MALIGNANCY BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MEDICINE SOPORE KASHMIR
SUB ACUTE BACTERIAL ENDOCARDITIS BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MEDICINE SOPORE KASHMIR
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Transcript of SUB ACUTE BACTERIAL ENDOCARDITIS BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MEDICINE SOPORE KASHMIR
INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
By Dr Bashir Ahmed DarChinkipora Sopore KashmirAssociate Professor MedicineEmail [email protected]
From Right to Left Dr.Smitha associate
prof gynae Dr Bashir associate
professor Medicine Dr Udaman
neurologist Dr Patnaik HOD
ortho Dr Tin swe aye paeds
From RT to Lt Professor Dr Datuk
rajagopal N Dr Bashir associate
professor medicine Dr Urala HOD
gynae Dr Nagi reddy
tamma HOD-opthomology
Dr Setharamarao Prof ortho
INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
A microbial infection of the endothelial lining of the heart; most commonly occurring as a vegetation on the valve leaflets
INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
Annual incidence: 15,000 to 20,000
Forth leading cause of life-threatening infectious disease
Male:female ratio is 1.7:1 (median age 50)
0%
10%
20%
30%
40%
50%
60%
Age
Age Distribution
<30 31-60 >60
INFECTIVE ENDOCARDITIS
100% fatal if undiagnosed and untreated
• 20% fatal even if diagnosed and treated appropriately.
•70% streptococcal• 20% staphylococcal
Predisposing factorsPredisposing factors
Any type of structural heart disease– Rheumatic heart disease (37-76%) like
MS,AS,AI,MI,etc– Congenital heart disease (6-24%) Like
ASD,VSD,PDA,etc– Degenerative cardiac lesions (30-40%)– Other (including prosthetic valves)
Predisposing factorsPredisposing factorsAlready damaged valves by Already damaged valves by
RHDRHD
Predisposing factorsPredisposing factors Already damaged damaged Already damaged damaged
heart by CHDheart by CHD– Congenital heart
disease (6-24%)
Predisposing factors Predisposing factors Prosthetic valves & Prosthetic valves &
pacemakerspacemakers High risk
– prosthetic cardiac valve
– prior episodes of endocarditis
– surgically constructed systemic-pulmonary shunts or conduits
– Pacemakers & pacemaker leads
Predisposing factors Predisposing factors Prosthetic valves & Prosthetic valves &
pacemakerspacemakers
PREDISPOSING FACTORS PREDISPOSING FACTORS IV drug abusersIV drug abusers
PREDISPOSING FACTORS PREDISPOSING FACTORS Alcohol abuse & sepsisAlcohol abuse & sepsis
PREDISPOSING FACTORSPREDISPOSING FACTORS
Neutropenia
&
Immunosupression
PREDISPOSING FACTORSPREDISPOSING FACTORS
Staph aureus accounts for the majority of cases of endocarditis in case of IV drug abusers and is recurrent polymicrobial
tricuspid valve, either alone or in combination, is most often infected
PREDISPOSING FACTORSPREDISPOSING FACTORS
Moderate risk– patent ductus arteriosus– VSD, primum ASD– coarctation of the aorta– bicuspid aortic valve– hypertrophic cardiomyopathy– acquired valvular dysfunction– MVP with mitral regurgitation
PREDISPOSING FACTORSPREDISPOSING FACTORS
Low risk– isolated secundum atrial septal defect– ASD, VSD, or PDA >6 months past repair– “innocent” heart murmur “
PREDISPOSING FACTORS PREDISPOSING FACTORS INVASIVE PROCEDURESINVASIVE PROCEDURES
– G.I. Barium enema Colonoscopy
– Genitourinary Prostatectomy
PREDISPOSING FACTORS PREDISPOSING FACTORS INVASIVE PROCEDURESINVASIVE PROCEDURES
Tooth extraction Periodontal surgery Teeth cleaning Tooth brushing,
flossing Using wooden
toothpicks Chewing food
PREDISPOSING FACTORS PREDISPOSING FACTORS INVASIVE PROCEDURESINVASIVE PROCEDURES
Biopsies, suture removal, placing orthodontic bands
Tonsillectomy,Adenoidectomy,Bronchoscopy.
