Infective Endocarditis Flashcards
Types of Endocarditis
by etiology
5 types
Infective
In myocardium activly multiplying in myocardium
Rheumatic
Strep imune response, antibody atack endocardium
Carcinoid syndrome
- H.T (serotonin) produced in massive amount => thickening of endocardium
Marentic Endocarditis
- Hypercoagulability state
- Formation of thromby on endocardium
SLE related endocarditis / Libman Sacks Endocarditis
Infective Endocarditis
Types by Time of onset and resonance of clinical seting
Chronic pathological condition - Jet Problem
Types
Acute Infective Endocarditis
- ONSET => Stormy
- High grade fever
- Destructive lesions in heart develop rapidly
- Cardiac Complications
- Leukocytosis (bone marrow iritated)
- New MURMUR
- If abcess in valve ring => Heart block
- Severe constitutional symptoms
- Die in few days if not treated well
- Highly virulent organism (highly destructive)
- S.Aureus
- Ocurs on Healthy Endocardium
Subacute Infective Endocarditis
- ONSET => Insidious
- Low grade fever
- Destructive lesions in heart develop slowly, and always a atempt for healing and fibrosis
- Spoted late
- Patient develops anemia of chronic diseases & Leukopenia(bone marrow suppression due to prolonged cytokine storm)
- Non specific symptoms of systemic disease (no target organ) = CONSTITUTIONAL SYMPTOMS ( Not pointing to any organ) -Cytokine storming gives ( Fatigue, low grade fever, Malaise, weight loss, bone marrow supression)
- Org. with low virulence (less toxic substances) normaly can not atack a healthy endocardium
- S.Viridans 50%(oral cavity - transient bacteriemia(neutralised by defenses) Septicemia (defenses beaten) )
“Bacteriemia not problem
- Comensal organism low virulence
- Not virulent enough to overcome defenses
- Endothelium & Endocardium is resistent to thrombus formation and colonisation”
- Predisposition to pathological conditions may be infected with low virulence
Pathological condition
- Flow defects that cause lesions
- Jet hits endocardium => Lesions => endocardium become procoagulative =>Platlet + Fibrin => microthrombi => Bacteria can stick=> go inside thrombus and make colonies, complement can not penetrate, Ab not
- Margins of the jet will create a Whirlpool effect that will prolong the bacteria contact on endocardium
- REGURGITATION MORE LIKELY THAN STENOSIS
- Catheter induced
Infective endocarditis
-Risk factors
- Individual
- Both
-Bugs
Acute Infective Endocarditis
Staph.Aureus
Subacute Infective Endocarditis
RISK FACTORS
VSD
Rheumatic Heart Dissease (M.v, T.v, A.v)
**Mitral valve prolapse (5%) **
- Midsystolic click - Leaflet touch in the middle of systole
- Murmur
Bicuspid aortic valve
Calcific Aortic Valve
VSD
FT
PDA
BUGS
-
S.Viridans 50%
- oral cavity - (transient bacteriemia(neutralised by defenses) Septicemia (defenses beaten) )
-
Staph Epidermidis
- Prosthetic Valve, in long run (1/2 month => Bug planted during surgery: S.Aureus or Coagulase -)
-
Enterococus
- UTI
-
Strep Bovis
- Colon carcinoma
- Ulcerative colitis
-
FUNGAL
- Manage surgicaly because the vegetations are big
- Antifungal cannot reach (it implants hard)
- Candida
- Aspergilus
RISK FACTORS IN BOTH TYPES
- Neutropenia
- AIDS
- Malignancy
- Therapeutic Immunosupression
- Anticancer
- Transplant
- Rheumatic disease
- DM
- Sugar make bug happy and lymphocytes sad
- Alcohoolic without balanced diet
- I.V Drug abusers
- needel share, non sterile
- usualy right side
- Polymicrbial
- Indweeling vascular catheter
Infective endocarditis
HACEK
- Haemophilus
- Actinobacillus
- Cardiobacterium
- Eikenella
- Kingenella
- Comensals in Oral
- Need lesion to adhere
- Can reach to blood through URI
Infective Endocarditis
Vegetation difference - Acute and subacute
ACUTE
- Describe Pathophysiology !! Make connection
- Define Ring abcess
- Describe local and metastatic complications
SUBACUTE
Describe Pathophysiology !! Make connection
Clinical connection => constitutional symptoms (how presents / missleading)
Chronic antigenemia
Splinter hemorage PATHOPHYS
Osler nodes PATHOPHYS
Janeway Lesions PATHOPHYS
NUTSHELL
FEVER MURMUR => immediatly blood culture (at least 3 diferent sites, at least 3 sets) and ecocardiography (transtoracic pick 60-65% => Transesophageal 95%)
Acute Infective endocarditis
- =>High virulent bacteria ataches endocardium
- =>Bacteria multiply on endocardium
- => Endocardium gets inflamed
- => Platlets and fibrin adhere to endocardium and microbes
- Inflamaion bring Neutrophils
- Time gives Positive feedback for all above bringing more
- NEUTROPHIL => Highly destructive
- MACROPHAGES => destructive
- => Lost parts of the vegetation (WBC inflamation–swelling–) pices can Embolise (Septic Emboli)=>metastatic abscesses
- Brain abcess
- Spleen
- etc.
