INFECTIVE

ENDOCARDITIS
Objectives
GENERAL SPECIFIC
To present and discuss a To identify the different etiologies
and clinical manifestation of Infective
case of Infective Endocarditis
Endocarditis  To discuss the pathogenesis of
Endocarditis
 To present a comprehensive
diagnostic and therapeutic
management plan
CASE
PRESENTATION
General Data
M.G, 30 year old, male
Married,
Roman catholic
Filipino
 work as an Engineer in plastic factory
Resides in Manila
Chief Complaint
Fever and generalized skin rashes
 HISTORY OF PRESENT ILLNESS
• Complained of malaise and poor appetite
• He also mentioned of having asthma attack which was well controlled by inhalers.
1 week PTA • No other symptoms noted. No consult done.

• Patient suffered from another attack of asthma, which was relieved by the prescribed
bronchodilator inhalers.
• He also had a brief episode of confusion following the attack.
1 day PTA
• No other symptoms were noted. No consultation was done.

• Patient was rushed to emergency department for high grade fever associated with
generalised body rash.
On the day of • No medication was taken.
consult
PAST MEDICAL HISTORY
(-) HTN
(-) DM
(+) Asthma, maintained on varying doses of prednisolone tabs
(-) Heart disease
(-) Rheumatic fever
(+) Atopic dermatitis, topical 2.5% hydrocortisone cream
FAMILY MEDICAL HISTORY
(-) HTN
(-) DM
(+) ASTHMA : PATERNAL
PERSONAL AND SOCIAL
HISTORY
(-) smoking
(-) alcohol
(-) iv drug use
Occupation : engineer in plastic factory
 REVIEW OF SYSTEM
General: (+) easy fatigability, (+) dizziness, (+) loss of appetite, (-) weight loss,
Integument: (+) rashes, (-) pallor, (-) pigmentations, (+) pruritus
Head and Neck: (-) stiffness, (-) masses, (-) swelling, (-) headache, (-) dizziness
Eyes: (-) eye redness, (-) use of corrective lenses, (-) discharge, (-) eye pain, (-) blurring of vision (-)
inecteric sclera
Ears: (-) difficulty hearing, (-) otalgia, (-) tinnitus, (-) vertigo
Nose and Sinuses: (-) colds, (-) mucoid discharge, (-) epistaxis, (-) obstruction
Mouth and Throat: (-) hoarseness, (-) sore throat, (-) dysphagia, (-) toothache, (-) ulcers, (-) tongue
fasciculation
Respiratory: (-) cough, (-) hemoptysis, (-) dyspnea, (-) tachypnea, (-) pleuritic chest pain
Cardiovascular: (-) angina, (-) palpitations, (-) orthopnea, (+) dyspnea
 REVIEW OF SYSTEM
Gastrointestinal: (-) vomiting, (-) nausea, (-) hematemesis, (-) diarrhea, (-) abdominal pain, (-)
constipation, (-) anorexia
Genitourinary: (-) increased frequency, (-) hematuria
Hematologic: (-) easy bruising, (-) easy bleeding
Endocrine: (-) polyuria, (-) polyphagia, (-) polydipsia, (-) heat/cold intolerance
Musculoskeletal: (-) joint pains, (-) back pains, (-) muscle aches, (-) fractures, (-) bipedal
edema
Neurologic: (-) syncope, (-) convulsions/seizures, (-) tremors, (+) one-sided weakness, (-)
slurring of speech
Autonomic: (-) fecal incontinence, (-) urinary incontinence
 PHYSICAL EXAMINATION
General survey: drowsy, weak looking, brought on stretcher
Vital signs:
BP 145/85 mmhg
H.R 110 bpm
RR 26 cpm
Temp 39◦C
O2 sats 90%
 PHYSICAL EXAMINATION
SKIN: (+) erythematous maculopapular non blanching rash, (-) scars, (-) lesions, (+) dry, (+) scales

