Endocarditis
Native: non-viridans strep, strep viridans, enterococci, staph aureus
Prosthetic: coagulase neg. staph (early <60 days postop), Staph Aureus (>60 days post op), Non-viridans strep, enterococci
IVDA/Immunocompromised: staph aureus, strep, gram-negative bacilli
Fever/Anemia/Murmur
Change in mental status due to embolization
Ptechiae, splinter hemorrhages, osler noders (palmar surface of fingertips; tender), janeway lesions (flat macular lesions on the palms; painless), Roths spots (pale c red halo)
Can present with microscopic hematuria (up to 50% of the time)
Get three sets blood cultures from three different sites. Better if separated by time.
Rheumatic Fever
Jones criteria (major)-carditis, polyarthritis, chorea, erythema marginatum (smoke ring of erythema), Sub-Q nodules
Antistrep antibodies stay positive 4-6 weeks post infxn
Native: PCN G and Naf and Genta or Vanco/Genta
Prosthetic: Naf, Genta, Rifampin or Vanco/Genta/Rifampin
virtually all bacteria have been implicated 2. vast majority cause by gram positive organisms a. viridans streptococci most common for abnormal native heart valve IE b. staph aureus most common in injection drug users (normal native valves) and in PV IE c. staph epidermidis (coag staph) relatively common in PV IE 3. fungal organisms in PV IE, immunosuppressed hosts, and indwelling vascular catheters 4. remember the fastidious gram neg bacilli that can cause endocarditis: HACEK organisms that will grow very slowly in culture a. Haemophilus parainfluenza, Haemophilus aphrophilus b. Actinobacillus actinomycetemcomitans c. Cardiobacterium hominum d. Eikenella corrodens e. Kingella kingae
Complications A. embolic phenomenon 1. seen in 22-50% of cases 2. mitral vegetations have highest rate (25%) especially anterior leaflet (37%) – followed by aortic (10%) 3. most cases occur within first two weeks of treatment 4. staph and fungus embolize most frequently 5. CNS most common site (65%) and most of these lodge in MCA 6. Splenic infarct common (40% of left sided IE) but only 5% of these go on to abscess formation 7. ECHO finding risk factor for embolization: vegetations >1 cm in diameter B. periannular infection/abscess 1. very common with prosthetic valve IE (56-100%) 2. 10-40% incidence in native valve IE (AV >MV or TV) 3. AV conduction block may result 4. myocardial fistulae can occur leading to intracardiac shunts 5. prosthetic valve dehiscence leading to CHF 6. rupture into the pericardium also a concern tamponade or purulent pericarditis may result 7. most will need surgery C. acute valvular insufficiency with acute CHF 1. perforation of valve 2. rupture of chordae tendinae 3. dehiscence of prosthetic valve 4. paravalvular leak D. valve obstruction from bulky vegetation 1. fungus is frequent pathogen in this setting 2. less common complication VII. Prophylaxis A. Recommended for whom? 1. High risk a. prosthetic heart valve b. h/o endocarditis c. complex cyanotic CHD (transposition, Tetralogy of Fallot) 2. Moderate risk a. Other congenital heart disease b. Acquired valvular dysfunction (e.g. RHD) c. MVP with regurgitation (or thickened leaflets) d. Hypertrophic cardiomyopathy 3. Not recommended a. isolated secundum ASD b. Surgical repair of ASD, VSD, or PDA c. MVP without regurgitation d. Previous CABG e. functional or physiologic heart murmurs f. pacemakers and implanted defibrillators B. For which ED procedures? 