Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiorespiratory > Lecture 18: CV infections > Flashcards

Lecture 18: CV infections Flashcards

1
Q

what is Infectious endocarditis?

A

An infectious inflammation of the endocardium that typically affects the heart valves but can affect the mural endocardium and septal defects. Typically caused by bacteremia (especially from gram-positive cocci). Divided into acute and subacute forms. Signs and symptoms include constitutional symptoms (e.g., fevers, chills, tachycardia, weight loss), cough, pleuritic chest pain, new heart murmur or arrhythmia, and extracardiac manifestations (e.g., cutaneous changes, renal injury).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the importance of IE?

A
  • -Uncommon, <0.1% of hospital admissions; potentially fatal; easily missed; need a high index of suspicion
  • -In the differential for a fever/pyrexia of unknown origin (F/PUO)
  • -Rheumatic fever important in resource-poor countries; IV devices often the risk factor in well resourced countries
  • -Microbiological role in diagnosis & treatment
  • -Preventable in some instances with prophylactic antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the types of infective endocarditis?

A

1) Native valve endocarditis
- -No health care contact
- -Nosocomial endocarditis
- -Healthcare related endocarditis resulting from invasive procedures
2) Prosthetic valve endocarditis
3) Endocarditis in intravenous (IV) drug users, often right-sided
4) Staphylococcal, streptococcal, fungal, etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the epidemiology of IE?

A
  • -Incidence increasing due to prosthetic valve surgery & iv drug use (IVDU)
  • -Mean age has increased (50 years) as the population has aged & rheumatic fever has declined
  • -Term ‘subacute’ & ‘acute’ less often used now
  • -Majority of patients have a recognized lesion, e.g. aortic stenosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the mean age of IE?

A

Mean age has increased (50 years) as the population has aged & rheumatic fever has declined

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the risk factors of IE?

A

1) Demographics
- -Male sex
- -Age > 60 years
2) Preexisting conditions
- -Previous IE
- -Pre-damaged or prosthetic heart valves
- -Congenital heart defects
- -Need for chronic hemodialysis
- -Impaired immune function (e.g., HIV infection)
3) Bacteremia
- -Infected peripheral venous catheters, surgery, dental procedures
- -Non-sterile venous injections (e.g., IV drug abuse)
- -Bacterial infections of various organs (e.g., UTIs, spondylodiscitis)
- —Investigations of, or procedures (e.g. surgery) involving the gastrointestinal, genitourinary or upper respiratory tracts
- -Indwelling devices
4) Animal exposure/pets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the pathogenesis of IE?

A
  • -localized infection or contamination → bacteremia → bacterial colonization of damaged valve areas → formation of fibrin clots encasing the vegetation → valve destruction with loss of function
  • -Preexisting valvular endothelial damage or prosthetic valves predispose to bacterial colonization, especially of those that cause subacute IE
  • -Platelets/fibrin act as a nidus for bacteria
  • -Bacteria adhere to clot/aggregate & vegetation develops
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what valves are frequently involved in IE?

A

Frequency of valve involvement: mitral valve > aortic valve > tricuspid valve > pulmonary valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the most commonly affected valve in IVDUs?

A

Tricuspid valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the clinical consequences of IE?

A
  • -Bacterial thromboemboli from bacterial vegetation → vessel occlusion with infarctions
  • -Formation of immune complexes and antibodies against tissue antigens → glomerulonephritis, Osler nodes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the factors that determine if the vegetation forms?

A
  • -Type of organism & or microbial load
  • -Site & or type of heart defect
  • -Host defense mechanisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the most common cause of IE overall?

A

S.Aureus

  • -a most common cause of acute IE for all groups (including IV drug users and patients with prosthetic valves or pacemakers/ICDs)
  • -Affects previously healthy valves
  • -Usually fatal within 6 weeks (if left untreated)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the most common cause of subacute IE?

A

Viridans streptococci

  • -Most common cause of subacute IE, especially in predamaged native valves (mainly the mitral valve)
  • -Common cause of IE following dental procedures
  • -Produce dextrans that facilitate binding fibrin-platelet aggregates on damaged heart valves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

name a common cause of IE in patients with prosthetic heart valves.

A
  • -Staphylococcus epidermidis
  • -IE transmitted via infected peripheral venous catheters
  • -Common cause of subacute IE in patients with prosthetic heart valves or pacemakers/ICDs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

name a common cause of IE following nosocomial urinary tract infections?

A
  • -Enterococci
  • -Multiple drug resistance
  • -Common cause of IE following nosocomial urinary tract infections (UTIs)
  • -Following gastrointestinal or genitourinary procedures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the significance of Streptococcus gallolyticus?

