Brief presentation on Neonatal sepsis

1. NEONATAL SEPSIS
LYNET BARASA MED/07/13
KINARA KENYORU MED/18/11

2. Def’n
• Clinical syndrome of systemic illness
accompanied by blood infection in infant
younger than 90 days old.

3. Importance
• Single most important cause of death in
community….. Accounts for over half.
• Can be treated with antibiotics if discovered
early.

4. Etiology
• Frequently bacterial, may also be viral
(enterovirus, adenovirus, HSV) fungal
(Candida spp), parasitic (TORCHES, malaria) or
as a result of toxins produced by these
microorganisms.

5. The largest East African study –
242 positive blood cultures
Age < 7 days Age 7 – 59 days
1 E. coli 19% 1
Group A
Streptococci
15%
2 Acinetobacter 12% 2
Group B
Streptococci
13%
3 Klebsiella 10% 3
Strep.
Pneumoniae
12%
4
Group B
Streptococci
9% 4
Staph.
aureus
12%

6. Epidemiology
• Occurs in 0.5-8.0 in 1000 live births
• Developing countries; 6-23 in 1000 live births
• Highest rates n low birth weight infants,
premature infants, ill infants, those with RDS
and those with maternal perinatal
predisposing factors
• High mortality rate (13-25%)

7. Risk Factors
1. Maternal; Chorioamnionitis, prolonged/preterm
rupture of membranes, maternal bleeding,
toxemia, precipitous delivery, maternal infection
(UTIs), maternal GBS colonisation, >6 DVEs
during labor in PROM, poor/no ANC, poor
nutrition, difficult delivery.
2. Neonatal; prematurity, twinning(especially 2nd
twin), galactosemia, IM administration of iron,
face presentation, low apgar, aspiration, fetal
distress,

8. 3. Environmental; overcrowding, understaffed
units, improper sanitation, sick staff around
neonates as well as poor delivery techniques.
• Intravascular cannulas (S.epidermidis, S.
aureus), intravenous feeding, prolonged
endotracheal intubation.

9. Classification
1. Early onset; Occurs rapidly. 85% within 24hr,
5% within 24-48hr and rest within 48-72hr.
• Associated with acquisition of microorganisms
from mother during passage through birth
canal. Commonly pneumonia
• Microorganisms commonly associated with
early onset; GBS, E. coli, coagulase neg Staph,
H. influenza and L. monocytogenes.

10. 2. Late onset; at 4-90 days of life. Organism first
colonises then invades, causing sepsis. Commonly
meningitis
Acquired from caregiving environment. Organisms
implicated; coagulase negative Staphylococcus, S.
aureus, E. coli, Klebsiella, Pseudomonas,
Enterobacter, Candida, GBS, Serratia and
Acinetobacter
Trends in late onset sepsis show an increase in
coagulase negative streptococcal sepsis, susceptible
to first generation cephalosprorins.

11. Portals of entry
• The infant’s skin, umbilicus, resp tract, GI tract,
conjuctiva may be colonised from environment
creating an entry point for invasive organisms
that cause late onset sepsis.
• Vectors for such may be vascular or urinary
catheters, other indwelling lines or contact with
caregivers who have bacterial colonisation.
• Pneumonia is more common in early onset sepsis
while meningitis and bacteremia are more
common in late onset.

12. Reasons for increased susceptibility in
preterm infants
1. Immunological; ↓ IgG transplacental
transfer, immaturity of immune systems
2. Poor surface defences; thin skin, easily
traumatised
3. Invasive procedures; ET tube, IV catheters
4. ↑risk of conditions predisposing to sepsis;
prolonged artificial ventilation, IV feeding
5. ↑postnatal exposure; other babies in
neonatal unit

13. Pathophysiology
• Spectrum of sepsis ranges from microbial
invasion of the bloodstream or intoxication
with early signs of circulatory compromise
(tachycardia, tachypnea, peripheral
vasodilation and fever or hypothermia) to full-
blown circulatory collapse with multiple organ
dysfunction syndrome (MODS) and death.

14. • In utero (transplacental)
• Intrapartum (ascending); due to disruption of
membranes and during passage along birth
canal.
• Postpartum (nosocomial/community
acquired)
• Inflammatory cytokines most commonly
produced in NNS; IL-6, 8 & TNFα.

15. • The bacterial capsule polysaccharide adheres
well to the plastic polymers of catheters.
• Proteins on the organism enhance attachment
to the surface.
• This creates a capsule between the microbe
and the catheter preventing C3 deposition and
phagocytosis.

16. • Pneumonia is the most common invasive
bacterial infection in the newborn.
• PMNs are vital in elimination of bacteria but they
are deficient in chemotaxis and killing in neonates
because of ↓ adherence to endothelial lining
reduced ability to marginate and leave
intravascular space.
• Deficient humoral deficiency due to ↓IgG.
• Infant T cells do not proliferate as fast as adult T
cells.

17. • Hypovolemia from intravascular fluid losses
occurs through capillary leak.
• Cardiogenic shock results from the
myocardial-depressant effects of sepsis.
• Distributive shock is the result of decreased
systemic vascular resistance.