1. dental procedure causing gingival bleeding 2. insertion of FC when UTI is present – controversial 3. I&D of abscess 4. Bronchoscopy C. Which antibiotics: 1. Oral or respiratory procedures b. amoxacillin 2 g po one hr pre-procedure (15 mg/kg for children) c. NPO: ampicillin 2 g IV or IM within 30 pre-procedure d. PCN allergic: clindamycin 600 mg, or cephalexin 2 g, clarithromycin/azithromycin 500 mg po 1 hr pre-procedure e. NPO/PCN allergy: clindamycin 600 mg IV or cephazolin 1 g IV/IM within 30 pre-procedure 2. GU procedures a. high risk: ampicillin 2 g and gentamicin 1.5 mg/kg IV/IM within 30 of procedure; 6 hr later, ampicilling 1 g iv/im or amoxacillin 1 g po; substitue single dose of vanco if PCN allergy b. moderate risk: amoxacillin 2 g po one hr pre-procedure or ampicillin 2 g IV/IM within 30 of procedure 3. Skin/soft tissue abscess (non-oral) a. dicloxacillin or cephalexin single dose one hr pre procedure b. vancomycin for those NPO or PCN- allergic SELECTED REFERENCES 1. Wilson WR, Karchner AW, Dajani AS, et al: Antibiotic treatment of adults with infective endocarditis due to steptococci, enterococci, staphylococci, and HACEK microorganisms: American Heart Association. JAMA 1995;274:1706. 2. Bayer AS, Bolger AF, Taubert KA, et al: Diagnosis and management of infective endocarditis. Circulation 1998;98:2936. 3. Dajani AS, Taubert KA, Wilson W, et al: Prevention of bacterial endocarditis: recommendations by the American Heart Association. JAMA 1997;277:1794. 4. Bayer AS: Infective endocarditis. Clin Infect Dis 1993;17:313. 5. Anonymous. Management of infective endocarditis. Drug & Therapeutics Bulletin. Apr. 2002 404):26-30. 6. Barnes PD, Crook DW. Culture negative endocarditis. Journal of Infection. 1997; 35(3):209-13. 7. Delahaye F, Hoen B, McFadden E, et al. Treatment and Prevention of infective endocarditis. Expert Opinion on Pharmacotherapy. 2002; 3(2):131-45 8. Giessel BE, Koenig CJ, Blake RL Jr. Management of bacterial endocarditis. American Family Physician. Mar 2000 61(6):1725-32. 9. Hoesley CJ, Cobbs CG. Endocarditis at the millennium. Journal of Infectious Diseases. Mar. 1999 179 Suppl 2:S360-5. 10. Keys TF. Infective endocarditis: prevention, diagnosis, treatment, referral. Cleveland Clinic Journal of Medicine. May 2000 67(5):353-60. 11. Mauri L, de Lemos JA, OGara PT. Infective Endocarditis. Current Problems in Cardiology, Sep. 2001 26(9):562-610.Farmer JA, TorreG. Endocarditis. Current Opinion in Cardiology. Mar 1997 12(2:123-30 12. Pawsat DE, Lee JY. Inflammatory disorders of the heart. Pericarditis, myocarditis, and endocarditis. Emergency Medicine Clinics of North America. Aug. 1998 16(3):665- 81. 13. Piper C, Korfer R, Horstkotte D. Prosthetic valve endocarditis. Heart (British Cardiac Society) May 2001 85(5):590-3. 14. Stamboulian D, Carbone E. Recognition, management and prophylaxis of endocarditis. Drugs Nov. 1997 54(5):730-44.
Prophylaxis
(1) a prosthetic valve of any kind, (2) a history of prior IE, or (3) a history of congenital cyanotic heart disease
EASE trial just reported shows early surgery should be the path instead of intial medical management
2023 Duke-International Society for Cardiovascular Infectious Diseases Diagnostic (Duke-ISCVID) criteria
Changes are in bold.