Resp tract procedure to drain abscess or empyema
PREDISPOSING FACTORS PREDISPOSING FACTORS INVASIVE PROCEDURESINVASIVE PROCEDURES
Central venous catheterization
Bladder catheterization, Endoscopies, shaving,
Skin or musculoskeletal infections
PREDISPOSING FACTORSPREDISPOSING FACTORS
– AIDS patients– Cancer patients– Leukemia– Lymphomas
MICROBIAL AGENTS MICROBIAL AGENTS RESPONSIBLE FOR IERESPONSIBLE FOR IE
The commonest cause is streptococci (alpha hemolytic) and constitutes about 70%.among which
Streptococci viridans is 35% that reside in oral cavity along with HACK associated with dental procedures.
Then is streptococcus bovis that resides in oral & colon.colonic cancers 15%
Then is enterococci 10%
And other streptococci 10%
MICROBIAL AGENTS MICROBIAL AGENTS RESPONSIBLE FOR IERESPONSIBLE FOR IE
Staphylococcus aureus: healthy or deformed valves, esp. in intravenous drug abusers and prosthetic valves.
Prosthetic valve
endocarditis during the perioperative period or 60 after operation also by s.epidermitides.
Prosthetic valve endocarditis also occurs by Candida and aspergillosis but form large vegetations.
MICROBIAL AGENTS MICROBIAL AGENTS RESPONSIBLE FOR IERESPONSIBLE FOR IE
HACEK group consists of Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, & Kingella (as I said are commensals of oral cavity)
MICROBIAL AGENTS MICROBIAL AGENTS RESPONSIBLE FOR IERESPONSIBLE FOR IE
Enterococcus Normal inhabitants of the GI tract, occasionally anterior
urethra Mostly subacute and affect men (mean age 59) after
genitourinary manipulations or women (mean age 37) after obstetrics procedures.
E. faecalis 85% of enterococcal IE
MICROBIAL AGENTS MICROBIAL AGENTS RESPONSIBLE FOR IERESPONSIBLE FOR IE
Others areFungi (Candida,aspergillosis).RickettsiaeChlamydiaThese infections occur in a particular
situation.
MICROBIAL AGENTS MICROBIAL AGENTS RESPONSIBLE FOR IERESPONSIBLE FOR IE
Still other organisms are Pseudomonas Brucella Diphtheroids Listeria Bartonella Coxsiella Chlamydia
PATHOGENESIS OF PATHOGENESIS OF INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
Previously damaged endocardial surface of valve for example by rheumatic heart disease forms rough surface over the damaged valve.
Due to this rough surface palatelets stick and adhere to this area forming small small thrombi over the cusp of valves.fibrin also deposits on this area, the lesions now called as Nonbacterial Thrombotic Endocarditis (NBTE).
PATHOGENESIS OF PATHOGENESIS OF INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
This deposition of sterile vegetations in the form of thrombi on the leaflets of cardiac valves, is also called MARANTIC ENDOCARDITIS
NONBACTERIAL NONBACTERIAL THROMBOTIC THROMBOTIC
ENDOCARDITIS (NBTE)ENDOCARDITIS (NBTE)
These vegetations are sterile, nondestructive, noninflammatory & small (1-5mm),made of platelets,fibrin & other blood elements and may occur singly or multiply along the lines of closure of heart valves
NONBACTERIAL NONBACTERIAL THROMBOTIC THROMBOTIC
ENDOCARDITIS (NBTE)ENDOCARDITIS (NBTE)
Probably occurs as a consequence of a hypercoagulable state
Seem with concomitant venous thrombosis &/or pulmonary embolism
May be seen with hyperestrogenic state, extensive burns, or endocardial trauma from indwelling catheters
NONBACTERIAL NONBACTERIAL THROMBOTIC THROMBOTIC
ENDOCARDITIS (NBTE)ENDOCARDITIS (NBTE)
Importance Local effect on valve unimportantMay produce emboli with resultant infarctsMay eventually heal with fibrosis.
PATHOGENESIS OF PATHOGENESIS OF INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
Bacteria reach this thrombotic vegetation site and produce colonization and deposit deep within this thrombi and remain hidden and protected and then multiply easily there.
The surface may further covered by platelets and fibrin.
Infectious EndocarditisInfectious Endocarditis
Infective endocarditis with perforation of mitral valve leaflet
Vegetation
Mitral Valve
Stick in Perforation
PATHOGENESIS OF PATHOGENESIS OF INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
The reason why bacteria lodge there is because of Venturi effect as the blood carrying bacteria flows with high jet and force from high pressure to low pressure chamber below.
