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Home , Endocarditis, Infective endocarditis, Vegetation (pathology)

□ CASE REPORT □

Infective and Acute Purulent in a Patient with Hyperglycemia

Kenji OKI, Wataru MATSUURA, Yasuhiro SAITO, Yujiro ONO, Kaoru YANAGIHARA, Masafumi SUESHIRO*, Satoru MORITA*, Junko KOIDE and Akihiro MAEDA

Abstract days prior to admission, he had general . His past medical history included mellitus at the age of 30 A diabetic patient was admitted to our hospital for and symptomatic diabetic neuropathy at the age of 40. He with acute purulent pericarditis was treated with insulin since the age of 41. Five months and diabetic ketoacidosis. revealed at- before this admission, he discontinued regular outpatient tachment of to the in the treatment. left ventricle and pericaridial effusion. The vegetation His temperature was 39.3°C, was 110 beats/min, was enlarged and pendulated for a few days despite and blood pressure was 90/56 mmHg. The physical findings maximal antimicrobial therapy. Surgical resection was on admission included dilated neck and multiple bilat- desirable to decrease the risk of embolic complications eral plantar ulcers that were 2–4 cm in diameter. No and cardiovascular collapse. We could not open the heart murmurs, crackles or rubs were audible over his chest. because of accumulation of purulent pericardial fluid, Neurologic examination revealed no abnormalities except for and right renal was complicated. We believe the loss of tendon reflexes. The bilateral dorsalis pedis arter- that the immunocompromised and hypercoagulable state ies were slightly palpable. All residual teeth were decayed, due to diabetes caused these conditions. and fistulae were found in the oral cavity. Laboratory data (Internal Medicine 44: 666–670, 2005) showed elevated inflammatory reactions [white blood cell count (WBC), 37,300/l (neutrophils, 94%); C-reactive pro- Key words: immunocompromised state, diabetic ketoacido- tein (CRP), 34.5 mg/dl]. Other laboratory values included the sis, operation, percutaneous pericardiocentesis following: serum urea nitrogen (BUN), 41.7 mg/dl; serum creatinine (Cre), 0.96 mg/dl; sodium, 132 mEq/l; potassium, 5.4 mEq/l; chloride, 86 mEq/l; aspartate aminotransferase, 25 IU/l;alanine aminotransferase, 15 IU/l; lactate dehydro- Introduction genase (LDH), 375 IU/l; creatine kinase, 100 IU/l; total pro- tein, 5.8 g/dl; albumin, 2.4 g/dl; plasma glucose, 642 mg/dl; Infective endocarditis is a disease with a very varied clini- glycosylated hemoglobin, 14.6%. His urine showed the fol- cal picture (1). Spread of to the from lowing: protein, –; glucose, 4+; ketones, 4+. Arterial blood the infective is uncommon. Attachment of gas while breathing room air showed the following: pH, vegetation to the chordae tendineae is also not common. 7.21; PCO2, 29.7 mmHg; PO2, 102.8 mmHg; base excess, – Here, we present an interesting case that focuses on the clini- –11.1 mmol/l; HCO3 ,14.1 mmol/l. Chest X-ray disclosed cal aspects of infective endocarditis with acute purulent . Electrocardiogram on admission showed ST pericarditis and hyperglycemia. elevation in leads I, II, III, aVF,V2–V6 (Fig. 1). Transthoracic echocardiography revealed attachment of a vegetation (12× Case Report 10 mm) to the chordae tendineae in the left ventricle, dilated inferior vena cava, and a small amount of pericaridial effu- On November 27, 2002, a 43-year-old unconscious man sion (Fig. 2). No evidence of valvular disease was detected. was admitted to our hospital with an elevated . Several Transesophageal echocardiography revealed no myocardial

From the Department of Internal Medicine and *the Department of Cardiovascular Surgery, National Hospital Organization Higashihiroshima Medical Center, Higashihiroshima Received for publication August 9, 2004; Accepted for publication December 28, 2004 Reprint requests should be addressed to Dr. Kenji Oki, the Department of Internal Medicine, National Hospital Organization Higashihiroshima Medical Center, 513 Jike, Saijo, Higashihiroshima 739-0041

666 Internal Medicine Vol. 44, No. 6 (June 2005) Infective Endocarditis with Diabetes

 

 

 

 

 

 

Figure 1. Electrocardiogram on admission showed ST elevation in leads I, II,

III, aVF,V2–V6.Aventricular extrasystole was present.

