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Emergency Medicine
Rounds
Dr. Edward LesSeptember 26, 2002
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Case
16 year old girl
c/o intermittent fever and bilateral leg pain x 5days unable to walk since yesterday feet,calves painful
nauseated; emesis x1 L arm, R abdo pain as well decreased energy/appetite dry cough
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w/i clinic x 2 in past 5 days Rxd tylenol and ibuprofen relief of symptoms
with same
CBC done @ 2ndw/i visit (3 days prior to ER): WBC 9.9, no shift Hb 142 Platelets 121
U/A: 10-20 WBC, 5-10 RBC, many epith
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PMH noted at triage:
VSD scheduled for f/u echo following week
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Course in ER
*Had taken Tylenol and ibuprofen 1 hour prior to
presentation
Initial VS: T 37.6, P 108, BP 97/47
Noted to be somewhat lethargic and unable tobear weight with some L leg swelling by triagenurse; tender RUQ
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Course in ER
Seen by ER doc 1 hour after triage:
Continued afebrile Symptoms abated since arrival Documented exam - generally normal apart from
cardiac murmur
Note made of low platelet count and abnormal U/A
Discharged dx: viral syndrome with myalgia
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2 days later
Presented to FHH with ongoing
intermittent fever, migratory arthritis,abdo pain, N/V, sore throat
Subsequently found to have endocarditis asdemonstrated by transesophageal echoand Group C Strep bacteremia
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Complicated course in hospital Abdominal wall abscess sx drained Pleural effusions chest tube
Coagulopathy Pericardial effusion/tamponade drained 300 mL
Rx with IV Pen V and gent, then Pen V alone x 4
weeks*Noted to have very poor dental hygiene
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Her cardiac anatomy
Based on echo 1 year prior to presentation
restrictive perimembranous VSD ~ 4 mm
LR flow gradient 78 mm Hg
LV size - upper limit of normal
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Infective Endocarditis
in childhood Background
Etiology Epidemiology Pathogenesis Clinical manifestations
Diagnosis Prognosis/complications Treatment Prevention
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Why?
Diagnosis can be difficult when delayed
Physicians/dentists/public not sufficiently aware ofthreat of IE and preventative measures available
Special risk groups have emergedSurvivors of cardiac surgeryPatients taking immunosuppressantsPatients with chronic IV catheters/ increased PICUcomplexityIV narcotics users
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Epidemiology
1 in 1280 pediatric admissions per year?Am Heart J. 1984:107:1235-1240
Probably higher now
Most often a complication of congenital orrheumatic heart disease Can also occur in children without a cardiac
malformation 8-10% of cases: usually S. aureus
Rare in infancy following open heart sx NICU kiddies with central lines
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EtiologyCommon:Native valve or othercardiac lesions
Uncommon:Native valve or othercardiac lesions
Prosthetic Valve
S viridans
roup
S aureus
Enterococcus
S. pneumoniae
Haemophilus influenzaeS. epidermidisHACEK groupCoxiella burnetti*Neisseria gonorrheaeBrucella*
Chlamydia spp*.Streptobacillusmoniliformis*Pasteurella multocida*Campylobacter fetus
S. epidermidis
S aureus
S viridans
P. aeruginosaSerratia marcescensDiptheroidsLegionella spp.*HACEK groupFungi
*fastidious organisms
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Culture negative
5-10% of cases
Fastidious organisms or anaerobes Prior antibiotic treatment Non-bacterial
R-sided endocarditis
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pathogenesis
Intact cardiac endothelium: poor stimulation of coagulationweakly receptive to bacterial attachment
Valve surface altered to produce suitable site for bacterial attachmentand colonization
Platelets and fibrin deposition in the formation of sterile vegetation Nonbacterial Thrombotic Endocarditis (NBTE)
Bacteria reach this site and produce colonization The surface is covered with platelets and fibrin clot propogates over
deposited bacteria Further bacterial multiplication and vegetation growth
- 107-1010cfu/g of tissue
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Localization of IE
high pressure areas: down stream from siteswhere blood flows at high velocity through a
narrow orificeVenturi effect: maximal deposition of bacteria in low-pressuresink
e.g.:
atrial surface of mitral valve (MR)ventricular aspect of aortic valve (AR)
RV wall (restrictive VSD)
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Transient bacteremia
Occurs whenever a mucosal surface heavilycolonized with bacteria is traumatized
If preexistent NBTE, it may result in
colonization and IE
Surgical or dental procedures can be
implicated in approximately 65% of cases Poor dental hygiene particular risk factor inkids with cyanotic CHD
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Generally Patients with IE and no underlying heart disease: Staph
aureus more common
S. viridans more common after dental procedures
Group D enterococci more often after lower bowel orgenitourinary manipulation
Pseudomonas or Serratia IV drug use
Fungal organisms after open heart surgery
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Sticky bugs
Organisms more frequently associated with IE adheremore readily to normal leaflets in vitroe.g.
