Pedi

1. Neonatal sepsis
1
Introduction
– Sepsis neonatorum describes any systemic
bacterial infection documented by blood culture
in the first month of life.
– Remain an important cause of neonatal mortality
and morbidity despite the advent of antibiotics
– It was almost always fatal in preterms with VLBW
before the antibiotic era and advancement in
neonatal care

2. Introduction…cont
2
– Why neonates, especially preterms are susceptible
to infections?
Immature and ineffective neonatal immune
system
oAntibodies
oComplement
oNeutrophils
oSkin/mucosal barriers
oLymphocytes
Socioeconomic and health care problems
exacerbates the incidence as well as the outcome

3. EPIDEMIOLOGY
3
– Incidence (during antibiotic era)
• Mortality
–13-63% world wide
–13-15% of neonatal deaths(USA)
–In Ethiopia… 33%, WHO/2006
• Meningitis
–0.4-2.8/1000 livebirths world wide
–Mortality 13-59% worldwide
• Sepsis
–1-21/1000 livebirths world wide
–Higher in preterms

4. Predisposing factors
1. Presence of maternal
(obstetric) risk factors
- PROM > 18 hrs
- intrapartum fever (>38°C),
- Maternal chorioamnionitis
- Prolonged labor > 18 hours
- Repeated vaginal
examination
2. Fetal risk factors
- Prematurity
- LBW
- Asphyxia
- Developmental or
congenital immune
defects
- Congenital anomalies

5. Epidemiology …cont
5
– Disease pattern based on postnatal age
• Early onset…within 7days of life
–Time of onset: 85% within 24hrs
• Late onset……within 7 to 30 days of life
• Late late onset…….30-90 days
–Preterms and VLBW who stayed in NICU

6. Characteristics of neonatal sepsis
6

7. Etiopathogenesis
7
Pathogenesis
• Early onset …vertical transmission
–Ascending intra-amniotic infection aspirated
by fetus
–Transplacental: syphilis and L.monocytogene
–Colonization of birth canal and poor nursery:
GBS, E.coli
–Invasive procedures
–Prolonged labor or ROM increases infection
• Late onset
–From maternal birth canal or postnatal

8. Etiopathogenesis …cont
8
Etiology
EONS LONS
* Group B streptococcus * Coagulase Neg.staph (CONS)
* E.coli * S.Aureus
* Viridans streptococci * E.coli
* Enterococci spp. * Klebsella spp.
* S.Aureus * Candida spp.
* Pseudomonas * Pseudomonas spp.
* Group D streptococcus * Enterococci spp.
* Listeria monocytogenes * GBS

9. Clinical manifestations
9
Strongly suggestive:
- Hypoglycemia / Hyperglycemia - Seizures
- Hypotension - Hepatomegaly
- Splenomegaly
- Metabolic acidosis - Petechiae
- Apnea - Hematochezia
- DIC - Bulging
fontanelles
- Shock - Respiratory
distress

10. Clinical manifestations …cont
10
Non-specific: manifestations
- Lethargy / Irritability
- Temperature Instability
- Poor feeding
- Cyanosis
- Abdominal distension
- Jaundice
- Tachycardia
- Tachypnea

11. Differential Diagnosis
11
Non-specific symptomatology
– Non-bacterial infections
• HSV and other viruses
• Fungal infections
• TORCH infections
– Non-infectious etiologies
• RDS: HMD, TTN, MAS
• Hypothermia, Hypoglycemia, Asphyxia
• ICH
• Drug withdrawal
• Errors in metabolism
• Many other disorders

12. Laboratory Investigations
12
A) Microbiologic tests
1) Culture (Blood, Urine, CSF)
I. Blood Culture (more than one sample)
»Growth within 24-48 hrs is possible
»Avoids contaminant pathogens
II. Urine Culture
»Can be positive in the absence of UTI
»Yield is low, especially in EONS
»May be positive in the absence of
sepsis in older newborns with UTI

13. Lab investigation
• Low total white count and absolute
neutropenia (< 1000/mL), all suggest neonatal
bacterial infection.
• •Thrombocytopenia (low platelet count in bd)
is also a common feature
• Definitive diagnosis is made by positive
cultures from blood, CSF, or other body fluids.

14. Neonatal Meningitis
• Any newborn with bacterial sepsis is at risk for
meningitis.
• The presence of seizure increases the suspicion
for meningitis.
• The most common organisms are GBS and gram-
negative enteric bacteria.
• Early diagnosis and therapy is mandatory
improve short and long term outcomes

15. Clinical manifestation
• Suspect neonatal meningitis if a neonate with
septicaemia have s/s of:
• fever
• seizures (convulsion or twitching)
• Staring look
• Bulging anterior fontanel
• Abnormal high pitched cry or excessive crying

16. Lab investigations:
Dx is suggested by:
• a CSF protein level higher than 150 mg/dL,
• glucose less than 30 mg/dL,
• leukocytes of more than 25/micro L, and a
positive Gram stain.
• The diagnosis is confirmed by culture.