HEENT: anicteric sclera, pink palpebral conjunctiva, moist lips, (-) tonsillar enlargement, no palpable
mass, (-) cervicolymphadenopathy, (-) jugular vein distention

Respiratory: Symmetrical chest expansion, (-) Retractions, (-) rhochi, (+) crackles , bibasal
Cardiovascular: adynamic precordium, (-) jugular vein distention, regular rhythm, (+) Grade 3/6
pansystolic murmur, radiated to the left axilla (-) s3 gallop, apex beat at 5th intercostal space, left of
mid clavicular line.
Abdomen : round, normoactive bowel sounds, soft, (+) tenderness , (+) palpable spleen edge
Extremities: (+) painful, red lesions on the soles (osler’s node), diminished peripheral pulses, CRT< 2
seconds, (-) edema, (+) rt leg weakness
Neurology: (+) rt ankle clonus, (-) sensory deficit, (+) palmar extensor stiffness
 Work up / Laboratory tests
Hb : 15.7 gm/dL
WBC : 14.5 x 10,000 /microL
Platelets : 50,000 x /microL
ESR : 15mm/hr
CRP : 292.9 mg/L (elevated)
Serum Na : 128 mmol/L (dec)
Serum K : 3.3 mmol/L
BUN : 7.5 mmol/L (elevated)
Crea : 207 micromol/L (elevated)
ECG, tee, Imaging studies & Culture studies
12 L ECG : sinus tachycardia; LVH
TEE : Mitral valve vegetation, severe MR and normal ejection fraction.
Chest X-ray : No significant findings
CT brain : no abnormal findings
MRI brain : multiple areas of White matter abnormality suggestive of embolism
around the periventricular area.
Blood culture : 2 sets showed (+) S aureus sensitive to gentamicin and
flucloxacin
SALIENT FEATURES
 30/M
 TEE : Mitral valve vegetation
 history of asthma, atopic dermatitis  12 L ECG : sinus tachycardia; LVH
Fever (39◦C ) and General skin  Blood culture : 2 sets showed
rashes (+) S aureus
 drowsy
 pansystolic murmur
Splenomegaly
Right Leg Weakness power (3/5)
 (+) Osler’s Node
DIFFERENTIAL DIAGNOSIS
RULE IN RULE OUT
Infective Endocarditis Fever, confusion,
pansystolic murmur, (+)
Osler nodes
Lobar pneumonia Fever, myalgia, cough, (-) chest X-ray, (-) sputum
fatigues, culture
(-) joint pain, (-)
Rheumatic fever Fever, cardiac murmurs rheumatoid factor, (-)
h/o sore throat
INITIAL WORKING DIAGNOSIS
Native valve Endocarditis due to S. aureus;
Atopic Dermatitis
Bronchial Asthma, Controlled
DISCUSSION
 INFECTIVE ENDOCARDITIS
IE- is a microbial infection of the endothelial surface
of the heart
Vegetations-
◦prototypic lesion of infective endocarditis,
◦is a mass of platelets, fibrin, microcolonies of microorganisms
◦ and scant inflammatory cells
Commonly involves:
◦Native or prosthetic valves
◦Low pressure side of the ventricular septum -site of the defect
◦Endocardium being damaged by aberrant jets of blood
◦Foreign bodies and intracardiac devices
CLASSIFICATION OF IE
Temporal evolution
Site of infection
Cause of infection
Predisposing risk factor
 Injection drug user
 Association with health care
CLASSIFICATION OF IE based on evolution
ACUTE ENDOCARDITIS SUBACUTE ENDOCARDITIS
Damage rate of cardiac Rapidly destroys cardiac Slowly
structures structures

Hematogenous seeding Seeds extracardiac structures Rarely Metastasizes

Untreated Death within a week Better than Acute IE,

Gradually progressive unless
complicated by a major embolic
event or a ruptured mycotic
aneurysm
 ETIOLOGY
Primary portals of entry: oral cavity, skin and upper respiratory tract
oViridans streptococci,
oStaphylococci, and
oHACEK organisms (Haemophilus species, Aggregatibacter species,
Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae)

