Infective endocarditis Flashcards

1
Q

Etiology

A
  • 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.
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2
Q

Pathogenesis

A
  • 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
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3
Q

Clinical picture - hard

A

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

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4
Q

Clinical picture senior - acute, subacute

A
  1. Acute:
    - increased perspiration, weakness, anorexia, sleeplessness, ↑ temperature > 39 degrees, lose weight.
    muscle dystrophy, hypovolemia with tachycardia, anemia, damage of valve, wide spread abscess,
    thromboembolism
  2. 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.
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5
Q

Syndrome

A
  1. 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
  2. intoxication syndrome
    - weakness, hyperhidrosis, headache, myalgia and arthralgia, poor appetite, pallor with icteric blue
  3. syndrome of thromboembolic complication
    - focal nephritis, MI, Infarction of spleen and intestine, Cerebral thrombo embolism
    - Embolism of retina and vessels of lower extremities
  4. syndrome of valvular lesions
    - involvement of aortic and mitral valves
  5. syndrome of immune disorders
    - immune complexes in circulating blood
  6. syndrome of immune lesions of organs and systems
    - diffuse glomerulonephritis, myocarditis, hepatitis, vasculitis
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6
Q

investigation - blood analysis, biochemical , urinalysis, instrumental, microbiology, ecg, chest x-ray

A
  1. Blood :
    - Aneosinophilia symptomatic for whole period of disease.
    - Plasmacytosis appear in blood.
    - Inflammatory markers. C-reactive protein (CRP) and ESR are increased.
  2. 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.
  3. Urine :
    - Proteinuria, hematuria, leucocyturia, cylinduria: Toxic kidney/glomerulonephritis.
    - Presence bacteria in blood : Not sterile.
  4. Instrumental :
    - US : Show bacteria situated in valve. shows vegetations & cond of chambers (size,etc).
    - US of spleen (enlarged), kidney.
    - valvular dysfunction, aortic root abscesses
  5. Microbiology
    - serological test
  6. PCR in culture-negative infective endocarditis
  7. ECG - atrioventricular block
  8. Chest X-ray
    - heart failure or, in right-sided endocarditis, multiple pulmonary emboli and/oral abscesses.
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7
Q

treatment

A
  1. 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.
  2. 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
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