Since the valve is deformed and stenosed so bubbles of blood are sprinkled that fall over the atrial surface of valve along free margins and deposit within thrombi.
Venturi EffectVenturi Effect
PATHOGENESIS OF PATHOGENESIS OF INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
In systemic lupus erythematosus the vegetations may form on the undersurface of valve towards ventricular side called as libman sacks syndrome.
PATHOGENESIS OF PATHOGENESIS OF INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
The adherence of the organism to NBTE is a crucial step.1. FimA is a surface adhesin of S.viridans that serves as
an important colonization factor. Homologues of fimA genes were found in many S.viridans strains and enterococci.
2. Fibronectin is implicated as the host receptor within NBTE.
PATHOGENESIS OF PATHOGENESIS OF INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
Adherence of some streptococci to blood clot is facilitated by dextran (a cell wall component) (especially of Streptococcus mutans, a viridans group.
Further Some strains of bacteria are stimulators of platelet aggregation
PATHOGENESIS OF PATHOGENESIS OF INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
Once these thrombotic vegetations are laden with microbial organisms they become large even upto 3cms,friable and easily detachable in contrast to vegetations of RHD that are not easily detachable.
The colour of vegetations is tan grey red or brown and situated along the line of closure of valve.
PATHOGENESIS OF PATHOGENESIS OF INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
Microscopic Pathology
Fibrin, platelets, masses of organisms,
+/- necrosis, +/- neutrophils
Later: +/-lymphocytes, +/- macrophages,
+/- fibroblasts, +/- fibrosis
LOCAL EFFECTS OF LOCAL EFFECTS OF INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
First the leukocytes are unable to penetrate the vegetations as additional layers of fibrin are added. Treatment with antibiotics can also be problematic because the bacteria within the vegetation often become less metabolically active, and many antibiotics require active bacterial growth to be effective.
LOCAL EFFECTS OF LOCAL EFFECTS OF INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
Infection may extends beyond valve cusp may erode & perforate valve, & may erode into underlying myocardium to produce an abscess (ring abscess) or Paravalvular abscess
Septal abscesses & adjacent abscessFistulaeProsthetic dehiscence
LOCAL EFFECTS OF LOCAL EFFECTS OF INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
Valvular distortion/destruction chordal rupture.
Conduction abnormalitiesPurulent pericarditisFunctional valve obstructionWith treatment, healing occurs by fibrosis
and occasionally calcification.
DISTANT EFFECTS OF DISTANT EFFECTS OF INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
Vegetations may become detached and produce embolic effects.
Embolic phenomena are common (15-35%). septic infarcts involving: renal, splenic, coronary, or cerebral circulation.
Risk for emboli is increased when vegetation >1cm.
IMMUNOLOGICAL EFFECTS OF IEIMMUNOLOGICAL EFFECTS OF IE
IE cause both humural and cellular response Rheumatoid factor:
– titers correlate with the level of hypergammaglobulinemia and decrease with therapy
Antinuclear antibodies:– may contribute to the musculoskeletal manifestations, low-grade fever, or
pleuritic pain
Circulating immune complexes:– Connected with long duration of illness, extravascular manifestations,
hypocomplemenemia– May cause diffuse glomerulonephritis, and some of the peripheral
manifestations such as Osler nodes
EFFECTS OF IE ON KIDENYEFFECTS OF IE ON KIDENY
Pathological processes: abscess, infarction, glomerulonephritis (focal, segmental), membranoproliferative GN
May be normal is size or slightly swollen 10 to 15% of IE exhibit immune complex GN (as in
SLE). Supporting IC rather than emboli:1. Bacteria rarely seen in lesion2. GN can occur with right-sided IE3. GN is rare in acute IE even though large vegetation result in
metastatic abscess formation4. IF staining reveals IC-typical distribution5. Antibacterial antibodies eluted from lesions
OTHER EFFECTS OF IEOTHER EFFECTS OF IE