Streptococcus gallolyticus originates from the gastrointestinal tract,

where it is associated with polyps and colonic tumors
Enterococci enter the bloodstream primarily from the genitourinary
tract
Classification of IE based on site of infection
NATIVE VALVE ENDOCARDITIS PROSTEHETIC VALVE
ENDOCARDITIS
Etiologies Staphylococcus aureus, Coagulase (-) staphylococci,
coagulase-negative staphylococci Facultative gm (-) bacilli,
(CoNS), and enterococci Diphtheroids, fungi
Community acquired (+) LATE PVE: >12 months after surgery

Health care associated Iatrogenic procedures EARLY PVE: occurs < 2 months of
(nosocomial) surgery
Delayed onset- 2 to 12 months
caused by CoNS, nosocomial S.
aureus
 ETIOLOGY
Injection drug use–associated
oinvolving the tricuspid valve,
ois commonly caused by S. aureus, resistant to methicillin
HIV infection in drug users does not significantly influence the causes of endocarditis
5 to 15% of patients with endocarditis have negative blood cultures due to prior antibiotic
exposure
Culture negative Infective Endocarditis
oFastidious organisms (S. Granulicatella and Abiotrophia species),
oHACEK organisms
oCoxiella burnetii
oBartonella species
oTropheryma whipplei causes an indolent, culture negative, afebrile form of endocarditis
PATHOGENESIS
Unless it is injured the endothelium is resistant to infection

 NBTE (non bacterial thromboendocarditis)

platelet fibrin thrombus

Endothelial injury Hypercoagulable state

• High velocity jet
• On the low pressure side
of a cardiac structural
lesion
PATHOGENESIS
PATHOGENESIS
NBTE (non bacterial thromboendocarditis)
arises as a result of a hypercoagulable state
Also called as marantic endocarditis
o uninfected vegetations seen in patients with malignancy and chronic
diseases
obland vegetations complicating systemic lupus erythematosus and the
antiphospholipid antibody syndrome (APAS).
PATHOGENESIS
Most common lesions resulting in NBTE:
◦ Mitral regurgitation (MR)
◦ Aortic stenosis (AS)
◦ Aortic regurgitation (AR)
◦ Ventricular septal defect (VSD)
◦ Patent Ductus Arteriosus (PDA)
◦ Tetralogy of Fallot (TOF)
◦ Degenerative heart disease- aortic sclerosis
PATHOGENESIS
Organism enter through the skin or sites of focal infection then enter the bloodstream

If resistant to the bactericidal activity of the serum and the microbicidal activity peptides from
the platelets

Adhere to the endothelium or exposed subendothelial tissue, attached to NBTE
Facilitate Adherence:
◦ Microbial surface components recognizing adhesin matrix molecules
◦ Fibronectin- binding proteins on Gm(+) bacteria ex. S. aureus
◦ Clumping factor- S. aureus
◦ Glucans or FimA – Streptococci
 PATHOGENESIS
Proliferation of the organism

Induce a procoagulant state by eliciting tissue factor from monocytes and
or from endothelium

Fibrin deposition, initiation of the coagulation cascade, platelet aggregation

Infected vegetations
CLINICAL MANIFESTATIONS
ACUTE ENDOCARDITIS SUBACUTE ENDOCARDITIS

Etiologies S. aureus, B hemolytic Viridans streptococcus,

streptococci, pneumococci enterococci, HACEK group,
Bartonella sp, Coxiella
burnetti, CoNS