and . Intravenous administration of ampicil- lin (ABPC) 8.0 g/day, panipenem betamipron 2.0 g/day, 2.4 g/day and immune globulin 2.5 g/day was initiated. Since enlargement of the vegetation was observed, administration of intravenous heparin 10,000 U/day was ini- tiated on the second hospital day. Although laboratory data showed improvement in inflammatory reactions (WBC, 14,800/l; CRP, 9.10 mg/dl), echocardiography showed marked progression of the mass size to 38 by 34 mm and pendulation of the vegetation on the third hospital day (Fig. 3). Percutaneous pericardiocentesis was not performed be- cause of inadequate accumulation of pericardial fluid. Although we decided to perform an operation, we could not open the heart due to the accumulation of purulent pericar- dial fluid on the third hospital day (Fig. 4). After a large vol- ume of pus was removed, improvement of hemodynamics Figure 2. On admission, transthoracic echocardiographic imag- and inflammatory reaction in laboratory data were observed. ing of the apical three-chamber view showed attachment of a A culture yielded vegetation (arrows), 12 by 10 mm, to the chordae tendineae in aureus. Since pectoris had been suspected on a past the left ventricle and a little pericaridial effusion. treadmill test procedure, coronary angiogram was performed before surgery. Coronary arteries were normal. Transthoracic echocardiography showed obvious diminu- or periannular abscess, corresponding to the abnor- tion in the size of the vegetation on the fifth hospital day. mality in transthoracic echocardiography. hemolytic strep- Laboratory data showed the following: LDH, 1,886 IU/l; tococcus C species and were isolated Cre, 1.65 mg/dl; BUN, 48.0 mg/dl. A computed tomographic from two separate blood cultures and multiple plantar ulcers. scan of the abdomen revealed right renal infarction. There The arterial blood gas, urinalysis and plasma glucose find- was no evidence of of the other organs. Trans- ings indicated the presence of diabetic ketoacidosis. Isotonic thoracic echocardiography revealed no vegetation three intravenous fluids (7,000 ml) and intravenous regular insulin weeks after admission. WBC and CRP values improved (110 U) were administered as an initial therapy over a 24- gradually and returned to the normal range six weeks after hour period. The glucose level decreased to approximately admission. The oral , (500 mg/day) was 200 mg/dl on the second hospital day. Arterial blood gas was substituted for ABPC and panipenem betamipron eight pH 7.37, and had a base excess of –0.2 mmol/l. The findings weeks after admission (Fig. 5). His diabetes was treated by on physical examination, transthoracic echocardiography and human premix (70% neutral protamin Hagedorn/30% regu- electrocardiogram led to a diagnosis of infective endocarditis lar) insulin 30 U per day. Decayed teeth, fistula in the oral

Internal Medicine Vol. 44, No. 6 (June 2005) 667 OKI et al

infective endocarditis (2). According to their criteria, a de- finitive diagnosis of infective endocarditis can be easily made based on the findings in the echocardiogram and blood cultures. In addition, a diagnosis of acute pericarditis can be easily made from echocardiographic evidence of pericardial effusion and electrocardiographic evidence of ST elevation in multiple leads. Since Staphylococcus aureus was isolated from plantar ul- cers, arterial blood and pericardial effusion, a chain of infec- tion was suspected to be the pathogenesis. Spread of infec- tion to the pericardium from the infected endocardium could occur by one of the following pathways: hematogeneous spread, septic embolization of the coronary artery, or rupture of myocardial abscess or periannular abscess (3). However, the of acute pericarditis complicated with infective endocarditis is not common. In the present case, echocardi- ography showed no myocardial abscess or periannular ab- scess and coronary angiogram revealed no abnormalities. Therefore, it was speculated that septicemia resulting from plantar ulcers or intraoral infection caused the infective Figure 3. On the third hospital day, transthoracic endocarditis and acute pericarditis. Acute bacterial peri- echocardiographic imaging of the apical three-chamber view is commonly observed in patients who are immuno- showed attachment of a vegetation (arrows) markedly enlarged logically compromised (4). We suggest that severe hyper- to 38 by 34 mm and pendulated. glycemia might lead the patient to be immunocompromised, leading to development of infective endocarditis and acute purulent pericarditis. It is generally known that most cases with native-valve endocarditis are more likely to have cardiac valvular disease or congenital heart disease. The existence of cardiac damage may be important for the binding of bacteria to cardiac endo- thelial cells (5). Both Staphyrococcal endocarditis and  hemolytic streptococci endocarditis sometimes occur in pa- tients without preexisting cardiac damage (6–8). The vegeta- tion attached to the chordae tendineae without cardiac disease observed in the present patient was uncommon. We suggested that specific binding of the vegetation was medi- ated in part by the hypercoagulable state due to hyperglyce- mia. The American Heart Association has issued a general guidline for medical management of infective endocarditis (9). High doses of are needed. Prolonged parente- ral administration of a bactericidal antimicrobial agent or a combination of agents is currently recommended (1, 10–12). The initial treatment usually cannot await re- Figure 4. Marked accumulation of purulent pericardial fluid and pus was found. sults when the symptoms progressively worsen, so the physi- cian must choose drugs to cover the species of organisms most likely to be present. species, coagulase- negative staphylococci, Gram negative bacilli and fungi are cavity and plantar ulcers subsided. common bacteria found in infective endocarditis (1, 5, 13). In a recent series, staphylococci, and in particular Staphylo- Discussion coccus aureus, has become the most common cause of infective endocarditis with native-valve endocarditis. The diagnosis of infective endocarditis requires the inte- Staphylococcus aureus, once the most common causative gration of clinical, laboratory, and echocardiographic find- agent of acute purulent pericarditis by far, remains the single ings. In 1994, a group at Duke University proposed most frequent etiologic organism. However, there has been a standardized criteria for assessing patients with suspected large increase in pericarditis caused by Gram-negative