1. Mycotic aneurysm is a localized, irreversible arterial dilatation due to destruction of the vessel wall by infection
More common with S.viridans
OTHER EFFECTS OF IEOTHER EFFECTS OF IE
May arise by the following mechanisms:– direct bacterial invasion
of the arterial wall with subsequent abscess formation or rupture
– septic or bland emoblic occlusion of the vasa vasorum
– immune complex deposition with resultant injury to arterial wall
OTHER EFFECTS OF IEOTHER EFFECTS OF IE
Tend to occur at bifurcation areas; middle cerebral artery is most common,Clinically silent until rupture
EFFECTS ON EFFECTS ON CNS,SPLEEN,LUNGCNS,SPLEEN,LUNG
CNS– cerebral emboli (>30% of IE)– Mycotic aneurysms
Spleen– infarctions (44% of autopsy cases)– enlargement associated with hyperplasia of lymphoid follicles,
increase in secondary follicles, focal necrosis,abscess Lung
– associated with right-sided IE– pulmonary embolism, acute pneumonia, pleural effusion, or
empyema
EFFECTS ON EFFECTS ON CNS,SPLEEN,LUNGCNS,SPLEEN,LUNG
CNS– cerebral emboli (>30% of
IE)– Mycotic aneurysms
EFFECTS ON EFFECTS ON CNS,SPLEEN,LUNGCNS,SPLEEN,LUNG
Spleen– infarctions (44% of autopsy
cases)– enlargement associated with
hyperplasia of lymphoid follicles, increase in secondary follicles, focal necrosis,abscess
EFFECTS ON EFFECTS ON CNS,SPLEEN,LUNGCNS,SPLEEN,LUNG
Lung– associated with right-sided
IE– pulmonary embolism, acute
pneumonia, pleural effusion, or empyema
EFFECTS ON SKIN&EYEEFFECTS ON SKIN&EYE
– Petechiae, may result from local vasculitis or emboli
– Petechiae are red because they contain red blood that has leaked from the capillaries
EFFECTS ON SKIN&EYEEFFECTS ON SKIN&EYE
Osler nodes, painful nodes on finger or toe pads
Due to immune complexes in dermal vessels
EFFECTS ON SKIN&EYEEFFECTS ON SKIN&EYE
Osler’s Nodes:
1. red, raised lesions Tender, subcutaneous
nodules.4 P’s: Pink Painful Pea-sized Pulp of the fingers/toes.
– Immunological origin?
EFFECTS ON SKIN&EYEEFFECTS ON SKIN&EYE
Janeway lesions (due to septic emboli), painless plaques on palms or soles.
non-tender, small erythematous or hemorrhagic macular or nodular lesions on the palms or soles only a few millimeters.
EFFECTS ON SKIN&EYEEFFECTS ON SKIN&EYE
Pathologically, the Janeway lesion is described to be a microabscess of the dermis with marked necrosis and inflammatory infiltrate not involving the epidermis, which is due to the deposition of circulating immune complexes in small blood vessels.
Janeway LesionsJaneway Lesions
EFFECTS ON SKIN&EYEEFFECTS ON SKIN&EYE
Splinter hemorrhage (linear lines beneath fingernails)
EFFECTS ON SKIN&EYEEFFECTS ON SKIN&EYE
Eye– Roth spots– Roth's spots are retinal
hemorrhages with white or pale centers composed of coagulated fibrin. They are typically observed via fundoscopy (using an ophthalmoscope to view inside the eye) or slit lamp exam
EFFECTS ON SKIN&EYEEFFECTS ON SKIN&EYE
Eye– Roth spots– They are usually caused by
immune complex mediated vasculitis often resulting from bacterial endocarditis. Roth's spots may be observed in leukemia, diabetes, subacute bacterial endocarditis, pernicious anemia, ischemic events, and rarely in HIV retinopathy.
EFFECTS ON SKIN&EYEEFFECTS ON SKIN&EYE
Infective endocarditis also can give rise to conjunctival haemorrhages
EFFECTS ON SKIN&EYEEFFECTS ON SKIN&EYE
Clubbing is also known to occur in infective endocarditis.
Summary of Infective Summary of Infective EndocarditisEndocarditis
Endothelial damage
Platelet-fibrin thrombi
Microorganism adherence
Summary of Summary of Pathogenesis BEPathogenesis BE
Turbulent blood flow (from congenital or acquired heart dz)Endothelial trauma
Platelets and fibrin deposit on damaged endothelium Nonbacterial Thrombotic Endocarditis (NBTE)
Bacteremia Colonization of NBTE Bacterial Vegetation
THINGS TO REMEMBER IN THINGS TO REMEMBER IN INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
Infective endocarditis affects Left-sided valves 75%
Right-sided valves 15%Both 5%Other 5%
THINGS TO REMEMBER IN THINGS TO REMEMBER IN INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
Mitral valve alone 35%Aortic valve alone 20%Mitral plus aortic 20%Tricuspid 14%Pulmonic 1%With changing murmurs in character
pitch duration etc.fungal vegetations are large vegetations.