Pattern of fever High Grade, (39.4-40◦C) Low grade, rarely exceeds

39.4oC

Murmurs heard on (+)abrupt, 85% of the cases (+) takes time to develop
presentation (auscultation) (-) Absent, normal valve
CLINICAL MANIFESTATIONS
HEART FAILURE
ABSCESS FORMATION
*myocardial infarction due to emboli occur in 2% of patients
Non-Cardiac Manifestation
ACUTE ENDOCARDITIS SUBACUTE ENDOCARDITIS
(+)More progressive if the AV gradual
is involved than the MV
(+)Valvular dysfunction leads
to murmurs
(+)Intracardiac fistula
(+) intracardiac fistulae with gradual
new murmurs
(+)heart block, when abscess
burrow and interrupt the
conduction system
(+) subungual hemorrhage, rarely
S.aureus
(+) Osler’s nodes, S.aureus
CLINICAL MANIFESTATIONS
Non- cardiac manifestations:
◦ Related to duration of illness
◦ Subungual hemorrhages
◦ Janeway lesions
◦ Roth’s spot
◦ Osler’s nodes
◦ Conjunctival petechiae
CLINICAL MANIFESTATIONS
Non- cardiac manifestations:
◦ Related to duration of illness
◦ Subungual hemorrhages
◦ Janeway lesions
◦ Roth’s spot
◦ Osler’s nodes
linear and black and affect the
◦ Conjunctival petechiae distal third of the fingernail – 20%
CLINICAL MANIFESTATIONS
Non- cardiac manifestations:
◦ Related to duration of illness
◦ Subungual hemorrhages
◦ Janeway lesions
◦ Roth’s spot
◦ Osler’s nodes
◦ Conjunctival petechiae
Non-tender, painless, small hemorrhagic
macular/nodular lesions on the palms or soles.
CLINICAL MANIFESTATIONS
Non- cardiac manifestations:
◦ Related to duration of illness
◦ Subungual hemorrhages
◦ Janeway lesions
◦ Roth’s spot
◦ Osler’s nodes
Retinal hemorrhages with pale center
◦ Conjunctival petechiae composed of coagulated fibrin caused by
immune complex mediated vasculitis via
fundoscopy
CLINICAL MANIFESTATIONS
Non- cardiac manifestations:
◦ Related to duration of illness
◦ Subungual hemorrhages
◦ Janeway lesions
◦ Roth’s spot
reddish, purple, tender erythematous nodules
◦ Osler’s nodes found distal pad of the finger/toes due to
immune complex deposition
◦ Conjunctival petechiae
CLINICAL MANIFESTATIONS
Non- cardiac manifestations:
◦ Related to duration of illness
◦ Subungual hemorrhages
◦ Janeway lesions
◦ Roth’s spot
◦ Osler’s nodes
◦ Conjunctival petechiae
CLINICAL MANIFESTATIONS

• Febrile – most common

• Fever may be absent
o Elderly
o Severely debilitated
o renal failure
CLINICAL MANIFESTATIONS
• Neurologic symptoms- occur 40% due to embolic strokes
o Meningitis/microabscess (S.areus endocarditis)
o Intracranial hemorrhage due to hemorrhagic infarcts;
o Ruptured mycotic aneurysms (focal dilatation of the
arterial wall that have been weakened by infection in the
vasa vasorum or where septic emboli have been lodged)
o Seizures
o Encephalopathy (15-35% of cases)
CLINICAL MANIFESTATIONS
Renal Manifestation
•Due to immune complex deposition
oGlomerulonephritis
oRenal dysfunction
•Flank pain and hematuria- due to emboli but rarely cause
renal dysfunction
CLINICAL MANIFESTATIONS
Manifestations of Specific Predisposing Conditions
•50% of injection drug users
oInvolvement of the TV
oFever, no murmur
oCough, pleuritic chest pain, nodular pulmonary infiltrates
oOccasional pyopneumothorax
•CIED endocarditis
o fever, minimal murmur, and pulmonary symptoms due to septic
emboli
DIAGNOSIS OF
INFECTIVE ENDOCARDITIS
DUKE CRITERIA

Definite endocarditis is defined by the

documentation of either:

- Two MAJOR criteria

- One MAJOR criterion and three MINOR
criteria
- Five MINOR CRITERIA
BLOOD CULTURE
Three 2-bottle blood culture sets, separated from one
another by at least 2 hr, should be obtained from different
venipucture sites over 24 hr.
If the cultures remain negative after 48-72 h, two or three
additional blood culture sets should be obtained.
NON BLOOD CULTURE TEST
Serologic tests: Brucella, Bartonella, Legionella, Chlamydia
psittaci, and C. burnetti.
Microscopic examination with special stains
Polymerase chain reaction (PCR) recovery of microbial DNA
or DNA encoding the 16S rRNA (bacteria) or 28S rRNA
(fungi)
CARDIAC IMAGING
Transthoracic echocardiography (TTE)
◦ Noninvasive and exceptionally specific
◦ Unable to image vegetations <2mm in diameter
◦ When initial results are negative, this warrants repeating the test in
7-10 days
◦ The optimal method for the diagnosis of PVE and CIED
endocarditis; detection of myocardial abscess, valve perforations,
or intracardiac fistulae
CARDIAC IMAGING
CARDIAC IMAGING
OTHER TEST
CBC, Creatinine, Liver function tests, Chest x-ray, and ECG
Erythrocyte sedimentation rate, C-reactive protein,
rheumatoid factor, and circulating immune complex titer –
commonly increased in endocarditis
Cardiac catheterization – assess coronary artery patency
APPROACH TO ECHOCARDIOGRAPHIC
EVALUATION OF PATIENTS WITH SUSPECTED
ENDOCARDITIS
TREATMENT
Antimicrobial Therapy
● Elimination of bacteria in the vegetation
● Bactericidal and prolonged
● Knowledge of susceptibility of causative microorganism and
other considerations
● Initiating empirical treatment
● The duration of therapy is measured from the time blood
cultures become negative
 CLASS MOA Clinical Use Adverse
Effects
Beta lactams Inhibit bacterial growth by Activity against gram positive organisms, gram negative Hypersensitivity
(Penicillin, Ampicillin, Oxacillin, interfering with the cocci, and non-B-lactamase producing anaerobes. Little
Nafcillin, Piperacillin) transpeptidation reaction of a activity against gram negative rods. Susceptible to hydrolysis
bacterial cell wall synthesis. by B-lactamases.

Glycopeptide (Vancomycin, Inhibits cell wall synthesis by Bactericidal for gram positive bacteria; active against gram Mostly minor and
Teicoplanin) binding to D-Ala-D-ala positive anaerobes reversible: chills and fever
terminus of nascent
peptidoglycan

