Neonatal Sepsis SCS.pptx8765434567uyfkki

nill

1. Neonatal Sepsis By Dr. Abu Bakarr Kanu

2. OUTLINE Introduction Aetiology Neonatal immunity Risk factors Pathogenesis Diagnosis: clinical manifestation, Investigations Treatment Prevention/ Prognosis Conclusion

3. INTRODUCTION Neonatal sepsis , prematurity and perinatal asphyxia remain major contributors to the burden of neonatal morbidity and mortality in Sub-Saharan Africa.* Sierra Leone (2019); NMR= 34 per 1,000 live births. Prematurity – 30%, Asphyxia – 27%, Sepsis – 23%.** ODCH: NNS is the 3 rd leading cause of neonatal death, after asphyxia and prematurity.*** * Nagalo K, Dao F, Tall FH, Ten years morbidity and mortality of newborns hospitalized at the Clinic El- FatehSuka (Ouagadougou, Burkina Faso). Pan Afr Med J2013; 14: 153-7. **Maternal, Neonatal, and Child Health/ UNICEF Sierra Leone. www.unicef.org ***ODCH Morbidity and Mortality review statistics

4. INTRODUCTION Neonatal Infection: the presence of a positive microbial isolate [viral, bacterial, protozoal and fungal] with clinical manifestations occurring within the first 28 days of life. Neonatal Sepsis (NNS) aka Sepsis Neonatorum: type of neonatal infection specifically referring to the presence of a bacterial blood stream infection.

5. INTRODUCTION Types:

6. AETIOLOGY Gram Positive : Clostridia , Enterococci, Group B streptococcus, Listeria monocytogenes, Staphylococcus aureus, Staphylococcus coagulase negative, Streptococcus pneumoniae , Viridans streptococcus Gram Negative : Bacteroides , Campylobacter , Citrobacter , Enterobacter, Escherichia coli, Haemophilus influenzae , Klebsiella , Neisseria gonorrhoeae, Neisseria meningitidis , Proteus, Pseudomonas, Salmonella

7. NEONATAL IMMUNITY Immature- there is a genetically programmed low response or lack of response of the fetal and newborn immune system. Inexperience- the newborn immune system has not yet had its first immunologic encounter.

8. NEONATAL IMMUNITY IMMUNOGLOBULINS: IgG is actively transported across the placenta, and levels are directly proportional to gestational age. Specific bactericidal and opsonic antibodies against enteric gram-negative bacteria are predominantly in the IgM class, which neonates lack.

9. NEONATAL IMMUNITY COMPLEMENT: No transplacental passage of complement from the maternal circulation. A fetus begins to synthesize complement components as early as the 1st trimester. Leads to diminished complement-derived chemotactic activity and to a diminished ability to opsonize organisms. Premature infants have lower levels of complement components and activity.

10. NEONATAL IMMUNITY MONOCYTE-MACROPHAGE SYSTEM: the function of macrophages is diminished, chemotaxis of monocytes is impaired, affecting the inflammatory response in tissues. NEUTROPHILS: Neonatal neutrophils have abnormal migration (chemotaxis), decreased adhesion, aggregation, and deformability, all of which may delay the response to infection.

11. RISK FACTORS Maternal Low socioeconomic status GBS colonisation PPP/ PROM/ prolong labour STIs Maternal WBC > 15,000 Peripartum MOD: Instrumentation, SVD Multiple vagina examination Ventilation/ Resuscitation Neonatal Sex: male Lower GA/ BW Asphyxia Bottle/ Formula feeding Facility Nurse-Patient ratio Overcrowding Environment Human traffic Indwelling materials

12. RISK FACTORS MAJOR RISK FACTORS: ROM > 24 hr Intrapartum maternal fever (>38.0 º C [>100.4 º F], Chorioamnionitis (see footnote below) Extreme prematurity

13. PATHOGENESIS: An ascending infection The human birth canal is colonized with aerobic and anaerobic organisms. Cervical mucus plug (operculum) acts as a protective barrier by deferring the passage of bacteria into the uterus. (see footnote ) High frequency of intercourse, multiple sexual partners, and frequent vaginal examination increases the risk for ascension of the vaginal bacteria into the amniotic cavity.

14. PATHOGENESIS

15. PATHOGENESIS LATE-ONSET POSTNATAL INFECTIONS : After birth, neonates are exposed to infectious agents in the nursery or in the community. Postnatal infections may be transmitted by direct contact with hospital personnel, the mother, or other family members; or from inanimate sources such as contaminated equipment. The most common source of postnatal infections in hospitalized newborns is hand contamination of health care personnel.

16. DIAGNOSIS Difficult Paucity of manifestations Non-specific Non- focalising High index of clinical suspicion All Systems CNS/ RS/ CVS GIT/ Digestive system/ UGS Haematopoeitic MSS/ Skin

17. DIAGNOSIS: Clinical Manifestation General: Fever, temperature instability, Poor feeding, oedema Gastrointestinal system : Abdominal distention, Vomiting, Diarrhoea, Hepatomegaly Respiratory system: Apnea, dyspnea, Tachypnea, retractions, Flaring, grunting, Cyanosis

18. DIAGNOSIS: Clinical Manifestation CVS: Pallor, mottling, cold, clammy skin, Tachycardia, Hypotension, Bradycardia CNS: Irritability, lethargy, Tremors, seizures, Hyporeflexia, hypotonia , Abnormal Moro reflex Hematologic system: Jaundice, Splenomegaly, Pallor, Petechiae , purpura, Bleeding

19. DIAGNOSIS : Investigations Microbiological Blood culture; Urine M/C/S CSF Analysis Haematological WBC/ I:T, Anaemia , Platelets Cytokines TNF α IL-6 Granulocyte CSF Acute-phase reactants CRP/ mESR Fibronectin C3 Complement Elastase α 1 -Protease Inhibitor Metabolic acidosis: pH, P co 2    Pulmonary function: PO 2 , P co 2    Renal function: BUN, creatinine    Hepatic injury/function : bilirubin , ALT, AST ammonia, PT, PTT Radiological

20. TREATMENT Empirical antimicrobial Most likely organism Infection site Tissue penetration Dose/ duration Combination Adjuvant IVF/ Hydration/ Electrolytes Ventilatory Support Total Parenteral Nutrition Shock (Fluids/ Inotropes ) Immunotherapy IVIG Human monoclonal IgM Ab Granulocyte transfusion Complement infusion Fibronectin administration Recombinant human Granulocyte CSF Granulocyte- Macrophage stimulating factor Exchange Blood Transfusion

21. PREVENTION/ PROGNOSIS Prevention Risk factors/ adherence to universal precautions Intrapartum Antibiotic Prophylaxis High clinical index of suspicion Prognosis Prompt/ Accurate diagnosis GA/ BW Immune Status Antimicrobial efficacy

22. Any Questions?

23. CONCLUSION NNS contributes significantly to the burden of neonatal morbidity and mortality in this sub-region. The risk factors for NNS are mostly preventable. A high clinical index of suspicion is required to make early diagnosis for prompt treatment.

24. Thank you