infective endocarditis-neonate
TRANSCRIPT
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