INFECTIVE ENDOCARDITIS PRESENTING AS MULTIPLE SEPTIC ARTHRITIS

Sibin*, Dileep.D**Sreejith.R***,Hitha.B***, Mohamedshaan****,Geetha.P****,P.K.Sasidharan*****

ABSTRACT

Infective endocarditis (IE) has been recognized as a distinct clinical entity for at least a century. A myriad of complications can result from this infection and occur in the majority of patients with IE.There are lots of articular manifestations of infective endocarditis including aseptic polyarthritis, typically involving the major joints, as well as vertebral osteomyelitis, low back pain (inflammatory or non-inflammatory), myalgiaand septic arthritis.It is very uncommon for infective endocarditis to present as multiple septic arthritis. Here we are reporting a case of Aortic valve infective endocarditis in a patient with chronic kidney disease presenting as multiple septic arthritis which is rarely reported.

Key words: Infective endocarditis; Multiple septic arthritis; Aortic valve

INTRODUCTION

Acute septic arthritis, involving one or more joints, may be the first clue to the presence of IE in a small percentage of patients. IE should be strongly considered in selected cases of septic arthritis1:

  1. When infections spontaneously arise in joints of the axial skeleton (eg, sacroiliac, pubis, or manubriosternal).
  2. When organisms with a known propensity to cause IE (eg, S. aureus, viridans streptococci or non-group A ß-hemolytic streptococci) grow from a joint aspirate, particularly in patients without a history of recent surgery, joint infection or trauma.
  3. When multiple joints are infected.

In our patient rapidly developing multiple septic arthritis was the clue towards a diagnosis of IE.

CASE REPORT

50 year old male, tile worker by profession, presented with pedal edema,facial puffiness for 1 week; fever, dysuria,decreased urine output for 2days and breathlessness for 1day. Complaints were of insidious onset and started initially as pedal edema followed by facial puffiness.Two days before admission, patient had high grade fever with chills, associated with severe dysuria and had decreased output at that time.Oneday back,he developed sudden onset of severe breathlessness with severe orthopnea. There was no history ofhematuria,frothing of urine, loin pain,chest pain,palpitations,cough or expectoration. He had history of hypertension for 2 years, had anterior wall myocardial infarction 5 years back. He was being treated as ischemic chronic kidney disease, diagnosed 1 year back. There was no history of similar illness in the past. He was an ex smoker and ex alcoholic stopped 5 years back.

On examination, there was pallor,bilateral pitting pedal edema, blood pressure was 160/100 mm Hg and there were right femoral and right subclavian bruits. JVP waselevated; there was cardiomegaly andan ejection systolic murmur at aortic area and basalcrepitations. There was no hepatosplenomegaly or free fluid in the abdomen. A Clinical diagnosis of acute pulmonary edema,acute on chronic kidney disease precipitated by urinary tract infection with underlying left ventricular dysfunction, calcific aortic stenosis and hypertension was made. Investigations showed Hemoglobin 7.2g/dl, total count 11900/µl, differential count P72 L21, platelet count 1.8lakhs,MCV81fl,ESR80 mm/1st hour and RDW14.3%.Urine examination showedpus cells10-12/HPF and RBC 6-8/HPF.His renal function was impaired with a Blood urea of 94 mg% and serum Creatinine 5.6 mg%. His serum electrolytes and liver function tests were within normal limts.ECG showed old anterior wall myocardial infarction along with left ventricular hypertrophy.

He was treated with diuretics and antibiotics. Patient improved with treatment. On fourth day, he developed right knee joint pain with gradually developed effusion of the knee joint. He had severe joint tenderness with fluctuation and he was febrile. Joint aspiration done showed purulent material and investigations were consistent with septic arthritis. Antibiotics were started according to culture and sensitivity. Patient improved with treatment. But one week later he began to develop left knee joint effusion and severe pain. Joint aspiration done showed total count 400 cells/µl with differential count P60 L40, with protein1.1g/dl, sugar-106mg%,gram stain was negative and culture was sterile. This was also suggesting septic arthritis of left knee. Considering his examination findings of ejection systolic murmur in aortic area with underlying infective focus like UTI with septic arthritis of bilateral knee joints, we strongly considered the possibility of infective endocarditis. A transthoracic echo was done which showedAortic stenosis and Aortic regurgitation with doubtful vegetation on non coronary cusp of aortic valve. A Trans Esophageal echo (TEE)showed 2x1 mm sessile structure overlying sclerosed aortic valve. Considering his clinical problems we strongly considered the possibility of aortic valve endocarditis with septic emboli leading to multiple septic arthritis. Therefore the final diagnosis was kept as Acute pulmonary edema,Acute onchronic kidney disease due to UTI,Acute aortic valve infective endocarditis with septic arthritis both knee joints (septic emboli),Aortic sclerosis and regurgitation,with left ventricular dysfunction and Systemic hypertension. The pulmonary oedema could have occurred due to the recent onset aortic regurgitation due to endocarditis. He was treated with antibiotics with adequate renal support for 4 weeks. Patient improved with treatment and was stable at time of discharge.

DISCUSSION

Musculoskeletal manifestations of infective endocarditis (IE) are particularly hard to diagnose,and until recently their frequency has been underestimated. Recent studies have shown an incidence of 19 to 28% of patients with IE have musculoskeletal manifestations2, though this phenomenon was partly or completely overlooked in earlier studies. The main peripheral manifestations were arthralgia,sometimes sequentially affecting several joints, and less often arthritis.An acute, sterile synovitis or tenosynovitis as well as myalgias are also common in bacterial endocarditis.Joint or bone infection are present in 15% of cases in some series2. These infections are much more common in intravenous drug users and may involve more than one joint.Arthralgia and arthritis preferentially involved the major joints; they showed rapid and complete resolution with antibiotics. The pathogenesis of arthralgia and arthritis in infective endocarditis is somewhat obscure. The hypothesis of septic foci in the joints would appear to be contradicted by the usual presence of sterile synovial fluid as well as by the rapid resolution of peripheral manifestations without radiological sequelae. Nevertheless, only few cases of septic arthritis during IE were reported in past, some of them confirmed by examination of synovial fluid and some cases by culture of a biopsy fragment of synovium, when the fluid was sterile.In our patient also presence of septic arthritis in multiple joints was confirmed by examination of synovial fluid, but culture of synovial fluid was sterile. The aortic valve and its adjacent ring are more susceptible to abscesses and the complications of paravalvular extension of infection which can lead to pyopericardium or acute aortic regurgitation; this kind of occurrence is less commonly seen with mitral valve and ring3,4.

In conclusion, Acute septic arthritis, involving one or more joints, may be the first clue to the presence of IE in a small percentage of patients,although it is very rarely reported.

REFERENCES

  1. Denis Spelman, Daniel J Sexton; Complications of infective endocarditis cmbi.bjmu.edu.cn
  2. Sapico FL, Liquete JA, Sarma RJ. Bone and joint infections in patients with infective endocarditis: review of a 4-year experience. Clin Infect Dis1996; 22: 783–87.
  3. Arnett, EN, Roberts, WC. Valve ring abscess in active infective endocarditis: Frequency, location, clues to clinical diagnosis from the study of 95 necropsy patients. Circulation 1976; 54:140.
  4. Omari, B, Nelson, RJ, Shapiro, S, et al. Predictive risk factors for periannular extension of native valve endocarditis. Clinical and echocardiographic analyses. Chest 1989; 96:1273.