Neonatal sepsis

1. Neonatal Sepsis
(NNS)
Presenter: Sakala Felix
6th year medical student
11/11/16
Moderator Dr. Kapakala. T.M

2. Outline
 Definitions
 Classification
 Aetiology
 pathophysiology
 Clinical presentation and investigations
 Treatment
 Bibliography list

3. Objectives
 At the end of the lecture SBAT
 1. define neonatal sepsis
 2. develop a holistic approach concerning
clerkship and identifying NNS

4. Definitions
 SEPSIS: The systemic inflammatory
response to an infectious process.
 SIRS: the system inflammatory response
to a variety of clinical insults, is
manifested by 2 or more of the following
conditions:
 Temperature instability <35 of >38.5
 Respiratory dysfunction; tachypnea >2SD
above the mean for age, hypoxia
(PaO2<70mmhg on room air

5. Definition
 Cardiac dysfunction : tachycardia >2
SD above the mean for age, delayed
CRT >3 secs, hypotension >2SD
below the mean for age
 Perfusion abnormalities: oliguria
(urine output <0.5ml/kg/hr), lactic
acidosis (elevated plasma lactate
and /or arterial pH< 7.25,altered
mental status.

6. What then is NNS????
NEONATAL SEPSIS: Is
the systemic
inflammatory response
to an infectious process
that occurs in the
neonatal period

7. Classification and aetiology
cont
 Classified into 2 as EONNS &
LONNS based on clinical
presentation
 Early onset neonatal sepsis occurs
within the 1st 48 hours post delivery
 Mostly due to acquisition of
microorganisms from the mother via
trans placental, ascending infection
from the cervix (GUT normal flora) or
colonised birth canal

8.  The organisms most commonly
associated with EONNS include
the following: Group B
Streptococcus (GBS), E.coli,
Coagulase negative staph,
Haemophilus influenzae and
listeria monocytegenes
Classification and
aetiology cont.’

9.  LONNS is one that occurs after
48hrs post delivery
 Organisms implicated in late
onset sepsis include the
following; Coagulase negative
staph,staph.aureus,E.coli,
Klebsiella., candida
Classification and
aetiology cont.’

10. Other causes (viral sepsis)
 Congenital
 Enteroviruses (ie. Coxsackievirus A & B)
 Herpes Simplex Virus
 TORCH infections ie. CMV,
 Acquired HIV, Varicella, Respiratory
syncytial virus
 Can be either early or late onset sepsis

11. Risk factors
 Risk factors implicated in
neonatal sepsis reflect the stress
and illness of the fetus at
delivery, as well as the
hazardous uterine environment
surrounding the fetus before
delivery.

12. EONNS risk factors
 Maternal GBS colonization
(especially if untreated
during labour)
 Prematurity
 Maternal urinary tract
infection esp @ delivery
 chorioamnionitis
 PROM (ROM after 37 wks
before onset of labor)
 Low apgar score(<6 at 1 or 5
mins)
 PPROM (<37weeks)  Maternal fever greater than
37.9💙C
 Prolonged rupture of
membranes >24hours
 Hx of NNS baby

13. LONNS risk factors
 Prematurity  Central venous
catherterization(>10
days)
 Nasal canula or
continous positive
airway pressure(CPAP)
use
 Gastrointestinal tract
pathology.

14. Pathophysiology
 The process begins with the invasion of
the pathophysiology of bacterial sepsis
and systemic contamination.
 The release of endotoxin by bacteria
cause changes in the function of the
myocardium, changes in uptake and
utilization of oxygen, inhibition of
mitochondrial function, and progressive
metabolic chaos.

