4-neonatal-septicemia.pdfdr. Haitham nsj

R

1. Your Date Here Your Footer Here
Neonatal infec,ons &
sepsis Rahma Ammar
-

2. •You are called to a/end an urgent cesarean sec3on delivery at 36 weeks' gesta3on
necessitated by maternal fever, fetal tachycardia, and a non-reassuring fetal heart
tracing. The prenatal course has been unevenEul, but the group B Streptococcus
status is unknown. Six hours before delivery, the mother began to develop fever,
nausea, and vomi3ng, followed by the onset of contrac3ons. Due to a history of
anaphylaxis to penicillin, she received one dose of vancomycin during labor.
Ar3Jcial rupture of the membranes occurs at the 3me of the cesarean sec3on and
reveals light meconium-stained Kuid. The infant emerges vigorous, and physical
examina3on reveals a faint erythematous rash, tachypnea, and grun3ng.
1.What is the most likely diagnosis?
2.What are the 3 most important inves3ga3ons he needs?
3.What ini3al an3bio3cs you will use?
Your Date Here Your Footer Here 3 -
-
-
-
-
-
-
- -
-
-
-
- >
-
-

3. Neonatal infec,ons
•They are frequent and important causes of morbidity and mortality in
the neonatal period. They aQect 2% of fetuses and 10% of infants in
the Jrst month of life.
•They are divided into: Viral, Bacterial, Fungal, mycoplasmal, Protozoal
infec3ons.
•Bacterial infec3ons are either speci7c (Minor, Major) or non-speci7c
(Neonatal sepsis).
Your Date Here Your Footer Here 8 -
-
-
-
*i
-- -
- -
-
-
-

4. Factors speci7c to neonatal infec,ons
1.Diverse modes of transmission of infec3ous agents from mother to fetus or newborns
during prenatal, or natal or postnatal period
2.Newborns may be less capable of responding to infec3ons because of one or more of
immunologic deJciencies.
3.Co-exis,ng condi,ons o]en complicate the diagnosis and treatment of neonatal infec3ons
like RDS, congenital pneumonia, CHD.
4.The extremely variable clinical manifesta,ons of infec3ous diseases of newborns that may
present as mild or severe manifesta3on of focal or systemic infec3ons.
5.The maternal infec3on is o]en undiagnosed during pregnancy as the mother is
asymptoma3c or with nonspeciJc signs and symptoms during acute infec3on.
6.The wide variety of e,ologic agents that infect newborns like bacteria, virus, etc..
7.7. The immature LBWN remain in the hospital for long period that put them at con3nuous
risk of nosocomial infec3on
Your Date Here Your Footer Here 9 ‘
-
-
-
X
ijs

5. Bacterial Neonatal infec,ons
Non-speci7c (Neonatal sepsis)
Speci7c (major, minor):
Minor Speci7c infec,ons: Omphali3s, oral thrush, Conjunc3vi3s, sep3c spots
Major Speci7c Neonatal infec,ons:
1.Pneumonia:
a.Congenital
b.Aspira3on
c.Staphylococcal
d.airborne
2.Pyogenic meningi3s
Your Date Here Your Footer Here 10
3.Pylonephri3s
4.Osteomyli3s + sep3c arthri3s
5.Epidemic diarrhea
6.Tetanus neonatorumBy the same pathophysiology
In older children and adults
they are seperate
By the same pathophysiology
In older children and adults
they are seperate -
-
--
-
-
-
- -
&j

6. Sepsis and Meningi,s
•Systemic and local infec3ons (lung, cutaneous, ocular, umbilical, kidney, bone-
joint, and meningeal) are common in the newborn period. Infec3on may be
acquired in utero through the transplacental or transcervical routes and during or
a]er birth. Ascending infec,on through the cervix, with or without rupture of
the amnio3c Kuid membranes, may result in amnioni3s, funisi3s (infec3on of the
umbilical cord), congenital pneumonia, and sepsis.
•The bacteria responsible for ascending infec3on of the fetus are common
bacterial organisms of the maternal genitourinary tract, such as group B
streptococci, Escherichia coli, Haemophilus inLuenzae, and Klebsiella. Herpes
simplex virus (HSV)-1 or more o]en HSV-2 also causes ascending infec3on that at
3mes may be indis3nguishable from bacterial sepsis. Syphilis and Listeria
monocytogenes are acquired by transplacental infec,on.
Your Date Here Your Footer Here 11 I
-
--
I
-
S
(S.agalact.)
-
-
-
-
viral
--
&

