1. NEONATAL SEPSIS
Dr.Sayid.,MD.
Dept.Paediatrics
Dept.of Paediatrics

2. What is neonatal sepsis?
Welcome !!
What is neonatal sepsis?
Definition
Causes
What will I learn?
Symptoms
Diagnosis
Treatments
Summary

3. DEFINITION
CLINICAL SYNDROME OF BACTERAEMIA CHARECTERIZED BY SYSTEMIC SIGNS AND SYPMTOMS OF INFECTION IN THE FIRST FOUR WEEKS OF LIFE.

4. What is Neonatal Sepsis?
When pathogenic bacteria gain access into the blood stream, they may cause overwhelming infection without much localization (septicemia) or may get predominantly localized to the lung (pneumonia) or the meninges (meningitis).
Arthritis.osteomylitis,and UTI.
Exception conjunctivitis and oral thrush.

5. More facts about Neonatal Sepsis
Neonatal Sepsis affects approximately 1- 2 infants per 1000 births with a higher incidence in premature & low birth weight infants. Incidence in India 30/1000(NNPD)

6. CLASSIFICATION Early onset <72 hours (RD,Pneumonia)
Late onset >72 hours nosocomial,
(Septicemia .pneumonia or meningitis)

7. RISK FACTORS LBW OR PREMATURITY ILLNES 2 WEEKS PRIOR TO DELIVERY
FOULSMELLING/MECONIUM LIQUOR
RUPTURE OF MEMBRANE>24HRS
PROLONGED LABOR.24HRS
ASPHYXIA
SINGLE/UNCLEAN OR>3 STERILE P/V-
MECHANICAL VENTILATION,IP,IVF,

9. Causes of Neonatal Sepsis
E.coli, Staphylococcus,Klebsiella and Group Beta Strep (GBS). neonates are more susceptible coz
Immature immune response
Genetic predisposition

10. What makes a neonate’s immune system immature?
Normally an immune system responds to a pathogen in a specific manner, but if there are problems with any element
the immune system is unable to function properly
Pathogen enters body
Neutrophils move in
Chemotaxis occurs
Opsonization causes
phagocytosis
Monocytes kill pathogen

11. Neutrophils: An important cell in immunity against pathogens
Neonatal neutrophils are deficient in
their ability to adhere to vessel walls at site of infection and
have a
decreased ability to “deform” &
migrate into tissues
Red Blood Cells
Neutrophils I

12. Chemotaxis Neonatal neutrophils have decreased chemotaxis due to
decreased chemoattractant .
Chemoattractants attract
neutrophils to the site of infection .

13. Opsonization
Neonates have a decreased amount of opsonins (antibodies that promote opsonization)
Opsonization
Pathogen

14. Monocytes: Another important cell in the fight against pathogens
Monocytes are deficient which are another main cells in fighting infection I

15. What makes a neonate’s immune system susceptible to sepsis?OR
Maturity
Immaturity

16. You’re Right!!!!
The immaturity of a neonate’s immune system makes them MORE SUSCEPTIBLE to sepsis.

17. Genetic Role
Polymorphisms cause either an over expression or under expression of proteins and/or genes that have significant roles in the immune response to infection. This alters their ability to properly function which makes a neonate more susceptible to sepsis.

18. CLINICAL FEATURES

19. SUBTLE/NON SPECIFIC
HYPOTHERMIA OR FEVER
LETHERGY/POOR CRY.REFUSAL OF FEED
POOR PERFUSION CRT>3sec.
HYPOTONIA WEAK OR ABSENT NNR
BRADY/TACHYCARDIA
RD,APNEA,GASPING RESPIRATION
HYPO/HYPERGLYCEMIA & ACIDOSIS

20. A CASE OF SEPSIS

21. heart rate changes tachypnea
SYSTEMIC FEATURES The symptoms of neonatal sepsis are not concrete and vary widely
heart rate changes tachypnea
hypotension DOB,Grunting
shock cyanosis
feed intolerance
vomiting / diarrhea DIC
abd. Distension bleeding
NEC petechia/purpura
hepatomegaly
jaundice umbilical redness/discharge
ARF sclerema
irritability mottling
high pitched cry,vacant stare pustule,abscess
bulging AF,seizures
stupor/coma

22. A Case of Septicemia

23. A CASE OF NEONATAL MENINGITIS

24. Inflammation in Neonatal Sepsis
It occurs because of an exaggerated systemic inflammatory response . Let’s find out how this is true
Inflammatory Process

25. Inflammatory Process Pathogen enters body Inflammatory mediators
released (cytokines)
Injury to endothelium
Tissue factors released
Production of thrombin
Increased activity of
fibrinolysis inhibitors
Coagulation promotes
clot formation
Decreased fibrinolysis

26. Inflammation
Overall, the imbalance among inflammation, over coagulation, and decreased fibrinolysis are the cause for the majority of deaths in sepsis.