Novel cyclic lipopeptide Binds to cell membrane via Similar to Vancomycin; active against vancomycin-resistant Myopathy, allergic
(Daptomycin) calcium dependent insertion organisms; rapid bactericidal activity compared to pneumonitis
of its lipid tail, causing Vancomycin
depolarization and cell death.
 CLASS
Cephalosporins (Ceftriaxone,
Cefotaxime, Ceftaroline)
Aminoglycosides (Streptomycin,
Gentamicin, tobramycin)
Antimycobacterial (Rifampin)
MOA
Similar to penicillins, stable to
many bacterial lactamases,
broad spectrum activity
Irreversible of protein
synthesis; binds to specific
30S-subunit ribosomal
proteins
Binds to B subunit of bacterial
DNA-dependent RNA
polymerase - inhibits RNA
synthesis
Clinical Use Adverse
Effects
Active against gram positive cocci; Ceftriaxone and Hypersensitivity reaction,
Cefotaxime have expanded gram negative coverage, able to local irritation,
cross BBB; hydrolyzed by constitutively produced AmpC B thrombophlebitis,
nephrotoxicity
lactamase thus not reliable against enterococci; most active
against penicillin-non-susceptible strains of pneumococci.
Ceftaroline have activity against enterococci.
Mostly used against aerobic gram-negative bacteria; used in Ototoxic and nephrotoxic
combination with B-lactam to extend coverage to gram
positive pathogens; combined with penicillin for bactericidal
activity against enterococcal endocarditis
Combined with second agent against staphylococcus; active Imparts harmless color to
against gram-positive and gram-negative cocci, some enteric urine, sweat, and tears.
bacteria, mycobacteria, and chlamydiae Rashes, thrombocytopenia,
nephritis, cholestatic
jaundice, hepatitis,
proteinuria
 Streptococci
● Minimal Inhibitory Concentration (MIC)
of Penicillin
● PVE or NVE complicated by cardiac or
extracardiac abscess
● Aminoglycoside-containing regimens
○ Aminogycoside toxicity
● Penicillin-resistant streptococci
regimens
○ Group B, C, or G streptococcal
endocarditis
● Moderately penicillin-resistant
streptococci regimen
○ Granulicatella, Abiotrophia,
Gemella species
 Enterococci
● Resistant to:
○ Oxacillin, Nafcillin, and Cephalosporins
● Inhibited but not killed by:
○ Penicillin, Ampicillin, Teicoplanin, and
Vancomycin
● Killed by:
○ Penicillin, Ampicillin, Vancomycin, or
Teicoplanin COMBINED with
aminoglycosides
● High level aminoglycoside phenomenon
● Considerations:
○ Aminoglycoside resistance
○ B-lactamase production
○ Penicillin, Ampicillin, Vancomycin, and
Teicoplanin susceptibility
 Enterococci
● Gentamicin
○ Smaller dose
○ Nephrotoxicity
○ 4-6 weeks duration vs 2-3 weeks
● Aminoglycosides are not given in presence of high level resistance
○ High dose Ampicillin plus Ceftriaxone or Cefotaxime eliminate E.
faecalis
● Resistance to all commonly used agents
○ Bacteremia suppression and surgical treatment
 Staphylococci
● Based on:
○ Presence or absence of prosthetic
valves
○ Involvement of native valves
○ Susceptibility
● All are considered potentially Penicillin
and Methicillin resistant
● NVE due to methicillin-resistant S.
aureus (MRSA)
○ Vancomycin - nephrotoxicity
● Vancomycin susceptibility
○ Vancomycin-intermediate S.
aureus (VISA)
○ Heteroresistant VISA (hVISA)
Staphylococci
● Daptomycin
○ Vancomycin alternative
○ Left-sided NVE
○ Enhanced activity against MRSA with Nafcillin or Ceftaroline
● British Society for Antimicrobial Therapy
○ Addition of second drug to Vancomycin or Daptomycin for MRSA NVE
● Uncomplicated MRSA endocarditis (tricuspid or pulmonic valve)
○ 2 week duration of Oxacillin or Nafcillin with Gentamicin
● Right-sided MRSA Endocarditis
○ 4 week duration with Vancomycin or Daptomycin
● Staphylococcal PVE
○ Rifampin, Vancomycin, Gentamicin
Other Organism
● Streptococcus pneumoniae endocarditis without meningitis
○ IV Penicillin, Ceftriaxone, Cefotaxime, or Vancomycin
● Pneumococcal
○ Strains with Penicillin MIC greater or equal to 2 ug/mL
■ Ceftriaxone or Vancomycin
■ Vancomycin and Ceftriaxone at advised dose if with meningitis
○ Pneumococcal NVE - 4 weeks; Pneumococcal PVE - 6 weeks
● Pseudomonas aeruginosa endocarditis
