A 44-year-old man with a 2-month A 44-year-old man with a 2-month history of weight loss, fatigue, history of weight loss, fatigue,

cough, and night sweatscough, and night sweats

Joe Kovaz, M.D.Joe Kovaz, M.D.

December 8, 2004December 8, 2004

No financial disclosuresNo financial disclosures

9/2/04 44 yo man with the following problems:

– Ischemic Heart Disease (stenting of right coronary artery 10/01)

– Ventricular Septal Defect and Atrial Septal Defect

– Tobacco Addiction (2 packs daily for many years)

– Type II Diabetes Mellitus

– Obstructive Sleep Apnea

– Hyperlipidemia

– Hypertension

– Chronic cellulitis/erysipelas of left leg

9/2/04

Discontinued all of his medications one week prior to his visit because: “They were killing me.”– Simvastatin 80 mg

– Niaspan 2000 mg

– Losartan/hydrochlorothiazide 100/25

– Aspirin 325 mg

– Atenolol 100 mg

– Spironolactone 25 mg twice a day

– Metformin 500 mg twice a day

– Flonase

Had multiple dental extractions done in early June while taking dicloxacillin 1 gram twice a day and benzathine penicillin 1.2 million units every four weeks. Had been on this regimen since 9/03.

Felt somewhat better after stopping his medications, but still had a cough and night sweats.

Past Medical History

Chronic cellulitis/erysipelas began in 10/02 after he was hit in the left leg with a sledge hammer by one son and a week later with a brick by another son.

Admitted for incision and drainage of an abscess of the left leg.

…had six additional episodes of cellulitis from 10/02 to 8/03 which responded to oral antibiotics, except for one episode requiring admission.

Past Medical History, continued

8/21/03 First seen by Dr. Vogelman, who

initiated treatment with dicloxacillin for recurrent cellulitis and terbinafine for tenia pedis.

9/4/03 Benzathine penicillin 1.2 million units

intramuscularly every four weeks was added for strep coverage.

Past Medical History, continued

Last seen by Dr. Vogelman on 8/26/04 who stopped antibiotics due to complete clearing of cellulitis/erysipelas.

Noted anemia (Hct 33) as well as a 2 month history of weight loss, fatigue, myalgias, and night sweats.

Physical Exam

Pulse: 112 bpm BP: 148/80 mmHg

Temperature: 99°F Chest: Clear

Heart: Harsh IV/VI systolic murmur along the left sternal margin, apex and base.

Well healed scar, left leg

Initial Lab and X-Rays

Sed Rate: 115

Normal PA and Lateral Chest Film/Sinus Series

Additional Lab and Imaging Studies

Initial blood culture grew Strep viridans (within 18 hours) followed by two subsequent sets which also grew Strep viridans (6 of 6 bottles)

Transthoracic echocardiogram—no vegetations. VSD and ASD noted.

Transesophageal echocardiogram—sub-pulmonic pedunculated mass in the RV outflow tract. Located where flow across the VSD hits the outflow track. Pulmonic regurgitation.

Hospital Course

Admitted and started on intravenous penicillin. Gentamycin was added later.

Infectious disease consult—Strep viridans probably due to dental work.

MIC Ceftriaxone .064 s Penicillin .064-.125 s

Discharged on Ceftriaxone 2 grams IV daily.

“I never knew I could feel this good.”

Learning ObjectivesLearning Objectives Recognize the protean signs and symptoms

associated with bacterial endocarditis

Become familiar with the common microorganisms which cause acute and subacute bacterial endocarditis

Become familiar with the Modified Duke Criteria for the diagnosis of infective endocarditis

Review the current recommendations for the treatment of, and prophylaxis for infective endocarditis

Definition Microbial infection of a cardiac valve or

mural endocardium

Mortality– Almost 100% in preantibiotic era– 10% streptococcal endocarditis– 35% staphylococcal endocarditis– 25-50% with prosthetic valve endocarditis

20,000-30,000 new cases/year primarily among newborn and elderly

Causes of Prosthetic Valve Endocarditis

Pathogenesis

Blood is driven from a high pressure area through a cardiac defect into a low pressure sink.

A platelet-fibrin aggregate forms in the low pressure sink.

During bacteremia, avirulent/virulent organisms adhere to the platelet-fibrin aggregate forming a vegetation.

Clinical presentations

Subacute bacterial endocarditis

– Duration of more than six weeks

Symptoms may begin insidiously and last for months

Fever, sweats, weakness, myalgias, arthralgias, malaise, anorexia, and fatigability are common

Subacute bacterial endocarditis, continued

May be caused by avirulent bacteria, such as streptococci which are part of the indigenous flora

Cutaneous manifestations– Petechiae-conjunctivae, oropharynx, skin

– Osler’s nodes—tender, purplish subcutaneous nodules in the pulp of the fingers

– Janeway lesions-nodular, nonpainful erythematous or hemorrhagic areas on the palms or soles.

Subacute bacterial endocarditis, continued

Musculoskeletal features—myalgias, arthralgias, arthritis 40-50%

Ocular findings—Roth spots—oval

white areas surrounded by a zone of hemorrhage 3-5%

Splenomegaly—15-30% with infarcts in 40% and abscesses in 5% of patients with SBE

Subacute bacterial endocarditis, continued

Renal manifestations

– Hematuria in 50%

– Embolic renal infarction—flank pain

– Membranoproliferative glomerulonephritis

Embolic phenomenon (cerebral or systemic)25-50%

Mycotic aneurysms 2-10%

Subacute bacterial endocarditis, continued

Neurological complications 30-40% due either to emboli or mycotic aneurysms

Cardiac findings– Murmur present in 90% of patients– Heart failure-usually due to involvement

of aortic or mitral valves– New conduction abnormalities due to

involvement of the membranous septum in the area of the AV node

Acute bacterial endocarditis

Organisms are more invasive (s. aureus,

s pneumoniae, gram negative bacilli) Onset is abrupt, with rigors and

temperatures over 102° F (duration less than six weeks)

Cutaneous manifestations, petechiae may be prominent, especially when caused by

s. aureus Emboli are common Metastatic infections-cause organ-specific

symptoms

Echocardiography 60% of vegetations can be detected

using transthoracic echocardiography

87-94% of vegetations can be detected with transesophageal echocardiography

Transesophageal echocardiography is indicated as the initial method for difficult to image patients, possible prosthetic valve infections, in patients with intermediate to high clinical suspicion or in patients for a high risk of complications