Endocarditis, Percarditis & Effusion Flashcards
What is Infective endocarditis
Infection of the endothelial lining of the heart. Commonly involves cardiac valves. May include margins of VSD and intracardiac devices.
Name and describe 4 types of infective endocarditis
Acute Bacterial Endocarditis:
- infection of normal valves with a highly virulent organism
(S.aureus, group A strep, Strep Pneumoniae)
Subacute Bacterial Endocarditis:
- indolent infection of abnormal valves with less virulent organism
(S. Viridans)
Native Valve Endocarditis
vs
Prosthetic Valve Endocarditis
Risk factors for Endocarditis
For an Abnormal valve
High risk;
- Prior endocarditis, Rheumatic valve disease, Aortic valve disease(bicuspid), prosthesis
Medium risk;
- Mitral valve disease, Hypertrophic cardiomyopathy
Abnormal risk of bacteraemia
- IV drug use, indwelling venous catheters, poor Dentition, Hemodialysis, pacemakers, ICD, MRSA
Microbiology etiology for the types of endocarditis
80% cases are:
Staphylococci, Streptococci and Enterococci (in older males following GI/GU procedures)
ABE = S.aureus, group A or other beta-hemolytic strep, Strep pneumo
SBE = Streptococcus Viridans
Prosthetic valve endocarditis
= Staphylococcus Epidermidis
Culture negative endocarditis
= HACEK (Hemophilus parainfluenzae, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
= Bartonella, Coxiella, Chlamydia, Legionella, Brucella
Fungal Endocarditis
= Candida, Aspergillus
Clinical manifestations
Infective Endocarditis syndrome is highly variable and spans a continuum between Acute and Subacute presentations.
Persistent bacteraemia;
(Fever, chills, night sweats, weightloss, fatigue, Anemia)
Valvular/perivalvular involvement;
(Murmur, CHF due to valvular dysfunction, conduction abnormalities)
Septic emboli;
( systemic emboli to CNS, kidney, speen, joints, periphery)
(Stroke)
(Pulmonary embolism if right sided)
(Coronary artery embolism = MI)
Immune complex phenomenon;
(Arthritis, Glomerulonephritis, ¡ESR, ¡CRP, ¡RF positive)
Work up and diagnosis + Criteria
When a febrile patient presents with endocarditis risk factors, cardiac or non-cardiac features or microbiological findings, then perform clinical, microbiologic and echocardiographic evaluation.
Modified Duke Criteria:
(2 major) OR (1 major + 3 minor) OR 5minor
OR
- Vegetation / intracardiac abscess on histology
OR
- Microorganism found by culture or histology of a vegetation or intracardic abscess.
Dukes Criteria brief description
1 of the following positive culture;
Typical microorganisms from 2 separate blood cultures:
- S. aureus
- S. Viridans
- S. Bovis
- HACEK group
- Enterococci (community acquired)
OR
persistently positive blood culture of
Typical organisms
*atleast 2 positive >12hrs apart
Skin contaminants
*3-4 cultures (1st and last atleast 1hr apart)
OR
Single positive blood culture for
Coxiella Burnetii or IgG >1:800
Evidence of endocardial involvement (1 of the following)
- Vegetation (TEE)
- Abscess
- new partial dehiscence of prosthetic valve
OR
New valvular regurgitation
Minor criteria;
1. Predisposition (e.g IV drug use, prosthetic valve, valve lesion with significant regurgitation or turbulence)
2. Fever >38°C
3. Vascular phenomena (e.g major arterial emboli, septic pulmonary infarcts, etc
4. Immunologic phenomena (e.g glomerulonephrits, Osler nodes, Roth spots, Rheumatic factor e.t.c)
5. Microbiologic evidence - positive blood cultures that do not meet major criteria
Management of Infective Endocarditis
ABE = empiric antibiotics started promptly after culture
Native valve - Vancomycin + Gentamycin
Prosthetic valve (add Ceftriaxone)
SBE = antibiotics may be delayed until blood culture results
Empiric Native valve (Ceftriaxone + Gentamycin)
For specific bacteria
Strep = Gentamycin + penicillin G
Or Ceftriaxone or Vancomycin
Enterococci = same
Or Ampicillin or Vancomycin
MRSA = Vancomycin + Gentamycin
HACEK = Ceftriaxone or Ampicillin
Coxiella Burnetii = Doxycycline + hydroxychloroquine
Bartonella = Ceftriaxone + Gentamycin
Early Surgery **** before completion of a full course of antibiotics.
Indications ;
- Aortic or mitral regurgitation
- paravalvular extension of infection
with development of annular or aortic abscess, fistula or Heart block.