I. DEFINITE ENDOCARDITIS
A. Pathologic Criteria
- Microorganisms identifieda in the context of clinical signs of active endocarditis in a vegetation; from cardiac tissue; from an explanted prosthetic valve or sewing ring; from an ascending aortic graft (with concomitant evidence of valve involvement); from an endovascular intracardiac implantable electronic device (CIED); or from an arterial embolus…
or - Active endocarditisb (may be acutec or subacute/chronicd) identified in or on a vegetation; from cardiac tissue; from an explanted prosthetic valve or sewing ring; from an ascending aortic graft (with concomitant evidence of valve involvement); from a CIED; or from an arterial embolus
B. Clinical Criteria
- 2 Major Criteria
or - 1 Major Criterion and 3 Minor Criteria
or - 5 Minor Criteria
II. POSSIBLE ENDOCARDITIS
- A. 1 Major Criterion And 1 Minor Criterion
or - B. 3 Minor Criteria
III. REJECTED ENDOCARDITIS
- A. Firm alternate diagnosis explaining signs/symptomse
or - B. Lack of recurrence despite antibiotic therapy for less than 4 d.
or - C. No pathologic or macroscopic evidence of IE at surgery or autopsy, with antibiotic therapy for less than 4 d or
- D. Does not meet criteria for possible IE, as above
Here are all the tiny footnotes:
- aBy culture, staining, immunologic techniques, polymerase chain reaction (PCR), or other nucleic acid–based tests including amplicon (16S, 18S, internal transcribed spacers) sequencing, metagenomic (shotgun) sequencing, or in situ hybridization on fresh or paraffin-fixed tissue. Molecular techniques and tissue staining (Gram stain, periodic acid–Schiff with diastase, Grocott, or silver stains such as Warthin-Starry, Steiner, or Dieterle) should be interpreted cautiously, particularly in patients with a prior episode of IE because such tests can remain positive for extended periods following successful treatment. Antibiotic therapy before tissue procurement may also significantly alter microorganism morphology and staining characteristics. Test specificity is influenced by several factors, and false positives can occur. Test interpretation should always be in the context of clinical and histological evidence of active endocarditis. A single finding of a skin bacterium by PCR on a valve or wire without additional clinical or microbiological supporting evidence should be regarded as Minor Criterion and not Definite IE [51].
- bActive endocarditis—vegetations, leaflet destruction, or adjacent tissue of native or prosthetic valves showing variable degrees of inflammatory cell infiltrates and healing. Many specimens demonstrate mixed features.
- cAcute endocarditis—vegetations or cardiac/aortic tissue lesions of native or prosthetic valves showing active inflammation without significant healing or organizational change.
- dSubacute/chronic endocarditis—vegetations or cardiac/aortic tissue lesions of native or prosthetic valves demonstrating evidence of healing or attempted healing: maturing granulation tissue and fibrosis showing variable mononuclear cell infiltration and/or calcification. Calcification can occur rapidly in injured tissue and vegetations or be part of the underlying valvular disease that was the original nidus for IE.
- eFirm alternate diagnosis explaining IE signs and symptoms consists of either microbiologic or nonmicrobiologic causes. Firm alternate microbiologic diagnosis includes (1) identifiable source for bloodstream infection with a nontypical IE pathogen, (2) rapid resolution of bloodstream infection, and (3) absence of evidence for IE on cardiac imaging. Firm alternate nonmicrobiologic diagnosis includes (1) presence of non-IE cause for cardiac imaging findings (eg, marantic or nonbacterial thrombotic endocarditis) and (2) absence of microbiologic evidence for IE.
Ah, yes but what are the Major and Minor Criteria? Fret not, gentle reader. We have them for you here! Changes are in bold.