668 Internal Medicine Vol. 44, No. 6 (June 2005) Infective Endocarditis with Diabetes

Figure 5. Intravenous administration of ABPC 8.0 g/day, panipenem betamipron 2.0 g/day and clindamycin 2.4 g/day were initiated on admission. Transthoracic echocardiography showed obvi- ous diminution in the size of the vegetation on the fifth hospital day, after the vegetation had be- come markedly enlarged. and panipenem betamipron were reduced to half doses because of renal insufficiency due to embolization. WBC and CRP improved gradually and re- turned to normal ranges 6 weeks after admission. Amoxicillin (500 mg/day), an oral antibiotic, was substituted for ABPC and panipenem betamipron 8 weeks after admission.

aerobic bacilli (3). In addition, facultative bacteria is fre- to the vegetation. Furthermore, it was suggested that virulent quently implicated in pericarditis (14). Therefore, ABPC, pathogens, such as Staphyrococcus aureus and hemolytic panipenem betamipron and clindamycin were chosen in the streptococcus C species led to destruction of valvular or present patient. Each antibiotic has a high sensitivity to the intracardiac structures and hemodynamic deterioration (17, causative pathogen, Staphylococcus aureus and hemolytic 18). Surgical resection was considered to be desirable to de- streptococcus C species. crease the possibility of embolic complications and collapse. Surgical therapy is recommended for patients with However, we had to forego removal of the vegetation be- infective endocarditis who have congestive , cause of the accumulation of purulent pericardial fluid. In a perivalvular invasive disease, uncontrolled infection despite patient with acute purulent pericarditis, it is very difficult to maximal antimicrobial therapy, or episodes of embolization perform . There have been no reports of the with residual large vegetation (9, 15, 16). The highest inci- treatment of patients with infective endocarditis having a dence of embolic is observed in infective large vegetation, complicated with acute purulent peri- endocarditis due to hemolytic streptococcus C species as carditis. The surgical indication for infective endocarditis well as Staphyrococcus aureus,resulting in a high mortality with purulent effusion has not been assessed. It was fortunate rate (17–20). It has been reported that size and mobility of that the present patient was successfully treated despite hav- the vegetation are highly sensitive in identifying patients at ing a complication of kidney embolism without mortal risk for embolic events (15). In the present patient, the size embolization of the other organs. In patients with acute puru- of the mobile vegetation became progressively enlarged over lent pericarditis with tamponade, percutaneous pericardio- afew days despite maximal antimicrobial therapy. There- centesis is recommended to remove pericardial fluid (3). In fore, we believed that there was a high risk of embolism due the present case, removal of pus from the pericardium