A
  • -S. gallolyticus is associated with colorectal cancer

- -If S. gallolyticus is detected, colonoscopy is indicated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Gram-negative HACEK group includes…

A

Haemophilus species, Aggregatibacter actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae

  • -Physiological oral pharyngeal flora (∼ 3% of cases of IE)
  • -In patients with poor dental hygiene and/or periodontal infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

does Candia and Aspergillus cause IE?

A

Yes

  • -Causes IE in immunosuppressed patients
  • -Causes IE in IV drug abusers
  • -Cause of IE after cardiosurgical interventions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the causes of prosthetic valve endocarditis?

A

1) Coagulase-negative staphylococci (30-35%) Staphylococcus aureus (20-25%)
- -Mostly early prosthetic valve endocarditis (first 60 days)
2) S. epiermidis

Others
culture-negative
fungal
polymicrobial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the most common cause o late-onset prosthetic valve endocarditis?

A

S. epiermidis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are the clinical features of IE?

A

1)Fever: often low grade; chills, rigors, night sweats
(persistent or unexplained bloodstream infection)
2)Murmur: new or changing; +/- other cardiac signs
3)Non-specific: malaise, fatigue, weight loss, arthralgia/ myalgia – often missed
4)Embolic phenomenon: arterial emboli (white leg), ‘stroke’, pulmonary infarcts (drug abusers)
5)Immunological phenomena e.g. Osler’s nodes, Roth Spots, etc. are now rarely seen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the clinical course of acute vs subacute IE?

A

1)Rapid, fulminant progression (days to weeks). More severe constitutional symptoms (e.g., high fever)
2)Insidious onset. Slow progression (weeks to months).
Less severe constitutional symptoms (e.g., low fever possible, often absent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the cardiac manifestations of IE?

A

1) New heart murmur development or change to a preexisting one
- -Mitral valve regurgitation → holosystolic murmur, loudest at the heart’s apex, and radiates to the left axilla
- -Tricuspid valve regurgitation → holosystolic murmur; loudest at the left sternal border ; seen in IV drug users and concomitant HIV infection, immunosuppressed patients, and patients with central venous catheters
- -Aortic valve regurgitation → early diastolic murmur; loudest at the left sternal border
2) Signs of progressive heart failure (e.g., dyspnea, edema)
3) Signs of acute cardiac decompensation (pulmonary edema)
4) Arrhythmias
- -Suspect perivalvular abscess in patients with infective endocarditis who develop a new conduction abnormality (e.g., a third-degree atrioventricular block)

24
Q

new-onset conduction defect in a patient with IE suggests?

A
  • -perivalvular abscess
  • -Infection spreads to the valve annulus and/or cardiac septum (paravalvular extension) → abscess formation → new-onset conduction delay → arrhythmia
25
Q

what are the extracardiac manifestations of IE?

A
  • -Petechiae; especially splinter hemorrhages (hemorrhages underneath fingernails)
  • -Janeway lesions: non-tender, erythematous macules on palms and soles (due to microemboli and microabscesses with neutrophilic capillary infiltration)
  • -Osler nodes: painful nodules on pads of the fingers and toes
  • -Roth spots: retinal hemorrhages with pale centers
  • -Signs of acute renal injury, including hematuria and anuria
  • -Splenomegaly and possible LUQ pain
  • -Neurological manifestations (e.g., seizures, paresis)
  • -Signs of pulmonary embolism (e.g., dyspnea)
  • -Possible arthritis
26
Q

what are the Osler nodes?

A

Painful subcutaneous nodules on the pads of the fingers and toes that typically occur in protracted cases of infective endocarditis. The lesions are due to immune complex-mediated vasculitis that most likely occurs as a sequelae of microthrombi occluding the vasculature.

27
Q

what are the Roth spots?

A

Retinal hemorrhages that can occur in infective endocarditis. Roth spots are most likely caused by septic microemboli that lead to vascular occlusion and localized immune-mediated vasculitis. Examination usually shows exudative, hemorrhagic lesions with pale centers.

28
Q

what are the Janeway lesions?

A

Nontender erythematous macules and papules on the palms and soles that can occur in infective endocarditis. The lesions are thought to be caused by septic embolization from the infected valve.

29
Q

when IE should be suspected?

A

Endocarditis should be suspected in all patients with fever & a heart murmur

  • -Endocarditis should be considered as a cause of F/PUO
  • -Endocarditis should be suspected in all patients with unexplained emboli
  • -Endocarditis should be suspected in patients with unusual cardiac dysfunction, even in the absence of a fever
30
Q

what are the other causes of Roth spots?