18. CLINICAL PRESENTATION
MED/18/11
KINARA KENYORU

19. • Age < 60/90days
• One or more of:
– Change in level of activity
– Bulging fontanelle
– History of convulsions
– Feeding difficulty
– Temp ≥37˚C or <35.5˚C
– Fast breathing? Resp rate ≥60bpm
– Severe chest wall indrawing
– Grunting
– Cyanosis/ Pulse oximetry

20. • Also check
– Jaundice
– Capillary refill
– Severe pallor
– PROM > 18hrs if aged <7days
– Localized severe infection – joints, abdominal distension
– Weight loss
• If no sign of serious illness check for:
– Pus from eye, ear, umbilicus and redness of abdominal
skin
– Few large, pus-filled blisters/ septic spots

21. HISTORY
• Characterise symptoms ruling out differentials
• Risk factors
• Interventions
• Complications

22. PHYSICAL EXAM
Initially nonspecific
General exam: sick looking, resp. distress, AVPU <A,
LBW, Hyper/hypothermia(temp instability), pallor,
mottled skin, skin rash, petechiae, jaundice
• RS-tachypnea >60, grunting, LCWI, Intercostal
recession, head nodding, Low SpO2
• CNS-Lethargy, excessive crying, bulging fontanelle,
irritability, convulsions, neck stiffness, sunset eyes,
• GIT- feed intolerance, abd distension,
hepatosplenomegaly
• CVS- Cap refill delayed, tachycardia or bradycardia,
• Septic spots
• Omphalitis- umbilical flare, oozing pus

23. Predicting severe illness in young infants (2)
Symptom / Sign WHO Kenya
Reduced Feeding Ability  
Reduced / Abnormal Movements  
Breathing difficulty  
History of convulsions  a
Temperature > 38.00C  
Respiratory rate > 60bpm  
Severe lower chest wall indrawing  
Cyanosis  
Prolonged capillary refill  b
Bulging fontanelle  
a – very uncommon, b – not assessed

24. Investigations
Lab:
Blood culture, Complete blood count(I/T ratio),
Lumbar Puncture(microscopy, culture, biochem,
sensitivity), Swab of infected cord or skin lesion,
Random Blood sugar (hypo/hyperglycemia),
Coagulation studies(DIC), CRP, PITC, HSV PCR
Supportive Ix such as UECs, LFTs as required
Imaging:
Chest xray, Cranial Ultrasound

25. TREATMENT

26. SUPPORTIVE
• Ensure hydration/electrolyte balance.
• Thermal-neutral environment.
• Ensure nutrition (parenteral if indicated). Weigh daily
• Isolate/barrier nursing especially if MRSA.
• Remove all indwelling catheters.
• Vit K 1ml PO and TEO if not given.

27. Things to take into account:
• Organisms
• Antibiotic sensitivity
• Is there meningitis?
Treatment could be supportive or definitive
with close monitoring of.

28. • Check for hypoglycaemia, treat if unable to measure
glucose. 2mls/kg of D10
• Give Oxygen if cyanosed or resp rate >60bpm
• Phenobarbital for seizures. IM LD 20mg/kg, MD 5mg/kg
IV ABX
Gentamicin 3mg/kg or 5mg/kg (if >2kg)OD and xpen
50,000IU/kg BD. Xpen can be substituted with 3rd gen
cephalosporin eg ceftriaxone 50mg/kg OD or cloxacillin if
Staph. suspected. Vancomycin for MRSA.
ORAL ABX
Amoxycillin/ampicillin/flucloxacillin 50mg/kg BD
• Acyclovir for HSV

29. Duration of treatment for neonatal sepsis
Signs of neonatal Infection in a baby breast feeding well.
IV/IM Abx could be stopped after 48 hours if all the signs of possible sepsis
have resolved and the child is feeding well and LP , if done, is normal.
Give oral treatment to complete 5 days in total. Advise the mother to
return with the child if problems recur.
Skin infection with signs of generalised illness such as poor feeding IV/
IM Abx could be stopped after 72 hours if the child is feeding well without
fever and has no other problem and LP , if done, is normal.
Oral Abx should be continued for a further 5 days.
Clinical or radiological pneumonia. IV/ IM Abx should be continued for a
minimum of 5 days or until completely well for 24 hrs.
Severe Neonatal Sepsis The child should have had an LP . I V/ I M Abx
should be continued for a minimum of 7 days or until completely well if
the LP is clear
Neonatal meningitis or severe sepsis and no LP performed I V/ I M Abx
should be continued for a minimum of 14 days.If Gram negative meningitis
is suspected treatment should be iv for 3 weeks.

30. Antibiotic prophylaxis
Xpen + Gentamicin given as soon as possible after birth to all
newborns (term and preterms) with any one of the following
risk factors:
PROM>18 hours
mother with fever (T > 38⁰ C)
Suspected or Confirmed chorioamnionitis
Mother Rx for sepsis at any time during labour or in the last 24 hours
before and after birth.
Given for 48-72 hours (at least 4 doses of Penicillin + 2 doses
of gentamicin) and may be stopped if the baby has remained
entirely well during this period. If there are no risk factors
then DO NOT initiate Abx treatment.
A well baby born preterm < 37 wks or Low birth weight with
low risk factors does not require antibiotic treatment.

31. PREVENTION
• Good antenatal care.
• Good delivery suite practices e.g aggressively
treat chorio-amnionitis with rapid delivery of
the infant.
• Prevent nosocomial infections by observing
infection control strategies such as hand
washing between infants, reduce over
crowding,good umbilical stump care.

32. COMPLICATIONS
• Shock,circulatory collapse, DIC, severe
jaundice, NEC.
• Long term…..due to meningitis/ mental
retardation and other neurological disorders.
……due to NEC / short bowel
syndrome following resection of non-viable
gut.