I. MAJOR CRITERIA
- A. Microbiologic Major Criteria
(1) Positive blood cultures
i. Microorganisms that commonly cause IEa isolated from 2 or more separate blood culture sets (Typical)b
or
ii. Microorganisms that occasionally or rarely cause IE isolated from 3 or more separate blood culture sets (Nontypical)b(2) Positive laboratory tests
i. Positive polymerase chain reaction (PCR) or other nucleic acid-based techniquec for Coxiella burnetii, Bartonella species, or Tropheryma whipplei from blood
or
ii. Coxiella burnetii antiphase I immunoglobulin G (IgG) antibody titer >1:800d, or isolated from a single blood culture
or
iii. Indirect immunofluorescence assays (IFA) for detection of IgM and IgG antibodies to Bartonella henselae or Bartonella quintana with immunoglobulin G (IgG) titer ≥1:800d - B. Imaging Major Criteria
(1) Echocardiography and cardiac computed tomography (CT) imaging
i. Echocardiography and/or cardiac CT showing vegetation,e valvular/leaflet perforation,f valvular/leaflet aneurysm,g abscess,h pseudoaneurysm,i or intracardiac fistulaj
or
ii. Significant new valvular regurgitation on echocardiography as compared with previous imaging. Worsening or changing of preexisting regurgitation is not sufficient.
or
iii. New partial dehiscence of prosthetic valve as compared with previous imaging
(2) Positron emission computed tomography with 18F-fluorodeoxyglucose ([18F]FDG PET/CT imaging)
Abnormal metabolic activityk involving a native or prosthetic valve, ascending aortic graft (with concomitant evidence of valve involvement), intracardiac device leads or other prosthetic materiall,m - C. Surgical Major Criteria
Evidence of IE documented by direct inspection during heart surgery neither Major Imaging Criteria nor subsequent histologic or microbiologic confirmationn
II. MINOR CRITERIA
- A. Predisposition
– Previous history of IE
– Prosthetic valveo
– Previous valve repairo
– Congenital heart diseasep
– More than mild regurgitation or stenosis of any etiology
– Endovascular intracardiac implantable electronic device (CIED)
– Hypertrophic obstructive cardiomyopathy
– Injection drug use - B. Fever – Documented temperature greater than 38.0 °C (100.4 °F)
- C. Vascular – Phenomena Clinical or radiological evidence of arterial emboli, septic pulmonary infarcts, cerebral or splenic abscess, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions, purulent purpura
- D. Immunologic – Phenomena Positive rheumatoid factor, Osler nodes, Roth spots, or immune complex-mediated glomerulonephritisq
- E. Microbiologic Evidence, Falling Short of a Major Criterion
1) Positive blood cultures for a microorganism consistent with IE but not meeting the requirements for Major Criterionr
or
2) Positive culture, PCR, or other nucleic acid based test (amplicon or shotgun sequencing, in situ hybridization) for an organism consistent with IEr from a sterile body site other than cardiac tissue, cardiac prosthesis, or arterial embolus; or a single finding of a skin bacterium by PCR on a valve or wire without additional clinical or microbiological supporting evidence - F. Imaging Criteria
Abnormal metabolic activity as detected by [18F]FDG PET/CT within 3 mo of implantation of prosthetic valve, ascending aortic graft (with concomitant evidence of valve involvement), intracardiac device leads or other prosthetic material - G. Physical Examination Criterias
New valvular regurgitation identified on auscultation if echocardiography is not available. Worsening or changing of preexisting murmur not sufficient
Here are all the footnotes…
- aStaphylococcus aureus; Staphylococcus lugdunensis; Enterococcus faecalis; all streptococcal species (except for Streptococcus pneumoniae and Streptococcus pyogenes), Granulicatella and Abiotrophia spp., Gemella spp., HACEK group microorganisms (Haemophilus species, Aggregatibacter actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae). In the setting of intracardiac prosthetic material, the following additional bacteria should be included as “typical” pathogens: coagulase negative staphylococci, Corynebacterium striatum and Corynebacterium jeikeium, Serratia marcescens, Pseudomonas aeruginosa, Cutibacterium acnes, nontuberculous mycobacteria (especially M. chimaerae), and Candida spp.
