A case of infective endocarditis

By Dr P. Arul

M4, Prof P. Vijayaraghavan’s unit

46 year old male presented with c/o◦Fever 3 weeks duration◦Slurring of speech 1 day◦Weakness of left upper and lower limbs 1

dayHistory of present illness:

◦Fever 3 weeks duration Intermittent High grade Not associated with chills, rigors.

◦Patient suddenly developed an episode of sudden loss of consciousness which lasted for 2 minutes and recovered spontaneously, following which he noticed difficulty in standing and walking due to weakness of his left lower limb. His family members also noticed that his speech was slurred.

◦No h/o seizure◦No h/o bladder, bowel disturbance◦No h/o regurgitation of feeds

◦No h/o burning micturition, increased frequency.

◦No h/o abdominal pain, vomiting, diarrhea.

◦No h/o cough with expectoration, breathlessness

◦No h/o skin ulcers, rash, jaundice

Past history:◦Was diagnosed to have cardiac

valvular lesion (?RHD) 1 yr back and on drugs since then.

◦Not a known diabetic, hypertensive, epileptic, COPD, PT, IHD.

◦No previous similar episodes.Personal history:

◦Not a smoker, drinks alcohol occasionally

Family history:◦No family h/o cardiac ailment

Treatment history:◦Patient consulted a private

practitioner 1 yr back for reduced exercise tolerance and was evaluated for cardiac causes. Echo picked up mitral regurgitation and patient was put on penicillin prophylaxis along with T. lasix.

General Examination Conscious Oriented Afebrile No cyanosisNo clubbingNo pallorNot ictericNo pedal edema

No petichiaeNo Splinter

hemorrhagesNo Oslers nodeNo Janway lesionRetinal

hemorrhage+-Roth’s spot

CVS:◦S1, S2 heard, ◦A pan systolic murmur with a musical

quality heard in the mitral area, ◦P2 loud.

RS:◦Normal vesicular breath sounds

heardP/A

◦Soft, no organomegaly

CNS◦HMF

Conscious Orientation

Time + Place +

Dysarthria with Anomic Aphasia(difficulty in naming persons and objects)

Memory intact

◦Cranial nerves I-VI – normal VII – UMN type facial palsy on left side VIII-XII – normal

◦Motor system Grade 4/5 power in both left lower and

upper limb Deep tendon reflex brisk in the left side Tone – mild increase in the left side Babinski positive on the left side

◦ Sensory system: Normal

◦ Cerebellar functions: Normal

◦ Spine and cranium: Normal

◦ No meningeal signs Imp:- RHD – mitral regurgitation/

infective endocarditis/ embolic CVA – left hemiparesis

Investigations ECG – NSR, WNLCXR - NADCBC

◦ Hb 11.2g/dl◦ PCV 31◦ TC 8600◦ DC P74 L24 E2◦ ESR 4/12◦ Platelets 1.8 lakhs

Blood sugar 108Blood urea 24Sr. creatinine 0.9

Lipid profile:◦TC◦TGL◦LDL◦HDL

CT Brain:◦Normal

MRI:◦Multiple small infarcts in the frontal

lobe, parietal lobe and basal ganglia

Blood culture◦Sample A no growth◦Sample B no growth◦Sample C coagulase negative

StaphylococciRepeat blood culture (5th day):

◦coagulase negative StaphylococciEcho:

◦Mitral regurgitation – moderate◦Rupture of chordae tendinae◦Valvular vegitations+

Treatment Inj Vancomycin 1g IV BD x

4weeksInj Gentamycin 80mg BD x 5days

Cardiologist opinion:◦Continue antibiotics repeat echo

weekly for assessing reduction in size of vegetations.

Follow upRepeat blood culture (3rd week)

◦No growthECHO

◦Mitral regurgitation (moderate)◦Rupture of chordae tendinae

Discussion Infective endocarditis is microbial infection of

cardiac valves.The features of infective endocarditis have

changed dramatically during the past three decades.

Patients with classic manifestations such as fever, splenomegaly, changing murmurs, signs of peripheral embolization and multiple positive blood cultures have become distinctly unusual.

Originally endocarditis was classified as acute or sub-acute depending on the duration of the disease.

Patients dying within 8 weeks were said to have acute form while those surviving more than 8 weeks were said to have sub-acute form.

Patients with endocarditis due to staphylococcus aureus, Neisseria meningitidis, Hemphilus influenzae or Streptococcus pyogenes were considered to have the acute form.

Streptococcus viridans or staphylococcus epidermidis were associated with the sub acute form.

Incidence 0.16 to 5.4 per 1000 hospital

admissions.Mean age is between 55 and 57

years.Uncommon in the first decade.When it occurs in infants it is of the

acute variety involving normal cardiac valves.

Men predominate with a ratio of 2:1 to as high as 9:1 in older age group.

Predisposing conditions 72% of patients have a preexisting

structural cardiac abnormality.Isolated valvular aortic stenosis was the

congenital defect most often associated with IE followed by VSD, TOF, idiopathic subaortic stenosis and ASD (uncommon).

In patients with valvular lesion mitral valve is involved most often followed by aortic valve, tricuspid valve involvement is uncommon (1%).

Cardiac prosthetic valves and parentral narcotic drug constitutes a major risk for IE.