A

Roth’s spots are retinal haemorrhages with white or pale centers composed of coagulated fibrin 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 anaemia, ischemic events, and rarely in HIV retinopathy.

31
Q

what are the immune complex manifestations of IE?

A

Osler nodes, Roth spots,glomerulonephritis

32
Q

what lab studies should be performed in suspected IE?

A
  • -Best initial test: blood cultures: Before starting antibiotic treatment. Transport blood cultures (3 to 5 separate sets) to the lab within 2 hours.
  • -Leukocytosis (with left shift), ↑ ESR, ↑ CRP
33
Q

in IE echocardiography shows…

A
  • -Detects valve vegetations , new valvular regurgitation, abscess, dehiscence of prosthetic valve
  • -Transthoracic echocardiography (TTE) usually performed first (sensitivity: ∼ 75%)
  • -Transesophageal echocardiography (TEE) to confirm findings; higher sensitivity (> 90%) than TTE
34
Q

what is the Duke criteria?

A

A set of diagnostic criteria for infective endocarditis. To be positive, a patient must have: two major criteria, one major and three minor criteria, or five minor criteria. Major criteria include: (1) two separate blood cultures positive for typical pathogens and (2) evidence of endocardial involvement in echocardiography. Minor criteria include: (1) underlying heart disease or IV drug abuse, (2) fever, (3) signs of embolism, (4) immunologic findings (e.g., Osler nodes), (5) Roth spots, and (6) positive blood culture for an atypical pathogen.

35
Q

what are the major Duke criteria?

A
  • -Two separate blood cultures positive for typical pathogens
  • -Evidence of endocardial involvement in echocardiography
  • -A new valvular regurgitation (worsening of a pre-existing murmur is not sufficient)
36
Q

what are the minor Duke criteria?

A
  • -Predisposition: underlying heart disease or IV drug abuse
  • -Fever ≥ 38°C (100.4F)
  • -Vascular abnormalities
  • -Immunologic disorder
  • -Microbiology (ositive blood cultures for atypical pathogens other than the ones typical in IE)
37
Q

can negative transthoracic echocardiography rule out IE?

A

Only negative findings on transesophageal echocardiography (TEE) can reliably rule out endocarditis, as transthoracic echocardiography (TTE) is not sensitive enough!

38
Q

Janeway lesions vs Osler nodes?

A
  • -Janeway lesions are non-tender, small erythematous or haemorrhagic macular or nodular lesions on the palms or soles only a few millimeters in diameter that are pathognomonic of infective endocarditis.Pathologically, the lesion is described to be a microabscess of the dermis with marked necrosis and inflammatory infiltrate not involving the epidermis. They are caused by septic emboli which deposit bacteria, forming microabscesses. Janeway lesions are distal, flat, ecchymotic, and painless.
  • -Osler’s nodes and Janeway lesions are similar, but Osler’s nodes present with tenderness (Olser–Ouch) and are of immunologic origin
39
Q

what are the management principles of IE?

A
  • -Unless the patient is very ill, confirm the etiology first before starting antibiotics
  • -Liaise with microbiology/infectious diseases regarding diagnosis, optimal therapy & follow-up
  • -Combination of antibiotics usually required for 4-6 weeks; shorter courses now increasingly being considered
  • -Early consultation with a cardiac surgeon if complications (e.g. recurrent emboli) or failure to respond to treatment; up to 40% require surgery
  • -Confirm diagnosis, e.g. Str. mitis from repeat blood cultures – a continuous bloodstream infection
  • -Minimum inhibitory concentrations (MICs), i.e. how antibiotic susceptible is the organism
  • -Choice of antibiotic to obtain synergy
  • -Regular antibiotic assays of aminoglycosides i.e. gentamicin & vancomycin, to avoid toxicity
40
Q

the pulmonary valve is most commonly affected in right-sided IE. True/False

A

False

  • -A minority, 5-10% of cases
  • -Associated with IVDU, cardiac device infections, central venous catheters, HIV & congenital heart disease
  • -Tricuspid valve often affected
  • -Signs of sepsis, respiratory symptoms (emboli), lung abscess
  • -Outcome good but poor compliance amongst IVDUs
41
Q

what are the causes of right-sided IE?

A

Associated with IVDU, cardiac device infections, central venous catheters, HIV & congenital heart disease

42
Q

what are the common causes of culture-negative endocarditis?