7. •Maternal humoral immunity may protect the fetus against some neonatal
pathogens, such as group B streptococci and HSV. Nonetheless, various
deJciencies of the neonatal an3microbial defense mechanism probably are more
important than maternal immune status as a contribu3ng factor for neonatal
infec3on, especially in the low birth weight infant.
•The incidence of sepsis is approximately 1:1500 in full-term infants and 1:250 in
preterm infants. The sixfold-higher rate of sepsis in preterm infants compared
with term infants relates to the more immature immunologic systems of
preterm infants and to their prolonged periods of hospitaliza,on, which
increase risk of nosocomially acquired infec,ous diseases.
•Preterm infants before 32 weeks of gesta3onal age have not received the full
complement of maternal an3bodies (IgG), which cross the placenta by ac3ve
transport predominantly in the la/er half of the third trimester.
Your Date Here Your Footer Here 12 (p8s9i(1)
-
I
-
->
-
-
- -
↓D
I
i
gity
x
58301
-
-
-
-
-
>32
W. -
2mp/-2 antibody599--
low
birthutI mili
dieh
i
·
girantibody
&
·
viSw
-
"¥
musous-gp
5)
.
Low
birthweight
·5
%
myJ245
.
/I

8. #
Preterm
more
riskthanothertermto
develope
sapses
:
why?
1
Prolonghospitalization
-Nasocomenal
infection
2.more
immature
System
.
Jessy
.
32w
Hig Ni 32w/
·
maternality
-
.
232w
Hig/
Stigh-rises
i

9. •In addi3on, although low birth weight infants may generate IgM an3bodies, their
own IgG response to infec3on is reduced. These infants also have deJciencies of
the alternate and, to a smaller degree, the classic complement ac3va3on
pathways, which results in diminished complement- mediated opsoniza3on.
Newborn infants also show a deJcit in phagocy3c migra3on to the site of
infec3on (to the lung) and in the bone marrow reserve pool of leukocytes.
•In addi3on, in the presence of subop3mal ac3va3on of complement, neonatal
neutrophils ingest and kill bacteria less eQec3vely than adult neutrophils do.
Neutrophils from sick infants seem to have an even greater deJcit in bacterial
killing capacity compared with phagocy3c cells from normal neonates.
Your Date Here Your Footer Here 13 -
-
-
-
Ideffective)
it was gG
LBW
118
,
-
·
ineutrophil
9j
,
a)
phagocyticfunction
in

10. •Defense mechanisms against viral pathogens also may be deJcient in a newborn.
Neonatal an3body-dependent, cell-mediated immunity by the natural killer
lymphocytes is deJcient in the absence of maternal an3bodies and in the
presence of reduced interferon produc3on; reduced an3body levels occur in
premature infants and in infants born during a primary viral infec3on of the
mother, such as with enteroviruses, HSV-2, or cytomegalovirus. In addi3on,
an3body-independent cytotoxicity may be reduced in lymphocytes of newborns
•Bacterial sepsis and meningi,s oVen are linked closely in neonates. Despite this
associa3on, the incidence of meningi3s rela3ve to neonatal sepsis has been on a
steady decline. The incidence of meningi3s is approximately 1 in 20 cases of
sepsis.
Your Date Here Your Footer Here 14 -
-
- -
I
-
-
-
-
-
-
>
- ->cellmediatedimmunity(NK
bylymphocyte)
20
sapsisI
meningitis

11. maneguitis&
Sapses
S254-
&
·
is

12. •The causa,ve organisms isolated most frequently are the same as for neonatal
sepsis: group B streptococci, E. coli, and L. monocytogenes. Gram-nega3ve
organisms, such as Klebsiella and Serra3a marcescens, are more common in less
developed countries, and coagulase nega,ve staphylococci need to be
considered in very low birth weight infants.
Your Date Here Your Footer Here 15Responsible for 50% of late onset
sepsis and nosocomial infec3on
Responsible for 50% of late onset
sepsis and nosocomial infec3on s
-
90
-
-

