Case Presentation

• B/o Veena ,23 day.

• Male child

• Wt : 2.7 kg.

• DOA:11/07/16 .

• 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.

• 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,hurriedbreathing ,bluish discoloration of extremities during hospital stay.

• Abscess over Left foot has been documented in referral letter

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.

Treatment History:

Treatment received in shivmogha

• Inj Linezolid-D12

• Inj Meropenem-D9

• Inj clindamycin-D6

• Inj Amphotericin B-D6

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.

• 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

• 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-

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

InvestigationsReferring 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 BClotrimazole,Flucanozole and Nystatin

• 2D Echocardiography:

Infective endocarditis.

Large vegetation on tricuspid valve.8*7 mm

Severe TR

PAH(+)

Good biventricular function

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

Diagnosis:

Course in hospital:

• Baby was started with IV Inj vancomycin ,Injcefotaxim 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.

Infective Endocarditis In Newborn

• Neonatal BE previously uncommon,about 60 cases reported before mid 80s.

• Prolonged survival of critically ill babies,complexCCHD,increase use of intravascular catheters,availabilty of echocardiography-responsible for increased recognition.

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

• 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.

• 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.

Pathogenesis:• Neonatal endocarditis frequently occurs on the

right side of the heart and is associated with disruption of endocardium or valvularendothelial 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

• 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 valvulardefects and hemangioma.

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).

• 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.

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 dopplerimaging improves diagnostic accuracy.

• 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.

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

Prognosis

• First survivor 1983,subsequently 2/3 cases have been cured.

• Death is usually due to overwhelming sepsis and CCF.

References

• Avery`s diseases of the Newborn,9e

• Nelson Textbook of pediatrics:First South Asia Edition,Robert M.Kleigmann

• Infective Endocarditis in Childhood: 2015 UpdateA Scientific Statement From the American Heart Association

• Remington and Klein's Infectious Diseases of the Fetus and Newborn Infant, 7th Edition.

Thank you