Infective endocarditis Flashcards
Etiology
- Microbial infection of a heart valve
- bacterium, rickettsia (Coxiella burnetti - Q fever endocarditis), chlamydia or fungus
- Streptococcal - viridans, enterococci
- Staphyl aureus
- Gram-negative bacilli, Haemophilus influencer
- Gram –ve Klebsiella, E-Coli, Viruses.
Pathogenesis
- presence of organisms in the bloodstream and abnormal cardiac endothelium facilitating their adherence
and growth. - may occur due to patient- (poor dental hygiene, intravenous drug use) or be associated with procedures
(dental treatment, intravascular cannulae, cardiac surgery, or permanent pacemakers). - Damaged endocardium promotes platelet and fibrin deposition allows organisms to adhere and grow
- Aortic and mitral valves are most commonly involved
Clinical picture - hard
Occur as an acute, fulminating, chronic or subacute illness with low-grade fever.
High clinical suspicion:
a. Regurgitant-murmur
b. embolic event
c. sepsis
d. haematuria, glomerulonephritis and suspected renal infarction
e. fever‘ plus:
- prosthetic material inside the heart
- other high predisposition for infective endocarditis, e.g. i.v. drug abuse
- newly developed ventricular arrhythmias or conduction disturbances
- first manifestation of congestive cardiac failure
- blood cultures (with typical organism)
- cutaneous (Osler, Janeway) or ophthalmic (Roth) manifestations
- peripheral abscesses (renal, splenic, spine)
- recent diagnostic / therapeutic interventions result in bacteraemia.
Low clinical suspicion. Fever only
Clinical picture senior - acute, subacute
- Acute:
- increased perspiration, weakness, anorexia, sleeplessness, ↑ temperature > 39 degrees, lose weight.
muscle dystrophy, hypovolemia with tachycardia, anemia, damage of valve, wide spread abscess,
thromboembolism - Subacute :
- Onset : Cold, weakness, malaise, headache, sweat, subfebrile 1-2months.
- After 2-3weeks, like in acute: ↑ temperature then drop to subfebrile level, lose weight, colour skin change
- clubbed fingers, splenomegaly, liver cirrhosis, disease of blood.
- inspiratory dyspnoe, palpitation, enlarged heart shape, sstolic & diastolic murmur.
- Vascular patho : Embolism & toxical vasculitis, myocarditis (enlarged heart by edema), pericarditis (pain)
exarcebate heart failure, embolism to coronary vessels.
- Petechial; spots HR in sclera & conjuctiva.
- Systemic immune vasculitis : Causes glomerularnephritis & HT. Hematuria.
- vasculitis on skin : Osler‘s Nodules in palm, soles. painful, red colour, protruded.
- Systemic vasculitis in liver with toxic effect & hepatitis - hepatomegaly.
- thrombosis of pulmonary artery with necrosis, infarction of lung. pneumonitis.
- Toxicity with depression of bone marrow: hyporegenerative anemia, lymphopenia, plasmocytosis.
Syndrome
- syndrome of inflammatory changes and septicaemia
- fever, chill, hemorrhagic rash, leucocytosis shift to left, accelerated ESR, high fibrinogen and α2-globulin contents, positive bl cultures - intoxication syndrome
- weakness, hyperhidrosis, headache, myalgia and arthralgia, poor appetite, pallor with icteric blue - syndrome of thromboembolic complication
- focal nephritis, MI, Infarction of spleen and intestine, Cerebral thrombo embolism
- Embolism of retina and vessels of lower extremities - syndrome of valvular lesions
- involvement of aortic and mitral valves - syndrome of immune disorders
- immune complexes in circulating blood - syndrome of immune lesions of organs and systems
- diffuse glomerulonephritis, myocarditis, hepatitis, vasculitis
investigation - blood analysis, biochemical , urinalysis, instrumental, microbiology, ecg, chest x-ray
- Blood :
- Aneosinophilia symptomatic for whole period of disease.
- Plasmacytosis appear in blood.
- Inflammatory markers. C-reactive protein (CRP) and ESR are increased. - Biochemical :
- Dysproteinaemia : alpha2-globulinaemia.
- transient azotemia
- serum Ig are increase, total complement and C3 complement are decreased
- Liver biochemistry. Serum alkaline phosphatase may be increased. - Urine :
- Proteinuria, hematuria, leucocyturia, cylinduria: Toxic kidney/glomerulonephritis.
- Presence bacteria in blood : Not sterile. - Instrumental :
- US : Show bacteria situated in valve. shows vegetations & cond of chambers (size,etc).
- US of spleen (enlarged), kidney.
- valvular dysfunction, aortic root abscesses - Microbiology
- serological test - PCR in culture-negative infective endocarditis
- ECG - atrioventricular block
- Chest X-ray
- heart failure or, in right-sided endocarditis, multiple pulmonary emboli and/oral abscesses.
treatment
- Antibacterial/Antiinfective Remedy :
- Penicillin. If mix flora, combination therapy with A‘glycoside (Gentamycin/Tobramycin).
- Monolactam AB : Tionam. last gen Penicillin : beta lactam, Amoxycoclaf. plus
Vancomycin/Cephalosporins of 3rd – 4th gen & Lincomycin.
- Enterococci : Vancomycin + Cephalosporins.
- Ampicillin; Pepericillin; Vancomycin; Tobramycin.
- Gram –ve : Cephalosporins (3rd & 4th gen), A‘glycoside last gen, Monolactam AB. - Remedy for immunity : Cephalosporins with A‘glycosides or Quinolones.
- Fungi : Diflucan, Ketokenazole, Fungisone.
- Antivirus : Cicloferon, Foskarnet.
- AB Fluoroquinolone before minor surgery.
- staphylococcal – vancomycin; gentamycin
- streptococcal – penicillin, gentamycin
- enterococcal – ampicillin / amoxicillin; gentamycin