1. FimA is a surface adhesin of S.viridansthat serves as an important colonizationfactor. Homologues of fimA genes were found in many S. viridans strains andenterococci.
2. Fibronectin is implicated as the host receptor within NBTE. Low-fibronectin-
binding mutants of S. aureushave decreased ability to produce IE.
3. Gm + coccus resistant to phagocytosis, platelet microbicidal proteins (PMP),and complement-mediated killing
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Who to worry about? High risk:
Children with VSDs, L-sided valvular disease, and systemic-pulmonary arterial communications
Most frequent structural lesions associated with IE: Tetralogy of Fallot VSD (esp restrictive) Aortic stenosis/coarctation PDA TGV
B-T shunts Valve replacements/valved conduits
Low risk:
pulmonic stenosis, ASD
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Others at risk
Congenital bicuspid aortic valve
Mitral valve prolapse with regurg Hypertrophic cardiomyopathy Ventriculo-atrial shunts
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Immunopathologic factors
IE cause both humoral and cellular responses
Rheumatoid factor: titers correlate with the level of hypergammaglobulinemia and decrease with therapy)
Antinuclear antibodies: may contribute to the musculoskeletal manifestations, low-grade fever, or pleuritic pain
Circulating immune complexes: Connected with long duration of illness, extravascular manifestations,
hypocomplementemia May cause diffuse glomerulonephritis, and some of the peripheral manifestations such as
Osler nodes
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Clinical manifestations
Relate to 4 underlying phenomena:
Bacteremia (or fungemia) Valvulitis Immunologic response
Emboli
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Symptoms
Fever Absent in 5-10% of cases Staph: hi spiking Strep: low grade
Chills Chest and abdominal
pain Arthralgia, myalgia
Dyspnea
Malaise Night sweats Weight loss CNS manifestations
Stroke, seizures,headache
Presentation is a
continuum
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signs
Fever Tachycardia
Embolic phenomena Roth spots Petechiae Splinter hemorrhages Oslers nodes CNS lesions
Janeway lesions Splenomegaly Arthritis
New or ing murmur CHF Arrythmias
Metastatic infection Arthritis Meningitis Mycotic arterial
aneurysm Pericarditis Abscesses Septic pulmonary emboli
Clubbing Long-term
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Famous but rarejaneway
Splinter
hemorrhage
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Lab
Hematology Anemia: normochromic, normocytic, Thrombocytopenia (5-15%)
Leukocytosis (20-30%) Elevated ESR, with mean value of 57mm/hr (90-100%) Hypergammaglobulinemia (20-30%)
Urinalysis Proteinuria (50-65%) Microscopic hematuria (30-60%) Red cell casts (12%)
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Lab
Serology Rheumatoid factor (40-50%)
Circulating immune complexes ANA hypocomplementemia
Blood culture Most important lab test Positive cultures in 90-95% of cases
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Sign/sx/lab
Very common
FeverPositive BCESR or CRP
Common
HA, myalgia,malaise
AnemiaHematuriaLeukocytosisRF
Infrequent
New or ing heartmurmur
CHFPetechiaePeripheral emboliSplenomegalyNeuro sEchocardiographic
vegetations
Rare
Oslers nodesJaneway lesionRoth spotsSplinter
hemorrhages
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Diagnosis Need a HIGH index of suspicion in a child with
an underlying contributory factor
