Heart & Lung 44 (2015) 448e450
Contents lists available at ScienceDirect
Heart & Lung journal homepage: www.heartandlung.org
Left ventricular pseudoaneurysm as a fatal complication of purulent pericarditis Bharath Sunkara, MD, Alexandros Briasoulis, MD, Luis Afonso, MD, FACC, Preeti Ramappa, MD, FACC * Division of Cardiology, Veterans Affairs Medical Center, Wayne State University, Detroit, MI 48201, USA
a r t i c l e i n f o
a b s t r a c t
Article history: Received 3 April 2015 Received in revised form 13 May 2015 Accepted 3 June 2015 Available online 8 July 2015
We report a case of a 48-year-old man with purulent pericarditis by Streptococcus viridans, despite aggressive treatment with antibiotics and partial pericardiectomy was complicated by left ventricle pseudo-aneurysm resulting in a fatal outcome. The case highlights the course of complicated purulent pericarditis and the use of noninvasive imaging for assessing early signs of pseudoaneurysm and its typical progression. Published by Elsevier Inc.
Keywords: Left ventricle Pseudoaneurysm Purulent pericarditis Streptococcus viridans Pericardial disease
Introduction Left ventricular pseudo-aneurysm (LVPA) occurs as a result of ventricular free wall rupture with adherent pericardium or fibrous tissue. It commonly occurs following myocardial infarction (MI) but it can infrequently complicate cardiac surgery, trauma, or pericarditis.1 LVPA as a result of purulent pericarditis in adults is extremely rare2 and limited to case reports. The typical etiological agent in all of these cases has been reported as Staphylococcus aureus. We report a rare case of purulent pericarditis by Streptococcus viridans, complicated by LVPA that led to a fatal outcome despite aggressive medical and surgical therapy. Case A 48 year-old diabetic, hypertensive male with history of alcohol dependence and chronic pancreatitis, presented with fatigue and poor appetite and was found to be in diabetic ketoacidosis (DKA). He had a recent history of multiple decayed tooth extraction and teeth abscesses 3 months prior to presentation. DKA resolved but
Funding: None. No ethical approval needed. Conflicts of interest: None. * Corresponding author. Tel.: þ1 313 576 3221. E-mail address: [email protected] (P. Ramappa). 0147-9563/$ e see front matter Published by Elsevier Inc. http://dx.doi.org/10.1016/j.hrtlng.2015.06.002
he subsequently developed chest pain and dyspnea and was noted to have clinical and echocardiographic evidence of pericardial effusion, which was initially a minimal accumulation along the posterobasal area and within 48 h, progressed to a large sized circumferential pericardial effusion with signs of cardiac tamponade (Fig. 1A and B). On presentation the patient appeared ill and cachectic and was afebrile, normotensive but in moderate respiratory distress with sinus tachycardia at a rate of 100 bpm, leukocytosis of 26,400 white blood cells/microliter with toxic granulation and elevated erythrocyte sedimentation rate (ESR) of 135 mm/h. No new electrocardiographic ST-T changes were observed and serial sets of cardiac biomarkers (Troponin I and creatine kinaseeMB subform) were negative, thus excluding the possibility that the initial presentation was ischemic in origin. He underwent emergent pericardiocentesis and 1 L of muddy brown, purulent fluid was drained which was positive for Streptococcus viridans. In spite of initial symptomatic improvement, his clinical condition deteriorated over the next 24 h and a repeat transthoracic echocardiogram (TTE) revealed thickened pericardium with moderate loculated pericardial effusion around the right ventricular (RV) free wall with signs of effusive constrictive pericarditis. Emergent pericardial window was performed. The pericardial tissue also grew streptococcus viridans. Initially, the patient was treated with an empiric antibiotic combination consisting of ceftriaxone 2 g IV once daily and vancomycin 20 mg/kg every 12 h with a serum trough level goal of 15 mcg/mL or greater. After
B. Sunkara et al. / Heart & Lung 44 (2015) 448e450
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Fig. 1. (A) Transthoracic echocardiogram (TTE) on presentation after pericardial drainage without evidence of pseudoaneurysm, (B) Follow-up TTE showed a moderate loculated pericardial effusion around the RV free wall with sustained RV free wall collapse with near cavity obliteration, (CeE) TTE shows akinetic inferoposterior wall with a basal wall pseudoaneurysm that measures 4.8 by 3.6 cm with a neck that measures 0.9 cm and free communication with the LV cavity as shown on color flow and continuous wave Doppler.
microbiologic diagnosis and sensitivities were available patient was treated with ceftriaxone 2 g IV daily for a total of 4 weeks. Patient’s condition markedly improved. He was hospitalized for 22 days with resolution of clinical signs of infection, normalization of white cell count, decreasing ESR, and adequate pericardial drainage with clearance of Streptococcus viridans from the pericardial fluid, and he was discharged on parenteral antibiotics. Serological evaluation for acquired immunodeficiency was negative. Four weeks following his pericardial window (1 week after his hospital discharge) the patient was re-admitted with signs and symptoms of tamponade. Echocardiogram revealed loculated effusion and an organized mass compressing RV with dyskinesis of basal inferolateral wall. He underwent partial pericardiectomy of markedly thickened, fibrotic pericardium and evacuation of large amount of pus and hematoma. A cardiac catheterization before the procedure showed no obstructive coronary artery disease. A transesophageal echocardiogram (TEE) was performed and didn’t show any evidence of infective endocarditis but revealed organized exudate around free wall of right atrium and RV partially compressing the RV free wall. The patient remained in critical clinical condition and a follow-up TTE showed a new large PA measuring 4.8 cm 3.6 cm along the basal infero-lateral LV with an orifice of approximately 0.9 cm, freely communicating with the LV cavity (Fig. 1C and D). The postero-medial mitral chordae appeared to be directly straddling
the mouth of the aneurysm. A CT angiogram of the chest confirmed the presence of a large ventricular PA and pneumopericardium. Massive adhesions between pericardium, left lung and myocardium were noted during surgical exploration. Cor-matrix double patch repair was attempted but the neck of the aneurysm could not be reached. Three days post-operatively, the LVPA became wider (Fig. 1CeE) and eventually ruptured. The patient died five weeks after the initial recognition of the LVPA and ten weeks after his initial hospitalization. Discussion Purulent pericarditis (PP) is a rare entity commonly caused by gram-positive cocci, S. aureus and S. pneumoniae. Infection occurs from either direct or hematogenous seeding of organisms to pericardium from primary source. Streptococci viridans are normal habitants of the oral cavity and upper respiratory tract. Because these bacteria are relatively avirulent and not invasive, the only infection that is associated with viridans streptococci is infective endocarditis due to bacteremia. The various species of streptococci that make up the viridans group account for 40e60% of native valve endocarditis in the community. Streptococcus viridans PP is rare and may result by seeding of bacteria in pericardium from dental caries and oropharyngeal abscesses as in our case. Our patient had
450
B. Sunkara et al. / Heart & Lung 44 (2015) 448e450
negative blood cultures and CT didn’t reveal any foci of infection other than inflamed pericardium. Left ventricular PA usually occurs after MI. Rarely, LVPA may complicate an infectious process as infection itself can cause weakening of the ventricular wall leading to dissection. In the few reported cases, post infectious LVPA occur in the inferolateral submitral region, few weeks after diagnosis and treatment of PP.3 One of the proposed mechanisms for the development of LVPA is that there seems to be contained rupture of ventricular wall at a site of weakening produced either by direct spread of infection from pericardium or by intramyocardial abscesses. Additionally, the inflamed myocardium might be inadvertently damaged during the pericardiectomy. There have been an equal number of cases reported in adults and children and the organism isolated in the majority of these cases is S. aureus, which caused generalized staphylococcal infection.4 Our case is unusual, in that, it is the first case reported to be due to streptococcus viridans without widespread streptococcal infection and bacteremia. Interestingly, none of the previously reported cases of purulent pericarditis due to Streptococcus species reported an associated LVPA as a complication.3 The site of origin of LVPA in this patient was the basal inferolateral wall, which is noted to be the common site for all the reported cases of infective LVPA in the current literature.3 Interestingly, our patient demonstrated regional wall motion abnormality on echocardiography, in the form of dyskinesis in this wall, one week preceding the appearance of LVPA. This is likely reflective of early signs of myocardial edema either secondary to direct spread of infection from pericardium or due to local intramyocardial abscesses rendering the muscle weak. This wall motion abnormality has not been described in earlier reports and we speculate if perhaps this is an early sign of impending rupture of the myocardial wall that calls for a more focused monitoring, using serial TTEs. This can aid early recognition and timely intervention that can remarkably change the course of outcome. Echocardiography is very useful for detecting tamponade in patients with purulent pericarditis, but cannot differentiate between purulent collections and sterile effusions. Echocardiographic findings such as new wall motion abnormalities in the absence of hemodynamically significant coronary artery disease (as in our case), dense adhesions, loculated effusion, recurrent tamponade, constrictive physiology, functional tricupid stenosis, and persistent infection may be related to high morbidity and risk of PA.
Unlike the overwhelming fatal outcome of LVPA secondary to infective endocarditis, the overall prognosis of LVPA secondary to purulent pericarditis has yielded good prognosis without recurrences in the reported cases that have all undergone timely surgical intervention in the form of LVPA repair.5 It is previously suggested that only patients with high-risk features (worsening symptoms, new onset, rapid expansion, size >3 cm) might benefit from surgical repair.6 In our case it is likely that the patient’s comorbidities, the size of LVPA, rapidity of the expansion, the dense fibrosis and adhesions rendered it less amenable for repair and led to poor outcome. In summary, this case provides an example of an entity that remains extremely rare and highlights the course of purulent pericarditis due to streptococcus viridans and raises awareness of the early echocardiographic signs preceding the formation of infective LVPA. In such cases, extensive pericardiectomy is essential to achieve adequate drainage. LVPA is a rare complication of PP and prompt surgical repair may prevent grave outcomes. Acknowledgments None. Supplementary data Supplementary data related to this article can be found online at http://dx.doi.org/10.1016/j.hrtlng.2015.06.002. References 1. Gould K, Barnett JA, Sanford JP. Purulent pericarditis in the antibiotic era. Arch Intern Med. 1974;134:923e927. 2. Majid AA, Omar A. Diagnosis and management of purulent pericarditis. Experience with pericardiectomy. J Thorac Cardiovasc Surg. 1991;102:413e417. 3. Desai M, Gandhi H, Mishra A. Post-infective pericarditis left ventricular pseudoaneurysm: a case report and review of literature. Cardiol Young. 2014;13:1e4. 4. Parikh SV, Memon N, Echols M, Shah J, McGuire DK, Keeley EC. Purulent pericarditis: report of 2 cases and review of the literature. Medicine (Baltimore). 2009;88:52e65. 5. Tokuyasu H, Saitoh Y, Harada T, et al. Purulent pericarditis caused by the Streptococcus milleri group: a case report and review of the literature. Intern Med. 2009;48(12):1073e1078. 6. Pretre R, Linka A, Jenni R, Turina MI. Surgical treatment of acquired left ventricular pseudoaneurysms. Ann Thorac Surg. 2000;70:553e557.
Contents lists available at ScienceDirect
Heart & Lung journal homepage: www.heartandlung.org
Left ventricular pseudoaneurysm as a fatal complication of purulent pericarditis Bharath Sunkara, MD, Alexandros Briasoulis, MD, Luis Afonso, MD, FACC, Preeti Ramappa, MD, FACC * Division of Cardiology, Veterans Affairs Medical Center, Wayne State University, Detroit, MI 48201, USA
a r t i c l e i n f o
a b s t r a c t
Article history: Received 3 April 2015 Received in revised form 13 May 2015 Accepted 3 June 2015 Available online 8 July 2015
We report a case of a 48-year-old man with purulent pericarditis by Streptococcus viridans, despite aggressive treatment with antibiotics and partial pericardiectomy was complicated by left ventricle pseudo-aneurysm resulting in a fatal outcome. The case highlights the course of complicated purulent pericarditis and the use of noninvasive imaging for assessing early signs of pseudoaneurysm and its typical progression. Published by Elsevier Inc.