Relative risk of various predisposing conditionsHigh risk Intermediate risk Low/negligible

risk

Prosthetic valves Mitral valve prolapse

Degenerative heart disease

Aortic valve disease

Mitral stenosis ASD

Mitral regurgitation Tircuspid valve disease

Luetic Aoritis (syphiis)

PDA HOCM CABG

AV fistula Calcific aortic stenosis

Surgically corrected congenital lesions

VSD TOF Pacemakers

Coarctation of Aorta

Non valvular intra-cardiac prosthesis

Previous IE

Marfan’s syndrome

Etiology Native valves Narcotic addicts Prosthetic valves

Streptococcus viridans

30-40

Saphylococcus aureus

50-60

Saphylococcus Epidermidis

20-30

Saphylococcus aureus

10-30

Streptococci 8-15 Saphylococcus aureus

15-20

Saphylococcus Epidermidis

1-3 Saphylococcus Epidermidis

2-5 Streptococcus Viridans

5-20

Enterococci 5-15 Enterococci 8-10 Enterococci 5-10

Other streptococci

15-20

Other streptococci

10-15

Other streptococci

1-5

Gram -ve bacilli 2-10 Gram -ve bacilli 4-8 Gram -ve bacilli

10-20

Fungi 2-4 Fungi 4-5 Fungi 5-15

Culture negative

5-10 Culture negative

5-8 Culture negative

<5

Pathogenesis Source of infection

◦The bacteremia or fungemia that initiates the infection is transient and arises form the oropharynx, genitourinary or gastrointestinal mucosa

◦Bacteremia following dental procedures occurs in 60% patients, 85% following suction abortion, 30% following tonsillectomy , 16% following nasotracheal intubation, 15% following bronchoscopy and10% after UGI scopy.

◦Staphylococcus aureus endocarditis are more likely to have a demonstrable source of infection.

Invasive predisposing factors to bacterial endocarditisDental procedures

Oral and upper respiratory tract surgery

Certain gastrointestinal procedures

Genitourinary surgery

Cardiac surgery

Certain trauma

Alimentation catheters in the right heart

Intravenous drug use

Cardiac pathologyEndocarditis develops following

implantation of a microorganism on a preexisting sterile thrombotic vegetation present at a point of structural endocardial abnormality.

It has been shown experimentally that bacteria are often deposited in areas of high blood flow velocity. Consequently vegetations develop more frequently in a regurgitant valve.

Valve affected Site of vegetation/complication

Mitral valve Along chordae tendinae toward papillary muscle causing their rupture

Aortic valve Develop ring abscess

VSD Right ventricular wall, the site of jet impact

Regurgitant mitral lesion Wall of left atrium in the area termed MacCallum’s patch

Regurgitant Aortic lesion Chordae tendinae of anterior mitral leaflet

Extracardiac pathologySystemic embolism is reported to

occur in over 50% cases in autopsy studies.

Most common sites are kidneys, skin, spleen, eye and CNS.

There is increasing evidence to show that embolic phenomena actually represent “immune complex” deposition in small systemic arteries.

Clinical manifestationsSymptoms %

Fever 84

Chills 41

Weakness 38

Dyspnoea 36

Sweats 24

Anorexia 24

Malaise 24

Cough 24

Skin lesion 21

Stroke 18

Nausea, vomiting 17

Chest pain 16

Physical findings %

Heart murmurs 89

Fever 77

Embolic events 50

Skin manifestations 50

Splenomegaly 28

Septic complications 19

Mycotic aneurisms 18

Glomerulonephritis 15

Digital clubbing 12

Retinal lesions 9

Heart murmurs◦Was the sine qua non for the diagnosis◦It has been found that 15% don’t have

murmurs at initial diagnosis, however most develop a murmur during the course of the disease

◦Changing murmurs – factors other than valvular integrity like change in cardiac output, temperature, hematocrit may play a role. However new onset regurgitant murmur in a setting of acute sepsis is virtually diagnostic.

Cutaneous manifestations◦ Petichiae (20-40%)◦ Subcunjunctival and subungual splinter

hemorrhages due to lipid microembolism.◦ Osler nodes

Tender, purplish erythematous papules in pulp of distal fingers

Due to hypersensitive angitis – cultures are negative

◦ Janeway lesions Erythematous, non-tender nodules on palms or soles.

◦ Clubbing found only in 10-20%.Ocular manifestations

◦ Roth spot- flame shaped hemorrhage occasionally takes the form of cotton wool spot.

Complications Congestive heart failureExtravalvular cardiac

manifestationsSystemic and pulmonary

embolismMycotic aneurismNeurologic – stroke,

neuropsychiatric syndromesRenal – glomerulonephritis, renal

infarctsHematological – anemia, TTP

Diagnosis – duke’s criteriaMajor Criteria1. Positive blood culture

Typical microorganism for infective endocarditis from two separate blood cultures or

Persistently positive blood culture, defined as recovery of a microorganism consistent with infective endocarditis from blood cultures drawn >12 h apart or

Single positive blood culture for Coxiella burnetii or phase I IgG antibody titer of >1:800

2. Evidence of endocardial involvement◦ Positive echocardiogram

Oscillating intracardiac mass on valve, or Abscess, or New partial dehiscence of prosthetic valve, or

◦ New valvular regurgitation

Minor Criteria 1. Predisposition:

◦ Predisposing heart condition or ◦ Injection drug use

2. Fever ≥38.0°C (≥100.4°F) 3. Vascular phenomena:

◦ Major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions

4. Immunologic phenomena: ◦ Glomerulonephritis, Osler’s nodes, Roth’s spots, Rheumatoid factor

5. Microbiologic evidence: ◦ Positive blood culture but not meeting major criterion as noted

previously or◦ Serologic evidence of active infection with organism consistent

with infective endocarditis

Documentation of two major criteria, of one major and three minor criteria, or of five minor criteria allows a clinical diagnosis of definite endocarditis

Treatment -medical

Surgical treatment

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