Neonatal infective endocarditis

1. Case Presentation

2. • B/o Veena ,23 day.
• Male child
• Wt : 2.7 kg.
• DOA:11/07/16 .

3. • H/o Fever- Day 8 of life .
• No h/o of convulsions, poor feeding ,lethargy,
abdominal distension, hurried respiration.
• Was admitted for same complaint and
treated with IV medications in pvt hospital
Bhadravathi for 4 days.

4. • Due to persistent fever baby was referred to
shivamoga.
• Admitted in private hospital Shivmoga for 12 days.
• Baby was treated with IV medications and fluids and
O2 inhalation, referred to our hospital for further
management.
• No h/o convulsions,white patches in oral cavity,hurried
breathing ,bluish discoloration of extremities during
hospital stay.
• Abscess over Left foot has been documented in referral
letter

5. Birth history:
• Primi gravida
• Regular ANC taken .
• Antenatal period uneventful.Antenatal USG
normal study.
• S/T/M/AGA delivered via naturalis ,in hospital
cried immediately. B wt-2.75kg.Breast fed
within one hour of birth.
• Baby was noted to be icteric on D3 given
phototherapy for 2days and discharged on D6
of life.

6. Treatment History:
Treatment received in shivmogha
• Inj Linezolid-D12
• Inj Meropenem-D9
• Inj clindamycin-D6
• Inj Amphotericin B-D6

7. On Examination:
• Vitals: HR-182/min SpO2:70% in room air
RR-48/min :85% with HBO2
CRAT-good CRT<3sec
Temp-98.6F
• Anthropometry:OFC-33 cm,Length-49cm.
• Oral examination-no e/o oral thrush.
• No abscess ,no e/o diaper dermatitis.

8. • CVS: S1 S2 heard.S2 Loud,
Systolic murmur,changing in quality best
heard in left lower sternal border.
• R/S :No retractions,bilateral air entry
adequate.No added sounds.
• P/A : Soft non distended,liver 2cm palpable,non
tender,Spleen palpable 2 cm below Lt
costal margin soft in consistency.
• CNS : AF at level.Reflexes and activity -Good

9. • B/O Veena day 23 male child, born through
NVD with h/o Fever from D8 of life with
examination findings of decreased Spo2,
tachycardia and changing murmur and loud S2
with splenomegaly provisional diagnosis-

10. Late onset sepsis with? infective
endocarditis with PAH not in CCF

11. Investigations
Referring Hospitals investigations
• Hb-14.4gm%,TLC-19,500/mm3,PMN-
65%,Platelet-28000/mm3.
• CRP-37mg/l.
• RFT and Electrolytes-normal
• Blood C/S-No growth.
• Urine examination-Scanty oval budding yeast
cell with pseudohypae.
• Urine C/S- Candida species grown.
Sensitive to Amphotericin B
Clotrimazole,Flucanozole and Nystatin

12. • 2D Echocardiography:
Infective endocarditis.
Large vegetation on tricuspid valve.8*7 mm
Severe TR
PAH(+)
Good biventricular function

25. LATE ONSET SEPSIS –POLYMICROBIAL
WITH INFECTIVE ENDOCARDITIS,
TRICUSPID VALVE VEGITATION-
?FUNGAL ? KLEBSIELLA WITH SMALL
PDA ,NOT IN CCF.
Diagnosis:

26. Course in hospital:
• Baby was started with IV Inj vancomycin ,Inj
cefotaxim and Inj flucanozole and continued
for 3 weeks.
• Change in murmur quality was noted multiple
times.
• Baby was weaned of from oxygen on D5 of
admission and shifted to mother side and
discharged at request after 3 weeks of
antibiotics.

30. Infective Endocarditis In Newborn
• Neonatal BE previously uncommon,about 60
cases reported before mid 80s.
• Prolonged survival of critically ill babies,complex
CCHD,increase use of intravascular
catheters,availabilty of echocardiography-
responsible for increased recognition.

31. Causative agents:
• University of New mexico with 3200-3500
admissions annually,12 cases occurred in children
younger than 3 months.
• Causative organisms-S.aureus-6
K.pneumoniae-1
Enterobacter cloace-2
Candida-1
S.viridans-1
CONS-1

32. • Etiological agents isolated by blood culture or
morphological characteristics of organisms
entraped in vegetation.
• Causative organisms
S.aureus(36),streptococci(6),S.epidermidis(5)
GBS(5),S.pneumonia,P.aeroginosa (2),
K.pneumonia,P.mirablis,S.faecalis(1).
• Candidal endocarditis becoming increasingly
prevalent particularly associated with CVC.

34. • In contrast to older children in whom CHD is
associated with IE,cardiac anomalies were
found only in 9 reported cases before 1994.
• Bacteremia arising from infected umbilical
stump,conjuctivitis and skin lesions were
source of valvular involvement in six infants.

35. Pathogenesis:
• Neonatal endocarditis frequently occurs on the
right side of the heart and is associated with
disruption of endocardium or valvular
endothelial tissue produced by catheter-induced
trauma,DIC,non specific stress hypoxia and
hypotension.
• Neonates often experience transient episodes of
bacteremia from trauma to the skin and mucous
membranes, vigorous endotracheal suctioning,
parenteral hyper alimentation, or placement of
umbilical or peripheral venous catheters.
• The combination of endothelial damage and
bacteremia is a critical one for the induction of IE

37. • Mitral valve alone or in combination of other
valve is involved in half of patients
• tricuspid valve in about 12,pulmonary valve 7,
Aortic valve in 7,infected mural thromi in 12
and unspecifeid site 3.
• D/D-NBTE,blood cysts,develoment valvular
defects and hemangioma.

38. Clinical findings:
• The clinical manifestations of IE in a neonate
are variable and nonspecific and may be
indistinguishable from septicemia or
congestive heart failure from other causes.
• Should be suspected in any neonate with
indwelling catheter,evidence of sepsis and
new or changing heart murmur
• Septic embolic phenomena are common,
resulting in foci of infection outside the heart
(eg, osteomyelitis, meningitis, or pneumonia).

39. • Although arthritis and arthralgia are common
findings in older children with IE, arthritis is
described infrequently in neonates.
• Osler nodes, Roth’s spots, arthritis have not
been described in neonates.
• Janeway lesions,generalised petechial rash
and splinter hemmorages have been
documented.

40. Investigations
• 2D Echocardiography:rapid ,non invasive
method for diagnosing IE.
- Cannot differentiate btw infected and sterile
vegetation
-Specific ,false positive readings are
uncommon.
-transesophageal echo and color doppler
imaging improves diagnostic accuracy.

41. • Blood ,CSF and urine culture should be sent for
bacterial and fungal culture.
• 2 periphreal venous blood sample 1-5ml for
culture to be collected before starting antibiotics.
• TLC ,DC and PLT count are usually indicative of
sepsis than cardiac valve infection.
• Chest x ray –to detect CCF or pulmonary
infection.
• Neuroimaging –in infants with neurologic signs ,in
L sided IE
• Baseline determination of inflammatory markers-
CRP and ESR .
• Microhematuria has been reported.

42. Treatment
• Intravascular catheter must be removed and sent
for c/s.
• Penillinase resistant pencillin +Aminoglycoside
started after sending cultures.
• Vancomycin substituted where MRSA is problem.
• Ampicillin is added or substituted if enterococci is
suspected.
• Fungal endocardits difficult to treat,DOC –
Amphotericin B+5-FU
• 4-8 weeks of parental treatment is adequate.
• CRP and ESR,serial echo,blood c/s.
• Surgical intervention-large or mobile vegetations
obstructing outflow tract or high risk of embolism

43. Prognosis
• First survivor 1983,subsequently 2/3 cases
have been cured.
• Death is usually due to overwhelming sepsis
and CCF.

44. References
• Avery`s diseases of the Newborn,9e
• Nelson Textbook of pediatrics:First South Asia
Edition,Robert M.Kleigmann
• Infective Endocarditis in Childhood: 2015 Update
A Scientific Statement From the American Heart
Association
• Remington and Klein's Infectious Diseases of the
Fetus and Newborn Infant, 7th Edition.

45. Thank
you