13. ①Most
common
cause
ofSapsis
in
newborn
②Most
common cause
ofmenengaitis
innewborn
-
-
>
Group
Bstreptococcal
-
F

14. Risk Factors
•Male infants seem to be more suscep3ble to neonatal infec3on than female
infants.
•Severely premature infants are at even greater risk secondary to less eQec3ve
defense mechanisms and deJcient transfer of an3bodies from the mother to the
fetus (which occurs mostly a]er 32 weeks’ gesta3on).
•Neonates in the neonatal intensive care unit live in a hos3le environment, with
exposure to endotracheal tubes, central arterial and venous catheters, and blood
draws all predisposing to bacteremia and meningi3s.
•Gene,c factors have been implicated in the ability of bacteria to cross the blood-
brain barrier. This penetra3on has been noted for group B streptococci, E. coli,
Listeria, Citrobacter, and Streptococcus pneumoniae.
Your Date Here Your Footer Here 16 -
=-
->
-
->
-
-- 2
.
55 88
-

15. Neonatal sepsis presents during three periods
1.Early (birth to 7 days)
2.Late oonset sepsis nset sepsis (8 to 28 days)
3.Nosocomially acquired sepsis (8 days to discharge)
Your Date Here Your Footer Here 17 -55
E
>
-
-
-
->
-- -
- -

16. Early onset sepsis (Birth – 7 days)
•It oVen begins in utero and usually is a result of infec3on caused by the bacteria
in the mother’s genitourinary tract. Organisms related to this sepsis include
group B streptococci, E. coli, Klebsiella, L. monocytogenes, and nontypeable H.
inLuenzae.
•Most infected infants are premature and show nonspeci7c cardiorespiratory
signs, such as grun,ng, tachypnea, and cyanosis at birth.
•Risk factors for early-onset sepsis include vaginal coloniza3on with group B
streptococci, prolonged rupture of the membranes (>24 hours), amnioni3s,
maternal fever or leukocytosis, fetal tachycardia, and preterm birth. African-
American race and male sex are unexplained addi3onal risk factors for neonatal
sepsis.
Your Date Here Your Footer Here 18 [
1:901)
--
&
-
-
-
-
I
"I
-
-a
-
-
- >
-
->
rheumaticfeverGAS
->Sepsis
&
meningitis
->
GBS Ed ze
gis
-
-
"¥
ascendinginfection
-
ofmothertothe
baby
.
&
1
-
Tachypnea
-
+
Cynoss 12
-
2- 3-
Y S 6 F
I

17. Riskfactorsofneonatal
sepsiss
.
-
Prolongedraptureof
mambrain
.
2.
covitaminunitis
.3-
vagainalColonization
.
30%
ofsepsis
4-
maternalfever
*
5-Leuckscytosis
.
=>
menengaitis
6-
Fetaltachycardia
.
7.
Pretermbirth
,8-
male
9
African
american
.

18. •Early-onset sepsis (birth to 7 days) is an overwhelming mul3organ system disease
frequently manifested as respiratory failure, shock, meningi3s (in 30% of cases),
disseminated intravascular coagula3on, acute tubular necrosis, and symmetrical
peripheral gangrene.
•Early manifesta,ons—grun,ng, poor feeding, pallor, apnea, lethargy,
hypothermia, or an abnormal cry—may be nonspeci7c.
•Profound neutropenia, hypoxia, and hypotension may be refractory to treatment
with broad-spectrum an3bio3cs, mechanical ven3la3on, and vasopressors such
as dopamine and dobutamine. In the ini,al stages of early onset sep,cemia in a
preterm infant, it is oVen di_cult to di`eren,ate sepsis from respiratory
distress syndrome. Because of this di_culty, premature infants with respiratory
distress syndrome receive broad-spectrum an,bio,cs.
Your Date Here Your Footer Here 19Especially in pre term
Especially in pre term any infant who is not doing well you should suspect sepsis so give ab
->-
-
specfic*
- -
-
- -
> -
$
-
,
*
-
-
- Sapsis
.
S
① ② ③
=DIC
i
due
t
term