17. Treatment
• •Sepsis can be treated IV for 10–14 days, but
meningitis often requires 21 days.
• •i.e Gram-negative infections, in particular, are
difficult to eradicate, and may relapse.
• •The mortality rate of neonatal meningitis is
approximately 10%, with significant neurologic
morbidity present in one-third of the survivors

18. • Neonatal Common Intravenous Antibiotic
• Ampicillin
• Cefotaxime
• Cefepime
• Ceftazidime
• Gentamicine
• vancomycine

19. Perinatal asphyxia
PNA

20. PERINATAL ASPHYXIA

21. Perinatal Asphyxia (PNA)
Insult to the fetus/neonate due to hypoxia
and/or ischemia to various organs
Defined 'Perinatal asphyxia' as "a condition in the
neonate where there is the following combination:
o Severely reduce oxygen delivery and lead to
acidosis; and
o A failure of function of at least two organs
(may include lung, heart, liver, brain, kidneys
and hematological) consistent with the effects of
acute asphyxia.

22. Introduction
PNA-is considered if:
Fetal acidosis (PH<7.0)
5th minute APGAR (0-3)
Hypoxic-Ischemic Encephalopathy
(abnormal tone, seizure, mental change--)
Multiorgan symptoms/signs

23. Consider PNA in our set up if:
• Low 1st minute APGAR (0-6)
• Hypotonia and
• Seizure
• Exceptional cases
– Preterm babies
– Babies who had birth trauma
– Babies with congenital neurological anomalies

24. PNA
• Incidence is 1-2% in developed countries
• Indirectly related with GA & birth weight
• Responsible for around 23% of perinatal deaths
• Causes:
Placental insufficiency (90%)- inability of the
placenta to provide O2 & remove CO2 & H from
the fetus
10% is due to CardioVascular, Pulmonary and
neurologic diseases

25. Risk factors:
The incidence of antenatal and intrapartal asphyxia is
higher in complicated pregnancies, particularly those
associated with diminished placental reserve:
Hypertensive disease of pregnancy or pre-
eclampsia,
Intrauterine growth restriction,
Placental abruption,
Maternal anemia,
Placental aging,
Malpresentation including vasa praevia.

26. Fetal hypoxia:
 Inadequate oxygenation of maternal blood
(Respiratory failure, cardiac diseases---)
 Low maternal BP
 Inadequate uterine relaxation
(e.g.:tetany with oxytocin)
 Premature placental separation
 Cord compression
 Placental insufficiency (post maturity,
PIH)

27. Postnatal/Neonatal Hypoxia:
Anemia
Shock
Low arterial O2 saturation (birth
injury, drugs---)
Failure of oxygenation of blood
(cyanotic CHD, Severe lung diseases)

28. As asphyxia progresses with severe hypoxia:
o Acidosis
o Decreased HR & BP
o Anaerobic metabolism with accumulation
of lactic acidosis
o Finally (hypotension, acidosis &
progressive hypoxia) leads to multiple
organ damage

29. Perinatal asphyxia may result in
–Fetal demise,
–Neonatal death, or
–A period of recovery during which
there is organ dysfunction with
possible long-term effects,
particularly in neurological function

30. • Target organs:
Kidneys (50%)
CNS (28%)
CVS (25%)
Pulmonary (23%)

31. Clinical manifestations:
• Depression of the neonate at
birth with a low APGAR score and
acidosis,
• Multiple organ involvement:
• Hypoxic ischemic encephalopathy
(HIE),

32. Multiple organ system dysfunction:
 Renal: ATN (Oligouria and elevated
creatinine)
 CVS: MI,CMP, poor contractility,
hypotension (25%),
 Pulmonary: respiratory distress and
persistent pulmonary hypertension of the
neonate, pul.hemorrhage (25%),
 Hematologic: DIC

33. Clinical manifestation…cont
 Adrenal insufficiency
 Subcutaneous fat necrosis
 Hepatic failure, and
 GI: ulceration with hemorrhage,
Necrotising enterocolitis, perforation
 Metabolic: SIADH, hypoglycemia,
hypocalcaemia, myoglobinuria,
hyperkalemia and hyponatremia

34. Sarnat H. & Sarnat M. staging of HIE
signs stage 1 stage 2 stage 3
Consciousness hyperalert lethargic stuporous/coma
Tone normal hypotonic flaccid
Posture normal flexion decerebration
Tendon reflexes hyperactive hyperactive absent
Moro strong weak absent
Pupils mydriasis meiosis unequal
Seizures none common decerebration
EEG normal seizure activity burst suppresion
Duration <24hrs 24hrs-14days days-weeks
Outcome good variable death, severe sequelae

35. Management of PNA
Principles
• Supportive care, correct metabolic
abnormalities
• Directed at the organ system manifestation
• Ventilatory support
• Hemodynamic stabilization
• Rx of seizure- aggressive

36. Prognosis of PNA
• Outcome ranges from complete recovery to death
• Depends on:
Whether metabolic & cardiopulmonary
complications (hypoxia, hypoglycemia, shock)
can be treated
Gestational Age (inverse relation) and birth
weight
Severity of HIE

37. • Poor prognostic features includes:
 Stage 3 HIE
 Refractory seizure
• Death, severe cognitive & motor deficit are also
predicted from:
Low APGAR at 20 minutes
Absence of spontaneous respiration at
20minutes
Persistence of abnormal neurologic signs at
2wks of age
Seizure occurring on the first day
Low voltage or suppression pattern on EEG

38. • Late sequalae of PNA:
o Cerebral palsy
o Mental retardation
o Microcephally
o Motor deficit
o Hearing loss

39. Prevention
• Perinatal assessment of fetal and
placental condition
• Effective neonatal resuscitation

40. Save me please!!!!!!
And
Good day!