THINGS TO REMEMBER IN THINGS TO REMEMBER IN INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
Infective endocarditis may be culture negative either due to prior antibiotic treatment or due to atypical microbial organisms or due to fungus etc.then called as non bacterial endocarditis.
CLASSIFICATION OF CLASSIFICATION OF BACTERIAL ENDOCARDITISBACTERIAL ENDOCARDITIS
1. Acute Bacterial Endocarditis (“ABE”) usually fulminant, due to highly virulent organisms (e.g. Staphylococcus aureus)
versus
Subacute Bacterial Endocarditis (“SBE”) with insidious onset over weeks, due to less virulent organisms (e.g. viridans streptococci)
CLASSIFICATION OF CLASSIFICATION OF BACTERIAL ENDOCARDITISBACTERIAL ENDOCARDITIS
Acute: Rapid progression of symptoms – Less than 6 weeks duration– Significant systemic signs/symptoms
Fever Elevated systemic WBC/ left shift
Subacute: Slower, more chronic progression of symptoms– Low grade fevers– Vague clinical signs/symptoms
weakness, anorexia, malaise,etc.
CLASSIFICATION OF CLASSIFICATION OF BACTERIAL ENDOCARDITISBACTERIAL ENDOCARDITIS Acute
– Toxic presentation– Progressive valve destruction & metastatic infection
developing in days to weeks– Most commonly caused by S. aureus
Subacute– Mild toxicity– Presentation over weeks to months– Rarely leads to metastatic infection– Most commonly S. viridans or enterococcus
CLINICAL FEATURES OF CLINICAL FEATURES OF ENDOCARDITISENDOCARDITIS
Common Symptoms Fever 80%Chills 40%Weakness 40%Dyspnea 40%
CLINICAL FEATURES OF CLINICAL FEATURES OF ENDOCARDITISENDOCARDITIS
Uncommon Symptoms
Cough 25%Sweats 25%Anorexia 25%Weight loss 25%Malaise 25%Skin lesions 20%Nausea/vomiting 20%Stroke 20%
CLINICAL FEATURES OF CLINICAL FEATURES OF ENDOCARDITISENDOCARDITIS
More Uncommon Symptoms
Headache 15% Myalgia/arthralgia 15% Edema 15% Chest pain 15% Abdominal pain 15% Delirium/coma 15% Back pain 10% Hemoptysis 10%
CLINICAL FEATURES OF CLINICAL FEATURES OF ENDOCARDITISENDOCARDITIS
Common Physical Signs Fever 90%Heart murmur 85% Splenomegaly 30%Petechiae 30%
CLINICAL FEATURES OF CLINICAL FEATURES OF ENDOCARDITISENDOCARDITIS
Uncommon Physical Signs
Osler nodes 15%(pea-sized tender finger/toe nodules)
Subungual splinter hemorrhages 15%
Changing heart murmur 10%
CLINICAL FEATURES OF CLINICAL FEATURES OF ENDOCARDITISENDOCARDITIS
More Uncommon Physical Signs
Janeway lesions 5%(small palm/sole hemorrhages)
New heart murmur 5%
Roth spots (on retina) 2%(white dots with surrounding hemorrhage)
LABORATORY FINDINGSLABORATORY FINDINGS
Laboratory Findings
Elevated ESR (mean 57 mm/hr) 95%(erythrocyte sedimentation rate)
Circulating immune complexes 90%
Anemia 80%
Proteinuria 60%
LABORATORY FINDINGSLABORATORY FINDINGS
Laboratory Findings
Rheumatoid factor 50%(anti-IgG antibodies)Hematuria 40%Leukocytosis 25%Hypergammaglobulinemia 25%Elevated creatinine 10%Leukopenia 10%Thrombocytopenia 10%
LABORATORY FINDINGSLABORATORY FINDINGS
ECG should be done in all pts with suspected IE– Nonspecific usually– Conduction abnormalities ( new LBBB, Prolonged PR
interval, new RBBB, complete heart block)– Junctional tachycardia
Chest Xray– Pulmonic emboli or CHF
LABORATORY FINDINGSLABORATORY FINDINGS
Blood cultures critical for specific diagnosis
3 sites 30-60 minutes apart
before starting antibiotics.
