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.
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-
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
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25. LATE ONSET SEPSIS âPOLYMICROBIAL
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.
27.
28.
29.
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.
33.
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
36.
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, Rothâs 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 âto detect CCF or pulmonary
infection.
⢠Neuroimaging âin 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 â
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.