○ Antipseudomonal b-lactam and high dose Tobramycin
Other Organisms
● Enterobacteriaceae endocarditis
○ Potent B-lactam plus aminoglycoside
● Corynebacterial endocarditis
○ Penicillin plus Aminoglycoside or with Vancomycin
● Candida endocarditis
○ Amphotericin B plus Flucytosine or high dose Echinocandin or Anidulafungin
○ Early surgery
○ Suppression with oral azole
Empirical Therapy and Treatment for
Culture Negative Endocarditis
● Considerations for formulating therapy for administration
○ Clinical clues to etiology
○ Epidemiologic clues
● Acute endocarditis in an injection drug user or health care associated NVE
○ Coverage of MRSA and potentially antibiotic-resistant gram-negative
bacilli
○ Vancomycin plus Gentamicin or Cefepime
● NVE with subacute presentation
○ Vancomycin plus Ceftriaxone
Empirical Therapy and Treatment for Culture
Negative Endocarditis
● Blood-culture pending PVE
○ Vancomycin, Gentamicin, and Cefepime if the prosthetic valve has
been in place for less than a year
● Endocarditis due to S. aureus, CoNS, Enterococci, Enterobacteriaceae
○ Empirical therapy targeting fastidious streptococci, nutritionally variant
organism, HACEK, Bartonella species
● Blood-culture negative subacute NVE
○ Vancomycin plus Ampicillin-Sulbactam or Ceftriaxone
○ Doxycycline for Bartonella coverage
CIED Endocarditis
● Antimicrobial therapy is adjunctive to complete removal of device
● Generator pocket infection without bacteremia
● CIED patients with S. aureus bacteremia and persistent CoNS bacteremia
○ Indicative of CIED endocarditis or valvular endocarditis
● Bacteremia relapse after antimicrobial therapy increases likelihood of CIED
endocarditis
● Treating CIED endocarditis with antibiotics alone is generally unsuccessful and
only done to patients whose devices cannot be removed or who refuse
removal.
Outpatient Antimicrobial Therapy
● Compliant, clinically stable patients with no bacteremia, afebrile, and
no other clinical findings as well as echocardiographic findings that
indicate a complication are managed as outpatients.
● Follow-ups, stable home setting, predictable IV access, and
antimicrobial agents in stable solution are necessary.
Monitoring Antimicrobial Therapy
● 25-40% of endocarditis patients - antibiotic toxicity, allergic reactions
● Periodic blood tests to detect toxicity - Renal, hepatic, and hematologic
● Aminoglycoside and Vancomycin serum concentrations
● Endocarditis due to S. aureus or difficult to treat organisms
○ Blood cultures repeated daily until sterile and 4-6 weeks after therapy
○ Check for recrudescent fever
○ B-lactam therapy results in sterile cultures in 3-5 days
○ Persistent positive culture for 7-9 days in MRSA endocarditis
● Persistent fever despite antibiotic therapy
Antithrombotic Therapy
● Initiation of antithrombotic therapy requires consideration of risks and benefits.
● Patients with infective endocarditis are at risk for:
○ Emboli
○ Hemorrhagic transformation of embolic strokes
○ Intracerebral hemorrhage from septic arteritis or ruptured mycotic
aneurysms
● Indication
○ Mechanical prosthetic valve
○ Atrial fibrillation with either mitral stenosis or a CHADS2 score ≥2
○ Deep vein thrombophlebitis
● Reversal of antithrombotic therapy
○ Unfractionated Heparin
○ Low-molecular weight Heparin
Surgical Treatment
● Intracardiac and nervous system complications - causes of morbidity and
death
● Indications for cardiac surgical treatment of endocarditis are varied; risks,
benefits, and timing of surgery are individualized.
○ Intracardiac complications and Congestive heart failure most
commonly cited indications
● Managed by multidisciplinary team
● 25-40% of patients with left-sided endocarditis undergo cardiac surgery
during infection.
● Significant survival benefits for surgeries for NVE and PVE.
Indications for Surgical Treatment
● Congestive Heart Failure
● Perivalvular infection
● Uncontrolled infection
● S. aureus endocarditis
● Prevention of systemic emboli
● CIED endocarditis
Timing of Cardiac Surgery
● Life-threatening indications is associated with greater survival