86 – 96% of 1st cultures positive
98 – 100% of 1st 2 cultures positive
Blood cultures may be negative if the patient
has already received antibiotics; a few cases
of infective endocarditis are “culture-negative”
LABORATORY FINDINGSLABORATORY FINDINGS
All patients with suspected bacteremia should have blood cultures drawn in the ED prior to abx
Blood cultures should be drawn in 3 different sites
Minimum of 10 ml blood in each bottleMinimum of one hour between first and last
bottle
LABORATORY FINDINGSLABORATORY FINDINGS
Negative culture can occur in 5% of patients.
1/3 to ½ are negative due to prior antibiotic use
In patients with culture negative IE, advise lab to allow specialized testing to recover the causative organism which is needed to adequately treat
LABORATORY FINDINGSLABORATORY FINDINGS
Transthoracic (TTE)echocardiography 60% sensitivity for vegetations
Transesophageal(TEE) echocardiography >90% sensitivity for vegetations
The absence of vegetations on echocardiogramdoes not exclude the diagnosis of endocarditis
Duke’s Criteria For Diagnosis Duke’s Criteria For Diagnosis of Infective Endocarditisof Infective Endocarditis
Duke Criteria – Simplified
Requires 2 major, or 1 major + 3 minor or 5 minor criteria
Duke’s Major CriteriaDuke’s Major Criteria
Major Criteria 1. Positive blood culture
– typical microorganism (strep viridans, strep bovis, HACEK group, staph aureus or enterococci in the absence of a primary locus) for endocarditis from two separate blood cultures
– persistently positive blood culture from: blood cultures drawn more than 12 hr apart, or all of 3 or a majority of 4 or more separate blood cultures, with
first and last drqwn at least 1 hr apart
Duke’s Major CriteriaDuke’s Major Criteria
2. Positive Echocardiogram showingVegetationAbscess,Detached prosthesisRegurgitation
Duke’s Minor CriteriaDuke’s Minor Criteria
Minor Criteria Predisposition (predisposing heart condition or iv
drug use) Fever of 100.40F or higher Vascular phenomena (major arterial emboli, septic
pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctive hemorrhages, Janeway lesions).
Duke’s Minor CriteriaDuke’s Minor Criteria
Immunologic phenomena (glomerulonephritis, Osler’s nodes, Roth spots, rheumatoid factor)
Microbiologic evidence (positive blood culture not meeting major criteria or serologic evidence of active infection with organism consistent with IE)
Echocardiogram (consistent with IE but not meeting major criteria)
COMPLICATIONS OF COMPLICATIONS OF INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
Heart failure 67%
Septic emboli 55% to kidneys 55%
to heart 50% to spleen 44% to brain 33%
COMPLICATIONS OF COMPLICATIONS OF INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS
Uncommon Complications
Myocardial abscess 20%
Glomerulonephritis 15%(immune complexes)
“Mycotic aneurysm” 10%
Pericarditis (S.aureus) rare
INDICATIONS FOR INDICATIONS FOR PROPHYLAXISPROPHYLAXIS
Prophylaxis is indicated for Prosthetic heart valves Congenital heart disease with manifestations Acquired heart disease with manifestations Hypertrophic cardiomyopathy Mitral valve prolapse with regurgitation Previous history of endocarditis Dental procedures known to produce bleeding Surgery involving GI, respiratory mucosa
INDICATIONS FOR INDICATIONS FOR PROPHYLAXISPROPHYLAXIS
Tonsillectomy Esophageal dilation ERCP for obstruction Gallbladder surgery Cystoscopy, urethral dilation Urethral catheter if infection present Urinary tract surgery Tonsillectomy Rigid bronchoscopy.
INDICATIONS FOR INDICATIONS FOR PROPHYLAXISPROPHYLAXIS
Esophageal sclerotherapy or stricture dilation Respiratory: Consider if pt will be cut or biopsied Periodontal procedures (surgery, scaling, and root
planing, probing, and recall maintenance) Implant placement and reimplantation of avulsed
teeth Endodontic instrumentation beyond the apex Subgingival placement of antibiotic fibers or strips Placement of orthodontic bands but not brackets.
