Endocarditis Pediatric

8/10/2019 Endocarditis Pediatric

1/56

Emergency Medicine

Rounds

Dr. Edward LesSeptember 26, 2002


2/56

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


3/56

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


4/56

PMH noted at triage:

VSD scheduled for f/u echo following week


5/56

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


6/56

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


7/56

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


8/56

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


9/56

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


10/56

Infective Endocarditis

in childhood Background

Etiology Epidemiology Pathogenesis Clinical manifestations

Diagnosis Prognosis/complications Treatment Prevention


11/56


12/56

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


13/56

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


14/56

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


15/56

Culture negative

5-10% of cases

Fastidious organisms or anaerobes Prior antibiotic treatment Non-bacterial

R-sided endocarditis


16/56

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


17/56

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)


18/56

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


19/56

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


20/56

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


21/56

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


22/56

Others at risk

Congenital bicuspid aortic valve

Mitral valve prolapse with regurg Hypertrophic cardiomyopathy Ventriculo-atrial shunts


23/56

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


24/56

Clinical manifestations

Relate to 4 underlying phenomena:

Bacteremia (or fungemia) Valvulitis Immunologic response

Emboli


25/56

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


26/56

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


27/56

Famous but rarejaneway

Splinter

hemorrhage


28/56

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%)


29/56

Lab

Serology Rheumatoid factor (40-50%)

Circulating immune complexes ANA hypocomplementemia

Blood culture Most important lab test Positive cultures in 90-95% of cases


30/56

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


31/56

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


32/56

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


33/56

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


34/56

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


35/56

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)


36/56

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


37/56

Blood volume related to culture

positivity

Towns, ML and LB Reller. ID Clinics NA 2002; 16(2)


38/56

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


39/56

Dx: procedures Echo

TTE rapid, noninvasive specificity: 98% sensitivity:


40/56

Remember ..

Absence of vegetations does not exclude IE

Vegetations are often not visualized in theearly phases or in patients with complex

CHD


41/56

Dx: procedures

EKG

May show arrhythmias or conductiondisturbances


42/56

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


43/56

Veggies eat your heart out


44/56

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


45/56

I.E. in the E.D.

Treatment Empiric abx:

Vanco + gent

or

Pen + gent(?talk to ID)

Treat CHF if present Admit


46/56

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


47/56

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


48/56

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


49/56

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


50/56

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%


51/56


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


52/56


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


53/56


What drugs?


54/56

retrospectroscope

The clues in our girl:

Hx: Restrictive VSDPersistent/intermittent fever, malaise, arthralgia

Exam: Murmur

Bad teeth

Lab: Hematuria, proteinuriaThrombocytopenia


55/56

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


56/56

Questions?

Endocarditis Pediatric

Documents

Transcript of Endocarditis Pediatric