following an early surgery rather than delayed.
● With less compelling indications, surgery may reasonably be delayed
to allow further treatment.
○ Justified when the infection is controlled and CHF is resolved wit
medical therapy
● Neurologic complications may be exacerbated during cardiac surgery
● Large non hemorrhagic embolic infarction - delayed for 2-3 weeks
● Cerebral hemorrhage - delayed for 4 weeks
● Ruptured mycotic aneurysm must be treated prior to cardiac surgery
Antibiotic Therapy after Cardiac Surgery
● Organisms are detected in excised valves in 45% of patients after
recommended therapy for endocarditis.
● Negative valve cultures in uncomplicated NVE by susceptible organisms
○ Recommended therapy duration = total duration of preoperative
and postoperative treatment
● Endocarditis complicated by perivalvular abscess, partially treated PVE,
culture positive valves
○ Full course of therapy is given postoperatively
Extracardiac Complications
● Extracardiac complications
○ Splenic abscess - 3-5% of patients
■ Image-guided percutaneous drainage
■ Splenectomy
○ Mycotic aneurysms - 2-15% of patients
■ Cerebral arteries - headache, focal neurologic symptoms,
hemorrhage
■ Monitored by angiography
■ Antimicrobial therapy/Surgery
○ Extracerebral aneurysms
■ Local pain, mass, local ischemia, bleeding
■ Surgery
Outcome
● Factors adversely affecting the outcome
○ Older age
○ Severe comorbid conditions and diabetes
○ Delayed diagnosis
○ Prosthetic valve involvement
○ Aortic valve involvement
○ S. aureus or antibiotic-resistant organisms
○ Intracardiac and neurologic complications
○ Associated of infection with health care
● Death or poor outcome is due to interactions of comorbidities and end
organ complications
Outcome
● Survival rates
○ NVE due to viridans streptococci, HACEK, or Enterococci - 85-
90%
○ NVE due to S. aureus
● PVE 2 months after valve replacements - 40-50% mortality
○ 10-20% mortality in late onsets
● Overall survival rates 1 year after successful endocarditis treatment
are 80-90%
Prevention
● Antibiotic prophylaxis for
endocarditis is not recommended for
widespread standard of care
● Prophylactic antibiotics only for
patients at high risk for severe
morbidity or death from endocarditis
● Maintain good dental hygiene for at
risk patients
● Prophylaxis not advised for patients
undergoing gastrointestinal or
genitourinary procedures
Case Therapeutic Management
● Admit patient to ICU
● Refer to cardiology specialist
● Diet: NPO
● Fluids: PNSS 1L x 24 hours
● Monitoring: VS Q15 I&O Q8
● Therapeutics
○ Paracetamol 1g IV
○ Flucloxacillin 2g IV Q4 (for 4-6 weeks)
○ Continue topical 2.5% hydrocortisone cream
● Hook to O2 via NC at 1-2 lmp for O2 sat <92%
● Refer
Take Home Points
● Infective Endocarditis is a microbial infection of the endothelial surface of
the heart, forming vegetations commonly involving prosthetic or native
valves.
● NBTE causes endothelial injury, predisposing affected valve to
microorganisms.
● Duke Criteria is used to diagnose infective endocarditis.
● Elimination of causative organisms in Infective endocarditis requires
multiple considerations such as susceptibility, resistance, side effects, and
patient’s predispositions.
● Early surgical managements warranted by life-threatening indications
presents with significant survival rates.
● Antibiotic prophylaxis only recommended for high risk patients.

Sources: Harrison's Principles of Internal Medicine 20th

Points taken
● Ceftriaxone is an alternative drug for in cases of Penicillin allergy.
● Doxycycline is drug of choice for Coxiella burnetti
● Ceftriaxone/ Vancomycin is the drug for Penicillin >2ug/mL
● Difference between:
○ Janeway lesion: Non-tender, painless, small hemorrhagic
macular/nodular lesions on the palms or soles.
○ Osler nodes: reddish, purple, tender erythematous nodules found
distal pad of the finger/toes due to immune complex deposition
• Duke Criteria for this case: Two major Criteria such as Positive blood culture
and mitral valve regurgitation

Sources: Harrison's Principles of Internal Medicine 20th

THANK YOU!
KEEP SAFE ALWAYS..