A

1) Prior antibiotic treatment
2) Fastidious organisms
3) Nutritionally variant streptococci
4) HACEK group (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella-kingella)
5) Uncommon bacteria or special growth requirements

  • -Bartonella spp.
  • -Chlamydia spp.
  • -Coxiella burnetti (Q fever)
  • -Brucella abortus
  • -Legionella spp.
  • -Tropheryma whippelii
  • -Non-Candida fungi
43
Q

what is the empiric treatment of native valve endocarditis?

A

1) Initial intravenous empiric antibiotic treatment with vancomycin → adapt intravenous antibiotics according to resistogram results from blood cultures
2) The duration of treatment depends on the patient’s profile, the pathogen’s resistance, and the patient’s response to treatment.
3) 4-week treatment
- -Drug of choice: penicillin G
- -Alternatives: ampicillin, IV ceftriaxone, IV vancomycin
4) 2-week treatment regimens
- -Drug of choice: gentamicin + penicillin G
- -Alternative: gentamicin + ceftriaxone

44
Q

what is the treatment of prosthetic valve endocarditis?

A
  • -Generally the same antibiotic regimen as for native valves, but longer duration (at least 6 weeks)
  • -Exceptions for staphylococci
    1) Methicillin-susceptible: nafcillin (or oxacillin, cefazolin) + rifampin + gentamicin
    2) Methicillin-resistant: vancomycin + rifampin + gentamicin
45
Q

does prosthetic valve IE is easier to treat?

A

No
Infective endocarditis in prosthetic valves is much harder to treat than in native valves. Surgical valve replacement may be required.

46
Q

what is the treatment of IE in IVDUs?

A
  • -Intravenous empiric antibiotic treatment with vancomycin
  • -After confirmation of a susceptible pathogen
    1) IV nafcillin (2 weeks)
    2) PO cloxacillin (2 weeks)
47
Q

what is the outcome of IE?

A
  • -Untreated–100% mortality

- -Treated–20% mortality (decreasing), 40% if prosthetic valve

48
Q

what are the indicators of poor prognosis in IE?

A
  • elderly patients
  • delay in treatment
  • Gram-negative bacilli (e.g. E. coli), fungal, Q. fever
  • > 1 valve involved
  • valve destruction or congestive cardiac failure
49
Q

what is the prophylaxis of IE?

A

1) Indicated for high-risk patients (Heart defects, prosthetic heart valves, history of endocarditis) undergoing procedures with a risk of bacteremia
2) Regimens
- -Usually PO amoxicillin (administer 1 hour before the procedure)
- -Patients who are unable to take oral medication: IV ampicillin
- -Patients with penicillin allergy: PO clarithromycin or azithromycin

50
Q

what is the pericarditis?

A
  • -Inflammation of the pericardium, often with pericardial effusion”
  • -presents with fever, chest pain & a pericardial rub may be present
51
Q

what are the causes of pericarditis?

A
  • -Coxsackie, influenza, adenovirus, Staphylococci/Streptococci etc.
  • -TB also to be considered
52
Q

what is the myocarditis?

A
  • -Inflammation of the heart muscle due to infection, usually viral”
  • -presents with fever, unexplained cardiac failure, arrhythmias etc.
53
Q

what are the causes of myocardium?

A
  • -Influenza virus
  • -Coxsackie B virus
  • -Corynebacterium diphtheriae(unusual in the industrialised world, due to toxins)
54
Q

how cardiac device infections present?

A

–Increasingly important as population ages
2% get infected in first 5 years
–Local cellulitis with discharge & pain or bloodstream infection, +/- endocarditis
–Diagnosis clinically, with culture of pus or excised, device & blood cultures
–Source control & weeks of antibiotics as for IE

55
Q

conditions that predispose to peripheral vascular infections?

A
  • -Should be considered in the context of post-operative infections
  • -The presence of a graft, e.g. aortic aneurysm repair, renders diagnosis & treatment more challenging
  • -Patients are often elderly with underlying cardiovascular (e.g. ischaemic heart disease) or systemic diseases (e.g. diabetes mellitus)
56
Q

what are the causes of peripheral vascular infections?

A
  • -Skin flora, e.g. Staph. epidermidis but also Staph. aureus the main causes
  • -Enteric flora, e.g. E. coli or Pseudomonas aeruginosa if groin infection
  • -Infections may be:
    1) Superficial like any surgical site infection
    2) Deep infection involving graft
    3) Associated with systemic infection such as bloodstream infection
  • -Treatment is challenging; prolonged antibiotics +/- removal of graft (source control)

Cardiorespiratory (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions