Ruptured myocardial abscess causing left ventricle to pulmonary artery communication in an infant with community-associated methicillin-resistant Staphylococcus aureus endocarditis.
A 12-month-old male infant presented to the emergency department (ED) with fever, irritability, and labored breathing. He had been previously healthy with no known medical problems until 5 days prior to admission, when he presented to an urgent care center with a small abscess on his left calf. The abscess was incised and drained and he was discharged home. Because of the interval development of fever, he returned to the urgent care center, where he was given a "shot of antibiotics" and a prescription for oral antibiotics. The prescription was not filled. He continued to be febrile and began to have labored breathing and fussiness 2 days prior to admission. As part of an evaluation in a local ED, a chest radiograph was performed which demonstrated mild cardiomegaly. He was subsequently transferred to our institution. Upon presentation, he was febrile, tachycardic, and in moderate respiratory distress. Initial vital signs were notable for a temperature of 38.7[degrees]C, heart rate of 185 beats per minute, respiratory rate of 90 breaths per minute, blood pressure of 81/49 mm Hg, and oxygen saturation of 97%. His extremities were cool and his capillary refill time was approximately 5 seconds. His brachial and femoral pulses were 1+ and his dorsalis pedis pulses were difficult to palpate. He had grunting respirations with subcostal and intercostal retractions. He had no murmur or gallop noted on the initial cardiac examination.
Laboratory studies included a complete blood cell count with a white blood cell count of 17000/[micro]L with 61% polymorphonuclear leukocytes and 29% bands. A chemistry panel was notable for a mild metabolic acidosis. A chest radiograph confirmed the cardiomegaly, but otherwise was negative. Initial echocardiogram performed in the ED showed a small circumferential pericardial effusion and borderline low global systolic ventricular function. The patient had trace aortic regurgitation and mild mitral regurgitation. No vegetations were seen. Cefotaxime and vancomycin were started, and the patient was admitted to the pediatric intensive care unit. He was fluid resuscitated with normal saline in the ED and later in the pediatric intensive care unit with a total volume of almost 80 mL/kg.
Because of progressive hypotension, respiratory failure, and worsening metabolic acidosis, the patient was intubated, placed on mechanical ventilation, and started on inotropic support with epinephrine and dobutamine. Milrinone at 0.25 [micro]g/kg/min was added because of the worsening of systolic ventricular function demonstrated on follow-up transthoracic echocardiography. A linear structure was identified extending from the chordae of the anterior mitral valve leaflet to the ventricular septum just below the aortic valve annulus. A subsequent transesophageal echocardiogram was performed to more clearly evaluate the structure. The structure could not be visualized; however, an echolucent area was noted in the anterior outlet ventricular septum just below the aortic valve, extending toward the pulmonary artery just superior to the pulmonary annulus (Figure 1, a and b). There was a thin wall separating the cavity from the pulmonary artery. There was low-velocity flow into and out of the cavity from the left ventricle; however, no flow was demonstrated entering the right ventricle or pulmonary artery by color Doppler.
On hospital day 3, the patient continued to have poor perfusion and was diffusely edematous with a tense abdomen. Blood cultures were positive for Staphylococcus aureus, which was resistant to nafcillin, cefazolin, and erythromycin, but sensitive to clindamycin, trimethoprim-sulfamethoxazole, doxycycline, gentamicin, and vancomycin, most likely representing the typical community-associated methicillin-resistant S aureus (CA-MRSA) strain seen at this hospital. Clindamycin susceptibility was confirmed with a double diffusion disk test per the microbiology laboratory routine. Cefotaxime was switched to gentamicin and vancomycin was continued after susceptibilities were obtained. Hydrocortisone was added to help maintain blood pressures. A peritoneal drain was placed for drainage of peritoneal fluid and to decrease intra-abdominal pressure. Later that day, the patient developed dilated and nonreactive pupils with an absent corneal reflex. A computed tomography scan of the brain showed infarctions in the posterior and middle cerebral artery distributions and multiple areas of infarction in the cerebellum, as well as diffuse cerebral edema.
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On hospital day 5, the patient became acutely hypotensive with signs of worsening organ perfusion and with decreased cerebral saturations as measured by noninvasive regional saturation monitoring. A 2/6 harsh S1 coincident systolic murmur was heard at the left upper sternal border. A transthoracic echocardiogram done at the bedside showed rupture of the septal cavity from the outlet septum into the left sinus of Valsalva of the pulmonary artery, creating a left ventricle to pulmonary artery communication with left to right shunting seen on color Doppler (Figure 2). Regional left ventricular systolic wall motion abnormalities were noted, with the basal, mid inferior-lateral, and inferior-left ventricular free walls being severely hypokinetic. The septal and apical segments had normal wall motion. Surgical consultation was obtained, but because of persistent bacteremia as well as multiple organ dysfunction, the patient was not deemed to be a suitable surgical candidate.
On hospital day 8, the patient had sudden onset of hypotension with sinus bradycardia. Resuscitative efforts were started. After a brief return of circulation, he again became hypotensive and bradycardic. The parents decided to withhold any further interventions and the patient subsequently died.
At postmortem examination, there was 30 mL of liquid blood and 65 g of clotted blood in the pericardial cavity. Fibrinous exudate on the visceral pericardium covered the anterior-superior right ventricular outflow tract and extended to the base of the pulmonary trunk and the right atrial appendage. Examination of the left ventricular outflow tract revealed a subvalvular cavity in the anterior-basilar interventricular septum just below the left coronary cusp of the aortic valve (Figure 3,a). There was no vegetation on the aortic valve leaflets and the valve was normally formed. The cavity had a 0.6 X 0.5-cm opening with a smooth rim. The interior was empty except for a thin fibrinous lining, and it was 0.5 cm deep. The superior wall of the cavity was formed by indurated epicardial soft tissue. Gentle manipulation of a probe through the back superior wall of the cavity demonstrated communication into the epicardial soft tissue and through a perforation in the pulmonary artery behind the left cusp of the pulmonary valve. The left pulmonary cusp sinus of Valsalva was filled with a 1 X 1 X 1-cm vegetation. The left cusp of the pulmonary valve was displaced away from the wall but was completely separate from the vegetation. The pulmonary valve was normally formed. Histologic sections showed adherent fibrin and patchy infiltration of mononuclear inflammatory cells along the inner lining of the cavity (Figure 3,b). There was no purulent exudate or intact endocardial lining in the cavity. The epicardial soft tissue forming the superior border of the cavity and extending to the pulmonary artery adjacent to the left sinus of Valsalva showed acute and chronic inflammation with foci of necrosis and purulent exudate. Focal transmural necrosis was present in the pulmonary artery adjacent to the left sinus of Valsalva vegetation, and the vegetation contained numerous gram-positive cocci. Additional findings included extensive, patchy recent coagulation necrosis in the left ventricular myocardium (focal near-transmural necrosis) including the papillary muscles and basilar interventricular septum adjacent to the cavity, luminal thromboemboli in the proximal left circumflex and left main coronary arteries, acute pneumonia with microabscesses, and multiple septic infarcts in the brain.
Myocardial abscesses arising as a complication of bacterial endocarditis or bacterial septicemia are relatively rare in the pediatric population. The presence of myocardial abscesses is commonly obscured by the symptoms of the associated generalized sepsis and is often only diagnosed by transesophageal echocardiography during evaluation for infectious endocarditis (IE) as the etiology for the sepsis. Most commonly, abscesses result from direct extension from an infected cardiac valve to the surrounding perivalvular structures leading to the formation of perivalvular abscesses. (1) Free-wall abscesses may result from septic coronary artery embolisms. Myocardial abscesses reported in association with septicemia have usually been multiple and small, and have been associated with abscesses in multiple organs, but most frequently in the kidneys, lungs, and brain. (2) Other miscellaneous clinical contexts associated with myocardial abscesses include complications of acute myocardial infarction, trauma and penetrating injuries, mechanical cardiac interventions, or human immunodeficiency virus. These contexts are much less common in the pediatric population.
Typically, the pathogens associated with IE and myocardial abscesses are S aureus and Streptococcus species, although other pathogens are occasionally reported. During the last decade, CA-MRSA has emerged as a significant pathogen in causing infection in multiple patient populations and in multiple organ systems. The prevalence of CAMRSA in IE has begun to increase and seems to be distinct from health care-associated MRSA in terms of epidemiology and clinical manifestations, (3) but overall is still relatively rare. Also, certain strains of CA-MRSA have been implicated in more severe invasive disease, such as those that include the genes that encode the Panton-Valentine leukocidin. Unfortunately, more specific molecular testing could not be performed in this case.