Keywords: Left ventricle Pseudoaneurysm Purulent pericarditis Streptococcus viridans Pericardial disease
Introduction Left ventricular pseudo-aneurysm (LVPA) occurs as a result of ventricular free wall rupture with adherent pericardium or fibrous tissue. It commonly occurs following myocardial infarction (MI) but it can infrequently complicate cardiac surgery, trauma, or pericarditis.1 LVPA as a result of purulent pericarditis in adults is extremely rare2 and limited to case reports. The typical etiological agent in all of these cases has been reported as Staphylococcus aureus. We report a rare case of purulent pericarditis by Streptococcus viridans, complicated by LVPA that led to a fatal outcome despite aggressive medical and surgical therapy. Case A 48 year-old diabetic, hypertensive male with history of alcohol dependence and chronic pancreatitis, presented with fatigue and poor appetite and was found to be in diabetic ketoacidosis (DKA). He had a recent history of multiple decayed tooth extraction and teeth abscesses 3 months prior to presentation. DKA resolved but
Funding: None. No ethical approval needed. Conflicts of interest: None. * Corresponding author. Tel.: þ1 313 576 3221. E-mail address: [email protected] (P. Ramappa). 0147-9563/$ e see front matter Published by Elsevier Inc. http://dx.doi.org/10.1016/j.hrtlng.2015.06.002
he subsequently developed chest pain and dyspnea and was noted to have clinical and echocardiographic evidence of pericardial effusion, which was initially a minimal accumulation along the posterobasal area and within 48 h, progressed to a large sized circumferential pericardial effusion with signs of cardiac tamponade (Fig. 1A and B). On presentation the patient appeared ill and cachectic and was afebrile, normotensive but in moderate respiratory distress with sinus tachycardia at a rate of 100 bpm, leukocytosis of 26,400 white blood cells/microliter with toxic granulation and elevated erythrocyte sedimentation rate (ESR) of 135 mm/h. No new electrocardiographic ST-T changes were observed and serial sets of cardiac biomarkers (Troponin I and creatine kinaseeMB subform) were negative, thus excluding the possibility that the initial presentation was ischemic in origin. He underwent emergent pericardiocentesis and 1 L of muddy brown, purulent fluid was drained which was positive for Streptococcus viridans. In spite of initial symptomatic improvement, his clinical condition deteriorated over the next 24 h and a repeat transthoracic echocardiogram (TTE) revealed thickened pericardium with moderate loculated pericardial effusion around the right ventricular (RV) free wall with signs of effusive constrictive pericarditis. Emergent pericardial window was performed. The pericardial tissue also grew streptococcus viridans. Initially, the patient was treated with an empiric antibiotic combination consisting of ceftriaxone 2 g IV once daily and vancomycin 20 mg/kg every 12 h with a serum trough level goal of 15 mcg/mL or greater. After
B. Sunkara et al. / Heart & Lung 44 (2015) 448e450
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Fig. 1. (A) Transthoracic echocardiogram (TTE) on presentation after pericardial drainage without evidence of pseudoaneurysm, (B) Follow-up TTE showed a moderate loculated pericardial effusion around the RV free wall with sustained RV free wall collapse with near cavity obliteration, (CeE) TTE shows akinetic inferoposterior wall with a basal wall pseudoaneurysm that measures 4.8 by 3.6 cm with a neck that measures 0.9 cm and free communication with the LV cavity as shown on color flow and continuous wave Doppler.
microbiologic diagnosis and sensitivities were available patient was treated with ceftriaxone 2 g IV daily for a total of 4 weeks. Patient’s condition markedly improved. He was hospitalized for 22 days with resolution of clinical signs of infection, normalization of white cell count, decreasing ESR, and adequate pericardial drainage with clearance of Streptococcus viridans from the pericardial fluid, and he was discharged on parenteral antibiotics. Serological evaluation for acquired immunodeficiency was negative. Four weeks following his pericardial window (1 week after his hospital discharge) the patient was re-admitted with signs and symptoms of tamponade. Echocardiogram revealed loculated effusion and an organized mass compressing RV with dyskinesis of basal inferolateral wall. He underwent partial pericardiectomy of markedly thickened, fibrotic pericardium and evacuation of large amount of pus and hematoma. A cardiac catheterization before the procedure showed no obstructive coronary artery disease. A transesophageal echocardiogram (TEE) was performed and didn’t show any evidence of infective endocarditis but revealed organized exudate around free wall of right atrium and RV partially compressing the RV free wall. The patient remained in critical clinical condition and a follow-up TTE showed a new large PA measuring 4.8 cm 3.6 cm along the basal infero-lateral LV with an orifice of approximately 0.9 cm, freely communicating with the LV cavity (Fig. 1C and D). The postero-medial mitral chordae appeared to be directly straddling