- b“Blood culture set” is defined as a simultaneously drawn pair of 1 aerobic and 1 anaerobic bottle. “Positive” blood culture set is defined as microbial growth from at least 1 of the bottles. Blood cultures from separate venipuncture sites are strongly recommended whenever possible for evaluating suspected IE.
- cAmplicon (16S or 18S) or metagenomic (shotgun) sequencing.
- dOr equivalent titer results on other methodologies.
- eOscillating intracardiac mass on valve or other cardiac tissue, endovascular CIED or other implanted material in the absence of an alternative anatomic explanation.
- fInterruption of valvular endocardial tissue continuity.
- gElongation with saccular outpouching of valvular tissue.
- hPerivalvular (or perigraft) soft tissue lesion with variable degree of evolution to an organized collection.
- iPerivalvular cavity communicating with the cardiovascular lumen.
- jCommunication between 2 neighboring cardiac chambers through a perforation.
- kFor prosthetic valve endocarditis (PVE), intense, focal/multifocal, or heterogeneous FDG uptake patterns; for native valve endocarditis and cardiac device leads, any abnormal uptake pattern.
- lPerformed at least 3 months after prosthetic valve surgical implantation.
- mSome prosthetic valves may have intrinsic non-pathological FDG uptake [42, 56]. An isolated FDG-PET positive generator pocket in the absence of intracardiac infection does not qualify as a Major Criterion. PET/CT can be useful in detecting extracardiac foci of infection [51, 57].
- nAddition of this major criterion should not be interpreted as giving license to not send appropriate samples for histopathology and microbiological studies.
- oPlaced either by open-heart surgical or transcatheter approach.
- pIncludes cyanotic CHD (tetralogy of Fallot, univentricular heart, complete transposition, truncus arteriosus, hypoplastic left heart); endocardial cushion defects; ventricular septal defect; left-sided lesions (bicuspid aortic valve; aortic stenosis and insufficiency, mitral valve prolapse, mitral stenosis and insufficiency); right-sided lesions (Ebstein anomaly, anomalies of the pulmonary valve, congenital tricuspid valve disease); patent ductus arteriosus; and other congenital anomalies, with or without repair [58–60].
- qDefined as either:
(1) Unexplained presence of either acute kidney injury (AKI, defined later) or acute on chronic kidney injury (defined later) plus 2 of the following: hematuria, proteinuria, cellular casts on inspection of urinary sediment, or serologic perturbations (hypocomplementemia, cryoglobulinemia, and/or presence of circulating immune complexes);
or
(2) renal biopsy consistent with immune complex-mediated renal disease.
AKI: new unexplained reduction of estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2.
Acute or chronic kidney injury: reduction by at least 1 ordinal level of function: eg, from “moderately decreased” to “severely decreased”; or from “severely decreased” to “kidney failure.” Interpretive ranges for eGFR: normal ≥60 mL/min/1.73 m2; moderately decreased 30–59 mL/min/1.73 m2; severely decreased 15–29 mL/min/1.73 m2; kidney failure <15 ml/min/1.73 m2. - rExcludes single positive blood cultures or sequencing based assays for microorganisms that commonly contaminate blood cultures or rarely cause IE.
- sApplicable only when echocardiography is unavailable. Based on expert opinion.
The 2023 Duke-International Society for Cardiovascular Infectious Diseases Criteria for Infective Endocarditis: Updating the Modified Duke Criteria. Clin Infect Dis. 2023 Aug 22;77(4):518-526. doi: 10.1093/cid/ciad271. Erratum in: Clin Infect Dis. 2023 Oct 13;77(8):1222.
Valvular Heart Disease
Prosthetic Valves
Mechanical
Last ~20 yrs, SEM murmur
Bioprosthetics
human, porcine, or bovine
8-10 yrs
anticoagulation optional, usually aspirin
Both types are prone to thromboembolism.