A review of the literature done in 1999 by Shah et al (4) found 16 patients with perivalvular abscesses associated with bacterial endocarditis during a 20-year period. The patients' ages ranged from 8 to 21 years, and 40% of the patients had infection with S aureus. There have been a few subsequent pediatric case reports in the literature, but overall the incidence of this complication remains rare in comparison to adults, in whom up to 30% to 40% of patients with native valve IE have evidence of a myocardial abscess. (5) A review (6) of infective endocarditis patients in India found that 7% (14 of 192) had cardiac abscesses; however, only 2 of those 14 had myocardial abscesses that did not involve the valve or perivalvular areas. A review (7) from Denmark in 1995 looked at 118 adult patients with IE and "perivalvular cavities" by echocardiography. The perivalvular cavities were either true abscesses (pus filled) or pseudoaneurysms formed because of tissue destruction by invasive bacteria. The microscopy was notable for a pseudoaneurysm appearance with endothelial/endocardial and intimal/subendocardial covering.
Rupture of a myocardial abscess is an even more uncommon finding in the pediatric population. There is only 1 case in the literature (8) involving a 17-year-old patient who developed an anterior left ventricle abscess that subsequently ruptured into the pericardial space. Because most cases of abscess rupture are associated with myocardial infarction, and most myocardial abscesses are small, the incidence of ruptured myocardial abscesses in children is quite low.
In summary, we theorize that this patient developed CA-MRSA bacteremia after incision and drainage of a superficial skin abscess, which resulted in seeding of multiple organs including the heart. It is unclear whether a wound culture was obtained at the time of initial drainage, but this case underscores the importance of obtaining cultures and starting appropriate antibiotic therapy as soon as clinically indicated. Although the pathogenesis cannot be clearly established, the absence of aortic valve endocarditis and the findings of other luminal coronary thromboemboli on autopsy support the theory that the septal abscess was the result of hematogenous origin via the coronary arteries instead of direct extension of valvular endocarditis. Aggressive tissue destruction most likely resulted in rupture of the abscess into the left ventricular outflow track. An alternative theory of a preexisting ventricular septal defect seems unlikely given several factors including the location of the cavity within the ventricular septum, the lack of any demonstrable communication of the cavity with the right ventricle, and the eventual rupture into the pulmonary artery. This unfortunate case demonstrates the effects of an emerging community-acquired virulent pathogen in a previously healthy, young patient with rapid and devastating clinical progression and unusual cardiac pathology.
(1.) Anguera I, Quaglio G, Ferrer B, et al. Sudden death in Staphylococcus aureus-associated infective endocarditis due to perforation of a free-wall myocardial abscess. Scand J Infect Dis. 2001;33(8):622-625.
(2.) Chakrabarti J. Diagnostic evaluation of myocardial abscesses: a new look at an old problem. Int J Cardiol. 1995;52(3):189-196.
(3.) Millar BC, Prendergast BD, Moore JE. Community-associated MRSA (CAMRSA): an emerging pathogen in infective endocarditis. J Antimicrob Chemother. 2008;61(1):1-7.
(4.) Shah FS, Fennelly G, Weingarten-Arams J, Yang L, Glickstein J. Endocardial abscesses in children: case report and review of the literature. Clin Infect Dis. 1999;29(6):1478-1482.
(5.) Choussat R, Thomas D, Isnard R, et al. Perivalvular abscesses associated with endocarditis: clinical features and prognostic factors of overall survival in a series of 233 cases: Perivalvular Abscesses French Multicentre Study. Eur Heart J. 1999;20(3):232-241.
(6.) Garg N, Kandpal B, Garg N, et al. Characteristics of infective endocarditis in a developing country--clinical profile and outcome in 192 Indian patients, 1992-2001. Int J Cardiol. 2005;98(2):253-260.
(7.) Tingleff J, Egeblad H, Gotzsche CO, et al. Perivalvular cavities in endocarditis: abscesses versus pseudoaneurysms?: a transesophageal Doppler echocardiographic study in 118 patients with endocarditis. Am Heart J. 1995; 130(1):93-100.
(8.) Harris DG, Rossouw GJ. Myocardial abscess with contained rupture: successful repair. Ann Thorac Surg. 2001;71(4):1360-1361.
Jared A. Hershenson, MD; Peter B. Baker, MD; Daniel G. Rowland, MD
Accepted for publication November 24, 2010.
From the Heart Center (Drs Hershenson and Rowland) and the Department of Pathology (Dr Baker), Nationwide Children's Hospital, Columbus, Ohio; and The Ohio State University, Columbus (Dr Baker).
The authors have no relevant financial interest in the products or companies described in this article.
Reprints: Jared A. Hershenson, MD, The Heart Center, Nationwide Children's Hospital, Columbus, OH 43205 (e-mail: jared.hershenson@ nationwidechildrens.org).
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|Title Annotation:||Case Reports|
|Author:||Hershenson, Jared A.; Baker, Peter B.; Rowland, Daniel G.|
|Publication:||Archives of Pathology & Laboratory Medicine|
|Date:||Aug 1, 2011|
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