the mouth of the aneurysm. A CT angiogram of the chest confirmed the presence of a large ventricular PA and pneumopericardium. Massive adhesions between pericardium, left lung and myocardium were noted during surgical exploration. Cor-matrix double patch repair was attempted but the neck of the aneurysm could not be reached. Three days post-operatively, the LVPA became wider (Fig. 1CeE) and eventually ruptured. The patient died five weeks after the initial recognition of the LVPA and ten weeks after his initial hospitalization. Discussion Purulent pericarditis (PP) is a rare entity commonly caused by gram-positive cocci, S. aureus and S. pneumoniae. Infection occurs from either direct or hematogenous seeding of organisms to pericardium from primary source. Streptococci viridans are normal habitants of the oral cavity and upper respiratory tract. Because these bacteria are relatively avirulent and not invasive, the only infection that is associated with viridans streptococci is infective endocarditis due to bacteremia. The various species of streptococci that make up the viridans group account for 40e60% of native valve endocarditis in the community. Streptococcus viridans PP is rare and may result by seeding of bacteria in pericardium from dental caries and oropharyngeal abscesses as in our case. Our patient had
450
B. Sunkara et al. / Heart & Lung 44 (2015) 448e450
negative blood cultures and CT didn’t reveal any foci of infection other than inflamed pericardium. Left ventricular PA usually occurs after MI. Rarely, LVPA may complicate an infectious process as infection itself can cause weakening of the ventricular wall leading to dissection. In the few reported cases, post infectious LVPA occur in the inferolateral submitral region, few weeks after diagnosis and treatment of PP.3 One of the proposed mechanisms for the development of LVPA is that there seems to be contained rupture of ventricular wall at a site of weakening produced either by direct spread of infection from pericardium or by intramyocardial abscesses. Additionally, the inflamed myocardium might be inadvertently damaged during the pericardiectomy. There have been an equal number of cases reported in adults and children and the organism isolated in the majority of these cases is S. aureus, which caused generalized staphylococcal infection.4 Our case is unusual, in that, it is the first case reported to be due to streptococcus viridans without widespread streptococcal infection and bacteremia. Interestingly, none of the previously reported cases of purulent pericarditis due to Streptococcus species reported an associated LVPA as a complication.3 The site of origin of LVPA in this patient was the basal inferolateral wall, which is noted to be the common site for all the reported cases of infective LVPA in the current literature.3 Interestingly, our patient demonstrated regional wall motion abnormality on echocardiography, in the form of dyskinesis in this wall, one week preceding the appearance of LVPA. This is likely reflective of early signs of myocardial edema either secondary to direct spread of infection from pericardium or due to local intramyocardial abscesses rendering the muscle weak. This wall motion abnormality has not been described in earlier reports and we speculate if perhaps this is an early sign of impending rupture of the myocardial wall that calls for a more focused monitoring, using serial TTEs. This can aid early recognition and timely intervention that can remarkably change the course of outcome. Echocardiography is very useful for detecting tamponade in patients with purulent pericarditis, but cannot differentiate between purulent collections and sterile effusions. Echocardiographic findings such as new wall motion abnormalities in the absence of hemodynamically significant coronary artery disease (as in our case), dense adhesions, loculated effusion, recurrent tamponade, constrictive physiology, functional tricupid stenosis, and persistent infection may be related to high morbidity and risk of PA.
Unlike the overwhelming fatal outcome of LVPA secondary to infective endocarditis, the overall prognosis of LVPA secondary to purulent pericarditis has yielded good prognosis without recurrences in the reported cases that have all undergone timely surgical intervention in the form of LVPA repair.5 It is previously suggested that only patients with high-risk features (worsening symptoms, new onset, rapid expansion, size >3 cm) might benefit from surgical repair.6 In our case it is likely that the patient’s comorbidities, the size of LVPA, rapidity of the expansion, the dense fibrosis and adhesions rendered it less amenable for repair and led to poor outcome. In summary, this case provides an example of an entity that remains extremely rare and highlights the course of purulent pericarditis due to streptococcus viridans and raises awareness of the early echocardiographic signs preceding the formation of infective LVPA. In such cases, extensive pericardiectomy is essential to achieve adequate drainage. LVPA is a rare complication of PP and prompt surgical repair may prevent grave outcomes. Acknowledgments None. Supplementary data Supplementary data related to this article can be found online at http://dx.doi.org/10.1016/j.hrtlng.2015.06.002. References 1. Gould K, Barnett JA, Sanford JP. Purulent pericarditis in the antibiotic era. Arch Intern Med. 1974;134:923e927. 2. Majid AA, Omar A. Diagnosis and management of purulent pericarditis. Experience with pericardiectomy. J Thorac Cardiovasc Surg. 1991;102:413e417. 3. Desai M, Gandhi H, Mishra A. Post-infective pericarditis left ventricular pseudoaneurysm: a case report and review of literature. Cardiol Young. 2014;13:1e4. 4. Parikh SV, Memon N, Echols M, Shah J, McGuire DK, Keeley EC. Purulent pericarditis: report of 2 cases and review of the literature. Medicine (Baltimore). 2009;88:52e65. 5. Tokuyasu H, Saitoh Y, Harada T, et al. Purulent pericarditis caused by the Streptococcus milleri group: a case report and review of the literature. Intern Med. 2009;48(12):1073e1078. 6. Pretre R, Linka A, Jenni R, Turina MI. Surgical treatment of acquired left ventricular pseudoaneurysms. Ann Thorac Surg. 2000;70:553e557.