27. How is Neonatal Sepsis Diagnosed?
There is no definite marker in neonatal sepsis, but there are determinants of infection. * Blood & Urine cultures * Septic screen: Complete Blood Count and DLC * Lumbar Puncture (LP) * Radiology CXR,Neurosonogram,CT * Line cultures

28. Sepsis screen CBC: white blood cell count and differential count.
Leukopenia <5000mm3
An absolute neutrophil count of < 1800 per cmm
Neutropenia
Immature neutrophils (Band cells + myelocytes + metamyelocytes) to total neutrophils ratio (l/T) > 0.20

29. Thrombocytopenia,
Toxic granules on peripheral smear and
Gastric aspirate smears showing more than 5 Polymorphs per high power field
Elevated micro- ESR->15mm in 1st hour
CRP-Positive >1mg/dl

30. NORMAL CSF IN NEONATES TERM PRETERM WBC /cmm upto 30 upto 90
Polymorphs % %
Protein mg/dl Upto
Glucose mg/dl

31. BAND FORM

33. Is there a diagnostic marker for neonatal sepsis?
True
False

34. Yeah!!! You are correct!
There is NOT a specific diagnostic marker, only determinants of infection (labs, x-rays).

35. Treatments for Neonatal Sepsis
It is of vital importance that treatment is initiated as soon as sepsis is suspected, especially for those infants at risk.
Why????

36. Why is it so important to start antibiotic treatment?
If not treated as soon as sepsis is suspected a neonate is more likely to die from sepsis and it’s complications.

37. INDICATIONS FOR ANTIBIOTICS
Presence of >3 risk factors
Presence of foul smelling liqour
Presence of 2 antenatal risk factors &positive septic screen
Strong clinical suspicion of sepsis

38. ANTIMICROBIAL THERAPY
Septicemia or Pneumonia 1 st line;
Inj Ampicillin 50 mg/kg/dose 7-10 days /
Inj Cloxacillin 50 mg/kg/ dose 7-10 days +
InjGentamicin 2.5mg/kg/dose 7-10 days /
Inj Amikacin 7.5 mg/kg/dose 7-10 days
3rd line drugs for resistant strains
CEFOTAXIME OR PIPERACILLIN-TAZOBCTAM
AMIKACIN

39. ANTIMICROBIAL THERAPY
I. Meningitis with or without positive blood/CSF C/S
(1) Inj Ampicillin 100 mg/kg/ dose 3 weeks
Inj Gentamicin 2.5 mg/ kg/dose 3 weeks
Add cefotaxime
II. Blood Culture positive,but no meningitis.
(2) Inj Cefotaxime 50 mg/kg/ dose 2 weeks
Inj Gentamicin 2.5 mg/kg/ dose 2 weeks
III.Culture and sepsis screen negative,but clinical course compatible;
continue 5-7 days.

40. SUPPORTIVE CARE Thermoneutral environment Establish IV line
Correct SHOCK
Correct hypoglycemia
Vitamin K
If cardiopulmonary compromise- CPR
Exchange transfusion in case of sclerema

41. DURATION OF ANTIBIOTICS
if baby appears ill with negative culture,sepsis screen positive ;Antibiotic should be continued for 7-10 days
Deep-seated infections (osteomyelitis) may require therapy for 3-6 weeks.

42. Superficial infections :local application of antimicrobial agents
Superficial infections :local application of antimicrobial agents. Pustules can be punctured with sterile needles and cleaned with spirit or betadine . Purulent conjunctivitis : neosporin or chloramphenicol ophthalmic drops. Oral thrush : local application of clotrimazole or nystatin (200,000 units per ml) and hygienic precautions

43. Prevention of infections
A good antenatal care
Tetanus toxoid to mother.
Any infection in antenatal period to be diagnosed early and treated early.
Exclusive breast feeding for 6m.
Cord care.
Hand washing

44. Prevention of infection in hospital
The nursery environment should be clean and dry with 24 hour water supply and electricity.
adequate ventilation and lighting.
temperature to be maintained between
Overcrowding to be avoided
Aseptic precautions

45. Unnecessary invasive interventions should be kept to the barest minimum.
use of disposables.
Stock solutions to be avoided.
separate thermometer and stethoscope and all barrier nursing measures for each baby

46. Strict house-keeping routines for washing, disinfection, cleaning of cots and incubators should be ensured and these policy guidelines should be available in the form of a manual in the nursery.
The use of prophylactic antibiotics for prevention of nosocomial infections is strongly condemned. They are not only useless but also dangerous because of the potential risk of emergence of resistant strains of bacteria.

47. PROPHYLACTIC ANTIBIOTICS
EXCHANGE TRANSFUSION
VENITILATED NEONATES

48. RESERVE ANTIOBIOTICS AZTREONAM against Gram negative organism
MEROPENEM most bacterial pathogen except MRSA and Enterococcus
IMEPENEM _generaly avoided—seizures
VANCOMYCIN /CIPROFLOXACIN WITH AMIKACIN for MRSA and ENTEROCOCUS

49. ADJUNCTIVE THERAPY EXCHANGE TRANSFUSION NO ROLE IVIg.
GM-CSF under trial.

50. SUMMARY
In conclusion, manifestations of neonatal sepsis are non-specific. A high index of suspicion with or without lab evidences of infection is the key for early diagnosis.
Prompt institution of antibiotic therapy and supportive care will save most of the cases of neonatal sepsis.

51. I hope you have enjoyed your experience and have learned some new information about neonatal sepsis.