INDICATIONS FOR INDICATIONS FOR PROPHYLAXISPROPHYLAXIS
ERCP Billiary surgery Prostate surgery Cystoscopy Cardiac transplants Extractions of teeth Intraligamentary injections Prophylactic cleaning of teeth or implants where
bleeding is anticipated
No ProphylaxisNo Prophylaxis
Vaginal delivery Hysterectomy Local anesthetic injections Placement of oral rubber
dams Post-op suture removal Placement of removable
appliances Fluoride treatment
Radiographs Orthodontic adjustments Shedding of primary teeth IUDs Circumcision MVP without
regurgitation Pacemakers but see if not
already infected Physiologic murmurs
Indications for SurgeryIndications for Surgery
(When removal of an infected valve is necessary). Refractory CHF Severe valvular dysfunction Uncontrolled infection Valve perforation Dehiscence Fistula Abscess
Indications for SurgeryIndications for Surgery
Embolic event with persistent large vegetation or >1 episode of embolization Prosthetic valve infection Fungal IE New heart block Refractory CHF Uncontrolled infection Ineffective antimicrobial therapy
Indications for SurgeryIndications for Surgery
Resection of mycotic aneurysms
antibiotic-resistant pathogens)
Local suppurative complications including perivalvular or myocardial abscesses
Persistent vegetations after a major systemic embolic episode
Large (>1cm diameter) anterior mitral valve vegetation
Acute mitral insufficiency Valve perforation or
rupture Increase in vegetation size
4 weeks after antibiotic therapy
Indications for SurgeryIndications for Surgery
Periannular extension of infection
Infected prosthetic material: less than 1 year out from original heart surgery
Refractory congestive heart failure (Leading cause of death)
Unresponsive infection/ continued infection despite appropriate antibiotics
Indications for SurgeryIndications for Surgery
Pt. experiences more than 1 major emboli
Severe valvular dysfunction: Acute CHF or impaired hemodynamic status
Relapsing prosthetic valve endocarditis
Fungal endocarditis New conduction defects or
arrhythmias
Persistent bacteremia Acute AR or MR with
heart failure. Acute AR with
tachycardia and early closure of the MV.
Annular or aortic abscess. Sinus or aortic aneurysm. Persistent bacteremia and
valve dysfunction
Indications for SurgeryIndications for Surgery
Recurrent emboli after appropriate Abx.
Mobile vegetations >10 mm.
Persistent pyrexia and leucocytosis with negative blood cultures.
Increase in vegetation size after antimicrobial therapy
Valvular dysfunction Fungal endocarditis
TREATMENT OF INFECTIVE TREATMENT OF INFECTIVE ENDOCARDITISENDOCARDITIS
Purpose of Prophylaxis To give antibiotics and kill blood-borne bacteria
or interfere with their metabolism, hindering their ability to adhere to a damaged heart valve.
However antibiotic resistance is increasing. Only administered prior to “high risk” surgeries Include dental procedures, surgery on the gastrointestinal or urinary tract, surgery on infected tissues
TREATMENT OF INFECTIVE TREATMENT OF INFECTIVE ENDOCARDITISENDOCARDITIS
50% of some valvular infections do not respond to antimicrobial therapy or surgery
Today’s highly virulent causative agents have led to an increase in dangerous complications
Don’t need to memorize individual procedures
PROPHYLACTIC PROPHYLACTIC TREATMENTTREATMENT
Standard Prophylactic RegimenSingle dose, 30-60 min prior to any
procedureAmoxycillin 2.0 grams orally or iv
Ampicillin 2gm IV/IM or Ceftriaxone 1g IV/IM
IV, PCN-allergic Ceftriaxone 1g IV/IM
PROPHYLACTIC PROPHYLACTIC TREATMENTTREATMENT
Prophylaxis for Patients Already Taking Amoxycillin or have allergy to pencillin or microbial may have developed resistance to Amoxycillin options then are
Ceftriaxone 1g IV/IM before and after procedure Clindamycin 600mg PO or Clarithromycin 500
mg or Azithromycin 500mg PO Quinolones or IV Vancomycin not recommended
for prophylaxis due to concern of creating new drug resistance
SUMMARY PROPHYLACTIC SUMMARY PROPHYLACTIC TREATMENTTREATMENT
Summary of Standard RegimenAmpicillin 1g IM/IV Gentamicin 1 to 1.5 mg/kg IV/IM (MAX
120 mg)Ceftriaxone 1gm IVVancomycin 1g IV over 1-2h
TREATMENT OF IE TREATMENT OF IE GENERAL COMMENTSGENERAL COMMENTS
IE treatment should be considered in All febrile IDUs Pts with a cardiac prosthesis and fever Pts with new murmur or change in murmur with
evidence of vasculitis or embolization Any cardiac risk factor with unexplained fever Any patient with a prolonged fever (>2 weeks)
TREATMENT OF IE TREATMENT OF IE GENERAL COMMENTSGENERAL COMMENTS
Most patients will require 4 to 6 weeks of antibiotic therapy.