Internal Medicine Vol. 44, No. 6 (June 2005) 669 OKI et al seemed to be useful to improve the hemodynamics and labo- 8) Lefort A, Lortholary O, Casassus P, et al. Comparison between adult ratory data. We wondered whether or not there are any alter- endocarditis due to beta-hemolytic streptococci (serogroups A, B, C, native treatments other than surgery for patients with similar and G) and streptococcus milleri: a multicenter study in France. Arch Intern Med 162: 2450–2456, 2002. conditions? In general, anticoagulant therapy has not been 9) Bonow RO, Carabello B, de Leon AC, et al. ACC/AHA guidelines for shown to prevent embolization (1). Since hyperglycemia, as the management of patients with . Executive sum- observed in the present case, is related to a hypercoagulated mary. A report of the American College of / American state, it may be important to assess the usefulness of antico- Heart Association Task Force on Practice Guidelines (Committee on agulant therapy in patients with hyperglycema. This calls for Management of Patients with Valvular Heart Disease). J Dis 7: 672–707, 1998. further controlled trials. 10) Bayer AS, Bolger AF, Taubert KA, et al. Diagnosis and management This case presents several interesting clinical observa- of infective endocarditis and its complications. Circulation 98: 2936– tions. The size of the vegetation was progressively enlarged 2948, 1998. despite maximal antimicrobial therapy. Infective endo- 11) Working Party of the British Society for Antimicrobial Chemotherapy. carditis complicated with acute purulent pericarditis that pre- Antibiotic treatment of streptococcal, enterococcal, and staphylococcal endocarditis. Heart 79: 207–210, 1998. vents cardiac surgery is uncommon. Attachment of the 12) Wilson WR, Karchmer AW, Dajani AS, et al. Antibiotic treatment of vegetation to the chordae tendineae is not common, either. adults with infective endocarditis due to streptococci, enterococci, We suggest that the immunocompromised and hyper- staphylococci, and HACEK . JAMA 274: 1706–1713, coagulable state due to severe hyperglycemia caused these 1995. conditions. It is necessary to keep in mind that infective 13) Nakatani S, Mitsutake K, Hozumi T, et al. Current characteristics of  infective endocarditis in Japan: an analysis of 848 cases in 2000 and endocarditis due to Staphylococcus aureus or hemolytic 2001. Circ J 67: 901–905, 2003. streptococcus C species with an immunocompromised state 14) Brook I, Frazier EH. Microbiology of acute purulent pericarditis. A 12- such as hyperglycemia may complicate acute purulent peri- year experience in a military hospital: Arch Intern Med 156: 1857– carditis that prevents cardiac surgery. 1860, 1996. 15) Mugge A, Daniel WG, Frank G, Lichtlen PR. Echocardiography in infective endocarditis: Reassessment of prognostic implications of References vegetation size determined by the transthoracic and the transesophageal approach. J Am Coll Cardiol 14: 631–638, 1989. 1) Mylonakis E, Calderwood SB. Infective endocarditis in adults. N Engl 16) Murtagh B, Frazier OH, Letsou GV. Diagnosis and management of JMed345: 1318–1330, 2001. bacterial endocarditis in 2003. Curr Opin Cardiol 18: 106–110, 2003. 2) Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of 17) Sanabria TJ, Alpert JS, Goldberg R, Pape LA, Cheeseman SH. infective endocarditis: utilization of specific echocardiographic find- Increasing frequency of staphylococcal infective endocarditis. Arch ings. Am J Med 96: 200–209, 1994. Intern Med 150: 1305–1309, 1990. 3) Sternbach GL. Pericarditis. Ann Emerg Med 17: 214–220, 1988. 18) Watanakunakorn C. Staphylococcus aureus endocarditis at a commu- 4) Shabetai R. Acute pericarditis. Cardiol Clin 8: 639–644, 1990. nity teaching hospital, 1980 to 1991. An analysis of 106 cases. Arch 5) Alestig K, Hogevik H, Olaison L. Infective endocarditis: a diagnostic Intern Med 154: 2330–2335, 1994. and therapeutic challenge for the new millennium. Scand J Infect Dis 19) Verhagen DW, van der Meer JT, Hamming T, de Jong MD, Speelman 32: 343–356, 2000. P. Management of patients with Staphylococcus aureus bacteraemia in 6) Thompson RL. Staphylococcal infective endocarditis. Mayo Clin Proc a university hospital: a retrospective study. Scand J Infect Dis 35: 459– 57: 106–114, 1982. 463, 2003. 7) Johnson CM. Staphylococcus aureus binding to cardiac endothelial 20) Venezio FR, Gullberg RM, Westenfelder GO, Phair JP, Cook FV. cells is partly mediated by a 130 kilodalton glycoprotein. J Lab Clin Group G streptococcal endocarditis and bacteremia. Am J Med 81: 29– Med 121: 675–682, 1993. 34, 1986.

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