19. I
i
/
is
RDS-wil
,
Sive
-
&
RDS
8
.
Nin
-
N
-
-
Broad-Spectrumantibiotic
,
DDS
-
_
sepsis

20. Your Date Here Your Footer Here 20
CBC Jndings - Leucopenia < 5000/mm3 (with severe sepsis) - Toxic granula3ons in neutrophils. - Bandemia:
Band cells (immature) >20% of total neutrophil count. - Less commonly leucocytosis (> 30.000 / mm3) -
Thrombocytopenia S⑧
?-
affectedby
neonatalsepsis
-
-
-
- & --
-
-die
--
-
- S
>
immunesystem
distrated
can'tdeffenceagainst
infaction
.

21. •The clinical manifesta,ons of sepsis are di_cult to separate from the
manifesta,ons of meningi,s in the neonate.
•Infants with early-onset sepsis should be evaluated by blood and cerebrospinal
Luid (CSF) cultures, CSF Gram stain, cell count, and protein and glucose levels.
•Normal newborns generally have an elevated CSF protein content (100 to 150
mg/dL) and may have 25 to 30/mm3 white blood cells (mean, 9/mm3), which
are 75% lymphocytes in the absence of infec,on. Some infants with neonatal
meningi3s caused by group B streptococci do not have an elevated CSF leukocyte
count but are seen to have microorganisms in the CSF on Gram stain. In addi3on
to culture, other methods of iden3fying the pathogenic bacteria are the
determina3on of bacterial an3gen in samples of blood, urine, or CSF.
Your Date Here Your Footer Here 21 -
a
CBC
-blood&
(sfculture
x,y
-
- >
-
-
"¥
bactivial
-
- - -
--- -
high -low

22. •In cases of neonatal meningi/s, the ra/o of CSF glucose to blood glucose
usually is less than 50%. The polymerase chain reac/on test primarily is used to
iden0fy viral infec0ons. Serial complete blood counts should be performed to
iden0fy neutropenia, an increased number of immature neutrophils (bands), and
thrombocytopenia. C-reac/ve protein levels are o:en elevated in neonatal
pa0ents with bacterial sepsis.
•A chest radiograph also should be obtained to determine the presence of
pneumonia. In addi0on to the tradi0onal neonatal pathogens, pneumonia in very
low birth weight infants may be the result of acquisi0on of maternal genital
mycoplasmal agent (e.g., Ureaplasma urealy0cum or Mycoplasma hominis).
Your Date Here Your Footer Here 22 ↑
Protein
-
?
->
bglucose
->
Icells
W
- -
D
- PCR
-
-
=>
-
--
-

23. •Arterial blood gases should be monitored to detect hypoxemia and metabolic
acidosis that may be caused by hypoxia, shock, or both. Blood pressure, urine
output, and peripheral perfusion should be monitored to determine the need to
treat sep0c shock with Huids and vasopressor agents.
•The mainstay of treatment for sepsis and meningi/s is an/bio/c therapy.
•An0bio0cs are used to suppress bacterial growth, allowing the infant’s defense
mechanisms 0me to respond.
•In addi0on, support measures, such as assisted ven0la0on and cardiovascular
support, are equally important to the management of the infant.
•A combina0on of ampicillin and an aminoglycoside (usually gentamicin) for 10 to
14 days is eNec0ve treatment against most organisms responsible for early-onset
sepsis.
Your Date Here Your Footer Here 23 -
- -
- -
-
-
-
-
-
-
-
grau(t) gran()
-B - --
=
-
=>
-
-
=°
zweeks Shock
+
Hypoxia
-
>
hypoxemia
+
Acidosis
"¥
C2
"¥
PH
D ↑
-
=>
-