Modified Dukes criteriaLi JS et al. Clin Infect Dis 2000: 30:633-8. Sensitivity >80% NPV 92%
Uses pathologic criteria and major and minorclinical criteria
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Dukes major clinical criteria
Typical bug from 2 separate BCs, or
Enterococcus in absence of primaryfocus, or
Persistently + BC with bug consistentwith IE drawn >12 h apart, or
All 3 or a majority of 4 or moreseparate BCs with 1stand last drawn atleast 1 h apart, or
+ Q fever serology
+ echo for IE: oscillating intracardiacmass, on valve or supporting
structures, or in path of regurgitantjets, or on implanted materials, in theabsence of alternative anatomicexplanation, or
Abscess, or
New partial dehiscence of prostheticvalve, or
New valvular regurgitation
Positive blood culture for IE Evidence of endocardial involvement
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Dukes minor clinical criteria
1. Predisposing heart conditionor IV drug use
2. Fever > 38 C
3. Vascular phenomena Major arterial emboli
Septic pulmonary infarcts Mycotic aneurysm Intracranial hemorrhage Conjunctival hemorrhages Janeway lesions
4. Immunologic phenomena Oslers nodes
Roth spots Glomerulonephritis Rheumatoid factor
5. Microbiologic evidence
+ BC but not meeting majorcriterion, or Serologic evidence of active
infection with organismconsistent with IE
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Pathologic criteria
Microorganismsby culture or histology
in a lesion/vegetation/
intracardiac abscessor
Lesions vegetation or intracardiac
abscess present,
Clinical criteria
2 major criteria, or1 major and 3 minor, or
5 minor
At least 1 major and1 minor,
or3 minor
Alternative diagnosisfor manifestations ofIE
or
Resolution ofmanifestations withabx
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Blood cultures
Prior to antibiotics Prep the skin
70% isopropyl alcohol, then iodine let dry
Peripheral blood Timing doesnt matter Need lots of blood!!
20 ml/draw in adults; 1-2 mL/draw in neonates, 2-3infants, 3-5 older kids, 10-20 adolescents
Low-grade bacteremia (1-10 cfu/mL venous blood Most of the bugs are buried - most of the damage is
occuring away from the surface (valve-ring abscesses and
ruptured chordae)
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Blood cultures in IETowns, ML and LB Reller. ID Clinics NA 2002; 16(2)
Acute IE: 2-3 cultures from several venipuncture sites w/i 5 minutes ofeach other then treat
Subacute IE: several BCs spaced 30 minutes to an hour apart prior toinstituting empiric abx therapy
Multiple cultures: More blood = single most important factor for successful recovery of
bug Rate of positivity increases as more cultures are obtained (up to a
point) Need multiple BCs to meet Duke criteria for diagnosis
ONE BC is inadequate!!! Doesnt maximize chance of isolating etiologic agent Cannot demonstrate presence of continuous bacteremia Cannot distinguish true bacteremia from contamination
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Blood volume related to culture
positivity
Towns, ML and LB Reller. ID Clinics NA 2002; 16(2)
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Notify the lab of suspected IE
May need prolonged culture (> 7 days) on
enriched media to detect nutritionallyvariant and fastidious bacteria or fungi
Indicate if received abx prior to collection
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Dx: procedures Echo
TTE rapid, noninvasive specificity: 98% sensitivity:
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Remember ..