Antifungals alone are not enough to cure fungal IE, although Amphotericin B is often administered in conjunction with surgery.
Culture-negative native-valve endocarditis should be individualized and generally includes ampicillin, Ceftriaxone, or Vancomycin, +/- Aminoglycoside
TREATMENT OF IE TREATMENT OF IE GENERAL COMMENTSGENERAL COMMENTS
Complete eradication takes weeks, relapses may occur. This is due to:
1. The infection exists in an area of impaired host defense and is tightly encased in a fibrin meshwork
2. The bacteria reach very high population densities, such that the organism may exist in a state of reduced metabolic activity and cell division
TREATMENT OF IE TREATMENT OF IE GENERAL COMMENTSGENERAL COMMENTS
Etiologic agent must be isolated in pure culture. MIC and MBC should be determined.
All patients with suspected bacteremia should have blood cultures drawn in the ED prior to abx
Blood cultures should be drawn in 3 different sites Minimum of 10 ml blood in each bottle Minimum of one hour between first and last bottle Aspirin may decrease the growth of vegetative
lesions and prevent cerebral emboli
TREATMENT OF IE TREATMENT OF IE GENERAL COMMENTSGENERAL COMMENTS
Parenteral antibiotics are recommended over oral drugs
Antibiotic combinations should produce a rapid effect
Selection of antibiotics should be based on susceptibility tests, and treatment should be monitored with clinical improvement.
Blood cultures should be obtained during the early phase of therapy to ensure eradication
Use of anticoagulants during therapy for native valve IE is not recommended. With mechanical valves, anticoagulation should be maintained (if indicated) within therapeutic range
TREATMENT OF IE TREATMENT OF IE GENERAL COMMENTSGENERAL COMMENTS
Effective antimicrobial treatment should lead to defervescence within 7 – 10 days
Persistent fever in IE may be due to staph, pseudomonas, culture negative IE or with microvascular complications/major emboli or due to drug reaction.
OOPS! You didn’t premedicate patient and you encounter unexpected bleeding!Don’t Panic
Stop procedure, administer antibiotics, and resume working
Antibiotics administered up to 2 hours following a procedure may still protective
TREATMENT OF IE TREATMENT OF IE GENERAL COMMENTSGENERAL COMMENTS
Anticoagulation for native valve endocarditis has not been shown to be beneficial because of Increase of risk of intracranial hemorrhage
Pts with prosthetic valves who are treated with anticoagulation can be maintained on their regimen with proper caution for CNS complications
TREATMENT OF IE TREATMENT OF IE GENERAL COMMENTSGENERAL COMMENTS
“If anticoagulation is indicated forAnother reason it should be continued. Anticoagulation does not prevent
TREATMENT OF IETREATMENT OF IE
Highly penicillin-susceptible Streptococcus viridans or bovis
Once-daily ceftriaxone for 4 wks cure rate > 98%Or Once-daily ceftriaxone 2 g for 2wks
followed by oral Amoxycillin qid for 2 wks
TREATMENT OF IETREATMENT OF IE
If organisms are resistant to this then giveVancomycin, 15mg/kg IV 12 hourly daily,
plus Gentamicin 1 to 1.5 mg/kg 8 hourly, both 4 to 6 weeks.
TREATMENT OF IETREATMENT OF IE
Ampicillin 2gm 4 hourly plus Gentamicin 60-80mg 8 hourly
HACEK organisms (IE) Ceftriaxone monotherapy (1 to 2gm IV/BD daily) or Ampicillin Plus Gentamicin x 4 to 6 weeks.
TREATMENT OF IETREATMENT OF IE
Staph IE with Prosthetic MaterialTriple drug regimensMethicillin-sensitive staph spp.Nafcillin/Oxacillin Plus Rifampin (6 weeks) Methicillin-resistant staph spp Vancomycin
Plus Rifampin 300mg PO 8hrly (6 to 8 weeks) Plus Ampicillin &Gentamicin (2 weeks).
TREATMENT OF IETREATMENT OF IE
Or Ceftriaxone (2 g/d IV as a single dose for 4 weeks) plus Rifampicin (300 mg PO q8h for 6-8 weeks).
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