24. •The combina0on of ampicillin and cefotaxime also is proposed as an alterna0ve
method of treatment. If meningi/s is present, the treatment should be
extended to 21 days or 14 days a:er a nega0ve result from a CSF culture.
•Persistently posi0ve results from CSF cultures are common with neonatal
meningi0s caused by gram-nega0ve organisms, even with appropriate an0bio0c
treatment, and may be present for 2 to 3 days aHer an/bio/c therapy.
•If gram-nega/ve meningi/s is present, some authori0es con0nue to treat with
an eNec0ve penicillin deriva0ve combined with an aminoglycoside, whereas most
change to a third-genera0on cephalosporin.
•High-dose penicillin (250,000 to 450,000 U/kg/24 hr) is appropriate for group B
streptococcal meningi0s.
Your Date Here Your Footer Here 24 Sepsis
-
weeks
meningitis
-
3weeks
->
asst
&
3weeks
&
5,5 &ass
culture
+
(contain
bactrial

25. •Inhaled nitric oxide, extracorporeal membrane oxygena5on (in term infants), or
both, may improve the outcome of sepsis-related pulmonary hypertension.
Intratracheal surfactant may reverse respiratory failure.
•Intrapartum penicillin empirical prophylaxis for group B streptococcal colonized
mothers or mothers with risk factors (fever, preterm labor, previous infant with
group B streptococci, and amnioni>s) has reduced the rate of early-onset
infec>on.
Your Date Here Your Footer Here 25RDS
Early onset sepsis
Pulmonary Hg
RDS
Early onset sepsis
Pulmonary Hg -
-I
-
VD
y
-
-
- -
-
-
- S
prophylaxis
↑
&
Panicillin
52/
3281s)

26. Late-onset sepsis (8 to 28 days)
•It usually occurs in a healthy full-term infant who was discharged in good health
from the normal newborn nursery.
•Clinical manifesta>ons may include lethargy, poor feeding, hypotonia, apathy,
seizures, bulging fontanelle, fever, and direct-reac>ng hyperbilirubinemia.
•In addi5on to bacteremia, hematogenous seeding may result in focal infec>ons,
such as meningi5s
•(in 75% of cases), osteomyeli5s (group B streptococci, Staphylococcus aureus),
arthri5s (gonococcus, S. aureus, Candida albicans, gram-nega5ve bacteria), and
urinary tract infec5on (gram-nega5ve bacteria).
Your Date Here Your Footer Here 26X- ray is non beneNcial because changes
are visible 7-10 days aRer onset
X- ray is non beneNcial because changes
are visible 7-10 days aRer onset يعني اكو انفكشن بادية بمكان وهي مسو ي ة sepsisI
-
1-
-
&
direct
&
>
S
indirect156
-
61-8E
-
bisigi
S
hyperbil.
-
-I
A-
-
-
Gibs<
I
fculture
S
- -
99,
186
-

27. Sepsis-
Direct indirect
Hyperbelirobenemia
-75-
of
Lateoncetsepsis
=
menergaitis
.=
mandetary
cs)
culture
+
Stain

28. •The evalua>on of infants with late-onset sepsis is similar to that for infants with
early-onset sepsis, with special aJen>on given to a careful physical examina5on
of the bones (infants with osteomyeli5s may exhibit pseudoparalysis) and to the
laboratory examina5on and culture of urine obtained by sterile suprapubic
aspira>on or urethral catheteriza>on.
•Late-onset sepsis may be caused by the same pathogens as early-onset sepsis,
but infants exhibi5ng sepsis late in the neonatal period also may have infec5ons
caused by the pathogens usually found in older infants (H. inSuenzae, S.
pneumoniae, and Neisseria meningi5dis). In addi5on, viral agents (HSV,
cytomegalovirus, or enteroviruses) may manifest with a late-onset, sepsis-like
picture.
Your Date Here Your Footer Here 27Not clean catch midstream urine
Not clean catch midstream urineCSF culture is mandatory here
CSF culture is mandatory here •CSF culture is mandatory
•physical examination to determine the site of focal infection
I
-- -
>-
- -
911
-
-1
- -
fections
-
in
-
-
-
-
&
-
-
-
-
-
X
T
- =>>

29. •Because of the increased rate of resistance of H. inLuenza and pneumococcus
to ampicillin, some centers begin treatment with ampicillin and a third-
genera>on cephalosporin (and vancomycin if meningi>s is present) when sepsis
occurs in the last week of the Mrst month of life.
•The treatment of late-onset neonatal sepsis and meningi5s is the same as that for
early-onset sepsis.
Your Date Here Your Footer Here 28 ase
n.
meningitis
->
ampicillin
&
3rd
cephalo.
I
vancomycin
-
if
no
meningitis
-->
-"
t
-
-
-
-
-> -
-
-