Absence of vegetations does not exclude IE
Vegetations are often not visualized in theearly phases or in patients with complex
CHD
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Dx: procedures
EKG
May show arrhythmias or conductiondisturbances
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Prognosis
Pre-antibiotic era fatal
With abx mortality still 25-50% Serious morbidity in 50-60% CHF in 30%: valvular veggies, myocardial abscesses,
pericardial effusions, ruptured sinus of Valsalva, acquired VSD,heart block
Systemic emboli: stroke, abscesses, osteomyelitis, arthritis,renal impairment, meningitis Pulmonary emboli Mycotic aneurysms
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Veggies eat your heart out
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Mycotic aneurysms
Develop during active IE More common with S.viridans May arise by the following mechanisms:
direct bacterial invasion of the arterial wall withsubsequent abscess formation or rupture
septic or bland embolic occlusion of the vasa vasorum immune complex deposition with resultant injury to
arterial wall Tend to occur at bifurcation areas; middle cerebralartery is most common
Clinically silent until rupture
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I.E. in the E.D.
Treatment Empiric abx:
Vanco + gent
or
Pen + gent(?talk to ID)
Treat CHF if present Admit
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Treatment
Prolonged ; usually at least 4-6 weeks abx
hi #s or bugs relatively protected locale; bacteria relatively
metabolically quiescent within the veggies
need b/w 5 and 20 times MIC
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Surgical intervention:
indications refractory CHF
physiologically significantvalve dysfunction asdemonstrated by echo
>2 serious systemic embolic
episode
uncontrolledinfection/ineffectiveantimicrobial therapy
resection of mycoticaneurysms
most cases of prosthetic valveIE (caused by more antibiotic-resistant pathogens)
local suppurativecomplications includingperivalvular or myocardialabscesses
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Surgical therapy:
echo features Persistent vegetations after a major systemicembolic episode
Large (>1cm diameter) anterior mitral valvevegetation Increase in vegetation size 4 weeks after
antibiotic therapy
Acute mitral insufficiency Valve perforation or rupture Periannular extension of infection
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Prevention:
in at risk groups Antimicrobrial prophylaxis prior to
various procedures Proper dental care and hygiene Vigorous treatment of sepsis and local
infections Careful asepsis during heart surgery andcatheterization
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I.E. prophyaxis in the E.D.
Whats the evidence?
Nonexistent: no RCT Uncommon disease even in highest risk kids Bacteremia from dental procedures accounts for
only ~10% of cases Efficacy of prophylaxis only ~50%
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I.E. prophyaxis in the E.D.
Which patients?Moderate risk
Congenital heart disease* Acquired valvular heart
disease Hypertrophic CM MV prolapse with regurg
*not isolated ASD, repaired VSD/PDA after 6months, pacemaker, defibrillator
High risk
Prev bacterial IE Prosthetic valve orsurgically constructedsystemic-pulmonaryshuns or conduit
Cyanotic congenitalHD (TGV, T of F, etc)
h h
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I.E. prophyaxis in the E.D.
Which procedures? I&D of odontogenic abscess
Urinary catheterization in setting of UTI ? I&D of cutaneous abscess
AHA recommendation, but..
Bibrow, BJ et al.Ann Emerg Med 1997; 29:407100 BCs after I&D of 50 abscesses:
0 of 100 positive
h h
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I.E. prophyaxis in the E.D.
What drugs?
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retrospectroscope
The clues in our girl:
Hx: Restrictive VSDPersistent/intermittent fever, malaise, arthralgia
Exam: Murmur
Bad teeth
Lab: Hematuria, proteinuriaThrombocytopenia
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Summary of endocarditis Serious complications
Death if untreated
Relatively non-specific signs
Importance of clinical suspicion Review of medical history, review of systems, careful exam
Immediate admission/referral
If you suspect it: draw appropriate cultures
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Questions?