15. Pathophysiology
 In sepsis sudden and severe,
complement cascade caused much
death and damage cells. The result is a
decrease in tissue perfusion, metabolic
acidosis, and shock, disseminated
intravascular coagulation resulting (DIC)
and death. (Bobak, 2004)

16. Pathophysiology
 Patients with immune disorders have an
increased risk for serious nosocomial
sepsis. Cardiopulmonary manifestations
of gram-negative sepsis can be
replicated by injection of endotoxin or
Tumor Necrosis Factor (TNF). Barriers to
employment TNF by anti-TNF
monoclonal antibody greatly weakens
manifestation of septic shock.

17. Pathophysiology
 When the bacterial cell wall components are
released in the bloodstream, cytokine-
activated, and can further lead to more
physiological mess. Either alone or in
combination, bacterial products and pro-
inflammatory cytokines trigger a physiological
response to stop the invaders (invader)
microbes. TNF and other inflammatory
mediators increase vascular permeability and
vascular tone imbalance, and the imbalance
between perfusion and increased metabolic

18.  Shock is defined as a systolic pressure below
the 5th percentile for age or defined with cold
extremities. Capillary refilling the late (more
than 2 seconds) is seen as a reliable indicator
of a decrease in peripheral perfusion.
Peripheral vascular pressure in septic shock
(heat) but be very up on a further shock (cold).
In septic shock tissue oxygen consumption
exceeds oxygen supply. This imbalance is
caused by peripheral vasodilatation in the
beginning, during further vasoconstriction,
myocardial depression, hypotension, ventilator
insufficiency, anemia. (Nelson, 1999).

19.  Septicaemia shows the emergence of a
systemic infection of the blood caused by the
rapid multiplication of microorganisms or toxic
substances, which can cause huge
psychological change. These substances can
be pathogenic bacteria, fungi, viruses, and
rickets. The most common cause of septicemia
is a gram-negative organisms. If the protection
of the body is not effective in controlling the
invasion of microorganisms, septic shock may
occur, which is characterized by hemodynamic
changes, imbalance of cellular functions, and
multiple system failures. (Marilynn E. Doenges,
1999)

20. In the history always look
for ,,,,,,,
 Was the babe compromised at delivery?
 Was there anything in the perinatal
history suggestive of an infectious risk?
E.g. maternal HVS esp. if pathogens
isolated, pyrexia,
 Is there risk of nosocomial infection from
relatives, staff, or other sick babies on
the unit??? The kiss of death
(remember herpes simplex virus don’t
kill the children)

22. At just 24 days old, Eloise
died in her mommy's arms
 .

23. Clinical presentation
 Signs and symptoms
 Constitutional Unstable temp. fever
37.9°C
 Hypothermia less than 35.5°C
 Respiratory RR > 60/min, Grunting,
Nasal flaring, Chest recession
 GIT Poor feeding, Abdominal distension,
Diarrhea, jaundice
 CVS Mottled, greyish skin, Poor CRT
>2sec, tachycardia

24. Clinical presentation
Cont.’
 CNS Lethargy,Irritabilty,Hypothermia
poor temp regulation, Seizures/Hypotonia
 Apnea, Bulging anterior fontanelle
 MS Cyanosis, pallor, Petechiae

25. Investigations
 Dx is clinical, no single investigation
exists thus dx is via evidence of infection
 Full septic screen
 Haematological FBC/DC, CRP
 Microbiology Blood culture, Urine M/C/S,
stool M/C/S, throat swab
 Biochemistry: CSF studies, RBS, U&Es
 Radiological: CXR

26. Treatment
 One blood is drawn Rx should be
instituted with empirical abx therapy
 1. 1st line Abxs for EONNS cefotaxime
50mg/kg/dose
 2. 1st line Abxs for LONNS
cefotaxime/cloxacillin
 2nd line abx is ciprobid unless culture
detects otherwise
 X pen and gentamycin - - - dosages

27. Bibliography/references
 Neonatal sepsis, Medscape
 UTH NICU protocol
 Manual of neonatal intensive care
 Images courtesy of littlethings,com and
dailymail.co.uk

28. End of presentation
 Thank you