis. JAMA 1992; 267: 1503-10. 13. Beck CS. Two cardiac compression triads. JAMA 1935; 104: 714-6. 14. Champion HR, Copes WS, Sacco W J, Flanagan ME. Injury severity scoring. In: Moore EE, editor. Early care of the injured patient. Philadelphia: BC Decker, Inc., 1990: 12-26. 15. Henao FR, Daes JE, Dennis RJ. Risk factors for muttiorgan
failure: a case-control study. J Trauma 1991; 31: 74-80. 16. Demey HE, Eycken M, Vandermast M, Bossaert LL. Purulent pericarditis due to methicillin-resistant Staphylococcus aureus. Acta Cardiol 1991; 46: 485-91. 17. Kumar VV, Herzog C. Purulent pericarditis caused by group G streptococcus. JAMA 1990; 264: 34-5. 18. Law EJ, Orlet HK, Still JM, Catalano PW, Mucha E. Purulent pericarditis in an adult burn patient treated with survival. Burns 1991; 17: 254-6. 19. Kraus WE, Valenstein PN, Corey GR. Purulent pericarditis caused by Candidtz'report of three cases and identification of highrisk populations as an aid to early diagnosis. Rev Infect Dis 1988; 10: 34-41. 20. Chow WH, Chow LTC, Suen HC. Purulent pericarditis: recognition from the chest radiograph. Int J Cardiol 1991; 30: 229-30. 21. Ku CS, Hsiung MC, Hsu TL, Ding YA, Shieh SH. Spontaneous contrast in the pericardial sac caused by gas-forming organisms. J Am Soc Echocardiogr 1991; 4: 67-8. 22. Horowitz MS, Schultz CS, Stinson EB, Harrison DC, Popp RL. Sensitivity and specificity of echocardiographic diagnosis of pericardial effusion. Circulation 1974; 50: 239-47. 23. Isner JM, Carter BL, Bankoff MS, Konstam MA, Salem DN. Computerized tomography in the diagnosis of pericardial heart disease Ann Intern Med 1982; 97: 473-9. 24. FifeTD, Finegold SM, Grennan T. Pericardial actinomyeosis: case report and review. Rev Infect Dis 1991; 13: 120-6. 25. Finland M. Changing ecology of bacterial infections as related to antibacterial therapy. J Infect Dis 1970; 122: 419-31. 26. Maier RV. Critical care and metabolism. Bulletin of the American College of Surgeons 1992; 77: 22-6. 27. Okoromora EO, Perry LW, Scott LR. Acute bacterial pericarditis in children: report of 25 cases. Am Heart J 1975; 90: 709-13. 28. Berk SL, Rice PA, Reyholds CA, Finland M. Pneumococcal pericarditis: a persistent problem in comtemporary diagnosis.Am J Med 1981; 70: 247-51. 29. Sethi GK, Nelson RM, Jenson CB. Surgical management of acute septic pericarditis. Chest 1973; 63: 732-5. 30. Majid AA, Omar A. Diagnosis and management of purulent pericarditis. J Thorac Cardiovasc Surg 1991; 102: 413-7. 31. Bouwels L, Jansen E, Janssen J, et al. Successful long-term catheter drainage in an immunocompromisedpatient with purulent pericarditis. Am J Med 1987; 83: 581-3. 32. Houghton JL, Becherer PR. Haemophilus influenzae pericarditis successfullytreated by catheter drainage. South Med J 1987; 80: 766-8. 33. Cameron EWJ. Surgical management of staphylococcal pericarditis. Thorax 1975; 30: 678-81. 34. Adebo OA, Adebonojo SA. Purulent pericarditis in children. J Thorac Cardiovasc Surg 1984; 88: 312-3. 35. Hardy CC, Raza SN, Isalska B, Barber PV. Atraumatic suppurative mediastinitis and purulent pericarditis due to Eikenella corrodens. Thorax 1988; 43: 494-5. 36. Palatanos GM, Thurer R J, Kaiser GA. Comparison of effectiveness and safety of operations on the pericardium. Chest 1988; 88: 30-3.
THE AMERICAN JOURNAL OF SURGERY VOLUME 165 MAY 1993 641