- => P.Feedback => can destroy heart
- Valve perfortion => ventricular failure
- Ring abscess (veget. move along the ring because surroundings are resistant) and can extend in surroundings
- Nodal tissue
- Myocard abscess
- Pericard supuration
Subacute Infective Endocarditis
- Valve abnormal
- => bacteria adhere slowly
- => vegetation is formed slowly eliciting CHRONIC RESPONSE (macrophages and Lympho’s
- => fibrosis due to Chronic response GF
- => VEGETATION HELD TIGHT
NONSPECIFIC FEATURES
- => Not pointing heart
- Doctors may give antibiotic to treat like other disease
- Keep running weeks and months without proper management
=> CHRONIC ANTIGENEMIA => (chronic = Lympo’s ) Antigen formed and streamed in blood => Antigen-Antibody complexes formed that lead to CIRCULATING IMMUNE COMPLEXES => bind to tissue and will activate the Complement System (TYPE III Hypersensitivity)
=> In nails subungual capilary take an acute turn so that is where the immune complexes will struck and cause vasculitic lesions => Splinter Hemorge (long strikes under the nails / most common case are in persons that work hard with hands)
=> If the Complexes get stuck in the acute turn of cappilary they get painfull and create Osler Nodes
=> If the complexes deposit in palms and feet than the patient develop Janeway Lesions
=> Immunecomplexes can develop Pericardial Rub, Pleural Rub, Joint deposits
=> Petichial hemorages
=> Roth Spots
=> Diffuse Glomerulonephritis
NUTSHELL
Acute
SYMPTOMS THAT PIN POINT TO HEART MORE LIKELY TO BE ACUTE
More chances of perforation in surrounding tissues due to lysis
Septic emboli form because of surounding tissue lysis, => ABCESSES => In renal ARF
Fever High
Subacute
SYMPTOMS THAT PIN POINT TOWARDS CONSTITUTIONAL SYMPTOMS ARE MORE LIKELY TO BE SUBACUTE
Less chances of perforation due to tighty held vegetation
Imunecomplexes formed embolise in tissues and create microvascular damage => In renal less likely ARF
Low grade fever
CONSTITUTIONAL SYMPTOMS
Infective Endocarditis Dukes Criteria
Major
- Blood culture (1 of below)
- Typical organism in 2 cultures
- Persistently + blood cultures 3 or more than 3 12h appart
- Endocardium involvement
- Ecocardiogram
- New valvular Regurgitation
Minor
- Predisposition for Infective Endocarditis
- I.V
- Flow
- Fever 38o
- Vascular / Imunological Signs
- Echo Finding
- Blood culture that not aplies in Major
Endocarditis RHE
- Multiple small vegetations forms along the line of closures Imune AB
- Sterile
- Platlet and fibrin
- Do not detach
Marentic Endocarditis
Apears in hypercoagulability
Seen
Malignancy, - especialy -
- Ca Pancreas (mucus producing)
- Ca Colon (mucus producing)
Mucus (procoagulant)
Can detach and produce Thrombembolism
Liibman Sacks ( SLE )
Are due to imunologic proceses
May form on any site
lot of fibrin platlets (verry sticky)
Valve is inflamed (contrast to thrombus)
Healing with scar
Carcinoid Syndrome - endocarditis
GIT formed
Can produce
Serotonine
Bradikinine
etc
Liver physiologic inactivaates them, but if metastasis in liver ocur than the substances that are secreted (serotnin etc) from the liver will go to right heart => in lung they will be inactivated
=>Produce intense fibrotic lesions in right heart endocardium
If lung has metastasis => left endocardium afected