Valves may fail leading to acute regurgitation
Paravalvular leak from disruption from annulus, can result from endocarditis
Endocarditis
Hemolysis
Get CBC, LDH, PT/PTT, ESR, Blood CX,
Aortic valves are lower risk for clot than mitral
The peak incidence of thromboembolism is during the first 3 months after surgery, probably reflecting the lack of endothelialization of the newly implanted prosthetic materials and delay in achieving therapeutic anticoagulation in the early days after operation
Mitral Valve Prolapse
can be associated with chest pain, palpitations, and hyperventilation in females.
May need b-blockers, dental prophylaxis,
Mitral Stenosis
from rheumatic heart disease, congenital, or left atrial myxomas
exertional dyspnea, hemoptysis, CHF sx
Can lead to a-fib, embolization
Mitral Regurgitation
acute is from ruptured chordae or papillary muscle dysfunction
chronic is most commonly from rheumatic or MVP, also Marfan’s
rate control, diuretics, anticoagulate
These patients need afterload reduction
Aortic Stenosis
congenital bicuspid valve, rheumatic heart disease, calcific aortic stenosis.
DOE, angina, exertional syncope, CHF, sudden death
Harsh systolic murmur
Symptomatic patients are at risk for sudden death, refer for valve surgery.
Most common cause in ICUs is senile calcific disease Causes LVH which predisposes to subendocardial ischemia
tachycardia decreases diastolic filling and therefore decreases coronary blood flow
Pts present with exertional dyspnea, angina, syncope, may progress to heart failure
Diuresis, IVF, and venodilators can all cause deterioration
avoid hypotension
Unload trial would say nitroprusside is a good move
OVERVIEW
Obstruction can be
- supravalvular
- valvular (most common)
- subvalvular
SEVERITY ASSESSMENT
- appearance
- mobility
- gradient
— continuous wave Doppler allows peak velocity to be measured -> peak gradient can be calculated using Bernoulli equation
— peak gradient = 4 x peak velocity across the narrowing squared
— normal peak gradient < 10mmHg, critical > 70mmHg
— gradient measurements are very dependent on ventricular function so can be misleading. - area
— normal 2.5-5.5 cm2
— critical < 0.92 cm2 - dimensionless severity index = ratio of LVOT velocity/aortic valve velocity (V1/V2)
— provides a dimensionless measurement of aortic stenosis which is independent of Q
— < 0.25 implies a valve area of 0.75cm2 (severe AS) - complications:
— LV hypertrophy or dilation
— LV systolic and diastolic dysfunction
— post-stenotic dilation
CATEGORIES OF AORTIC STENOSIS SEVERITY (From Vahanian et al, 2010)
Aortic sclerosis |
Mild | Moderate | Severe | |
---|---|---|---|---|
Aortic jet velocity (m/s) | <2.6 | 2.6–3.0 | 3–4 | >4 |
Mean gradient (mmHg) | — | <30 (25) | 30–50 (25–40) | >50 (40) |
AVA (cm2) | — | >1.5 | 1.0–1.5 | <1.0 |
Indexed AVA (cm2/m2) | >0.9 | 0.6–0.9 | <0.6 | |
Velocity ratio | >0.50 | 0.25–0.50 | <0.25 |
Above from Life in the Fast Lane CCC
Aortic Insufficiency
acutely from infective endocarditis, dissection, trauma
chronic from rheumatic heart disease, bicuspid valve, marfan’s
widened pulse pressure
try judicious use of nitro or nitroprusside
reduce bradycardia to decrease diastolic filling and therefore degree of regurg
never use IABP
Withholding Anticoagulation
much more dangerous in mitral and tricuspid
can hold aorta anti-coag 2 days before surg and drift INR t to <=1.5
then restart
for mitral/tricusp bridge with heparin until procedure
(Emerg Med Clin 2011;29:801)
Which Valve has been Replaced?
http://www.raddaily.com/whitepaperarticle.php?articleTitle=Cardiac+Valves:+Assessment+and+Identification