- Unstable prosthetic valve
- difficult to treat pathogen e.g fungi
- persistent bacteraemia or fever >7days
- large >10mm hypermobile vegetation
What is Pericarditis
An inflammation of the pericardium
Characterized by pericarditic chest pain, precardial friction rub (left sternal border triphasic grating sound), and ECG changes (e.g new widespread ST elevation or PR depression; new or worsening pericardial effusion)
Pathophysiology of pericarditis
In most cases, the pericardium is acutely inflammed and has an infiltration of PMN leukocytes and pericardial vascularization. Eventually it leads to a fibrinous reaction with exudate and adhesions.
Granulomatous pericarditis occurs with tuberculosis, fungal infections, Rheumatoid arthritis and sarcoidosis.
Types of pericarditis
Acute Pericarditis
Viral infection
- is the most common cause of acute Pericarditis. Usually self limited lasting 1-3 weeks
**Coxsackievirus B & Influenza, ***HIV and others.
Patients may have associated Myocarditis.
Bacterial Infections
- result from direct pulmonary extension, hematogenous spread, myocardial abscess or endocarditis. Trauma or surgery.
** Strep pneumo, other strep and staphylococcus species, E.coli, Pseudomonas, proteus, klebsiella, salmonella, Shigella, neisseria meningitidis and H.influenzae
*** Thoracic surgery, renal disease and Immunosuppression****
(Serous Pericarditis)
- usually caused by non-infectious inflammation like in Rheumatoid arthritis and SLE. Fibrous adhesions rarely occur.
(Fibrous & serofibrous)
- most frequent types with the same basic process. Common causes include AMI, post- MI Dressler syndrome, Uremia, radiation etc. Severe infections and routine cardiac surgery as well.
(Purulent or Suppurative)
- due to a causative organism which may arise from hematogenous seeding, lymphatic extension, or direct introduction during cardiotomy. ***Immunosuppression***
Clinical features
Fever, chills, and Spiking temperatures.
***Constructive Pericarditis ***
(Hemorrhagic Pericarditis)
- blood mixed with a fibrinous or Suppurative effusion. Most commonly caused by tuberculosis or direct neoplastic invasion.
Also in severe bacterial infections in patients with a bleeding problem.
Common after cardiac surgery or trauma and may cause tamponade.
Until proven otherwise, caseation within the pericardial sac is Tuberculous in origin.
Untreated is most common cause of Chronic Constrictive Pericarditis.
Chronic Pericarditis:
Adhesive mediastinopericarditis is a reaction that usually follows suppurative or caseous percarditis, cardiac surgery or irradiation. The pericardial potential space is obliterated and adhesion of the external parietal layer to the surrounding structures occurs.
Systolic contraction of the ribcage and diaphragm + pulsus paradoxus may be observed.
Increased workload = massive cardiac hypertrophy and dilation.
Constrictive Pericarditis is caused by Suppurative, caseous or Hemorrhagic Pericarditis. Heart is encased in thick layer of scar or calcification with no hypertrophy.
Patient presentation of pericarditis
Chest pain - precordial or retrosternal with referral to the trapezius, neck, left shoulder or arm.
Pain is worse with inspiration, laying flat or during swallowing. May be released by leaning forward while seated.
Palpitations
Dyspnea, Tachypnea
Low grade intermittent fever
Findings on physical examination for Pericarditis
Pericardial friction rub (grating sound, triphasic -atrial & ventricular systolic rub and early diastolic rub)
Auscultation of left lower sternal edge (Apex) with patient sitting up and leaning forward.
Ewart sign = dullness and bronchial breathing between the tip of the left scapula and the vertebral column
ECG
1. Widespread concave ST elevation and PR depression in most leads
2. aVR has reciprocal ST depression and PR elevation +/-V1
3. Sinus tachycardia due to pain or Pericarditis effusion
Stages
1 - ST elevation + PR depression
(first 2 weeks)
2 - flattened T waves 1-3 weeks
3 -3 weeks T waves become inverted
4 - several weeks later = normal
Pericarditis in Myocardial Infarction.
After a transmural infarction, a fibrinous pericardial exudate appears within 24 hrs, begins to organise at 4-8 days and completes organisation at 4 weeks.
Pericardial pain occurs less frequently than the friction rub detected on the 2nd or 3rd day after an AMI.
Pericardial involvement indicates a larger infarction, greater incidence of left ventricular dysfunction and greater mortality. The pericarditis usually heals without consequence.
Describe the Dressler syndrome
Observed 2-3 weeks after an MI
A secondary pericarditis.
This may be an autoimmune inflammatory reaction to myocardial neo-antigens formed as a result of MI. Or an unrecognised post-MI pericarditis.
May develop pulmonary infiltrates and large pericardial effusions.