30. Nosocomially acquired sepsis (8 days to discharge)
•It occurs predominantly in premature infants in the neonatal intensive care unit;
many of these infants have been colonized with the mul5drug-resistant bacteria
indigenous to the neonatal intensive care unit. The risk of such serious bacterial
infec>on is increased by frequent treatment with broad-spectrum an>bio>cs
for sepsis and by the presence of central venous indwelling catheters,
endotracheal tubes, umbilical vessel catheters, and electronic monitoring
devices.
•Epidemics of bacterial (coagulase-nega5ve staphylococci, fungi, enteric bacteria)
or viral sepsis, bacterial or asep5c meningi5s, staphylococcal bullous skin
infec5ons, celluli5s, pneumonia (bacterial or caused by adenovirus or respiratory
syncy5al virus), omphali5s (caused by S. aureus or gram-nega5ve bacilli), and
diarrhea (staphylococcal, enteroviral, or caused by rotavirus or enteropathogenic
E. coli) are common in the neonatal intensive care unit and in the nursery for well
infants.
Your Date Here Your Footer Here 29Sepsis Tx is 10-14 days
Meningi5s Tx is for 21 days
Sepsis Tx is 10-14 days
Meningi5s Tx is for 21 days -
-
>
-> - resistantbactria
50

31. •The ini5al clinical manifesta>ons of nosocomial infec5on in a premature infant
may be subtle and include apnea and bradycardia, temperature instability,
abdominal disten>on, and poor feeding. In the later stages, signs of infec5on
are shock, disseminated intravascular coagula>on, worsening respiratory status,
and local reac>ons, such as omphali>s, eye discharge, diarrhea, and bullous
impe>go.
•The treatment of nosocomially acquired sepsis depends on the indigenous
microbiologic Sora of the par5cular hospital and the an5bio5c sensi5vi5es.
Because S. aureus (occasionally methicillin-resistant), Staphylococcus epidermidis
(methicillin-resistant), and gram-nega5ve pathogens are common nosocomial
bacterial agents in many nurseries, a combina5on of vancomycin or
oxacillin/nafcillin (some use ampicillin) with an aminoglycoside (gentamicin or
tobramycin) is appropriate
Your Date Here Your Footer Here 30 دائما الpremature يصي ر ل ه non specific
symptoms -ن هن هذني اليعرف يسويهن
(nonSpecific)
mostlyhypothermia
>
-
- ->
-
-
-
-
"¥
grau. ①
-

32. •The dose and interval for administering all aminoglycosides, such as gentamicin,
vary with postnatal age and birth weight. In addi5on, treatment with
aminoglycosides for more than 3 days necessitates monitoring of the serum
peak and trough concentra5ons to op5mize therapy and to avoid ototoxicity and
nephrotoxicity.
•Persistent signs of infec>on despite an>bacterial treatment suggest candidal or
viral sepsis.
Your Date Here Your Footer Here 31 -
- -
=

33. DiUeren>al Diagnosis
•Other causes of cri5cally ill neonate: THE MIS FITS
•T: Trauma e.g. intracranial hemorrhage
•H: Heart disease e.g. congenital ,hypoxic, hypovolemic
•E: Endocrine e.g. congenital adrenal hyperplasia
•M: Metabolic disturbances e.g. hypoglycemia , hypocalcemia
•I: Inborn errors of metabolism
•S: Sepsis
•F: Fits(seizures)
•I: Intes5nal catastrophes e.g. intes5nal obstruc5on, NEC
•T: Toxins
•S: Severe asphyxia
Your Date Here Your Footer Here 32 55,
b
-
-
-
-
-
-
-
-

34. Principles for the Preven>on of Nosocomial
Infec>on in the Neonatal Intensive Care Unit:
•Observe recommenda>ons for universal precau>ons with all pa>ent contact:
1.Gloves
2.Gowns, mask, and isola>on as indicated
3.Nursery design engineering:
•Appropriate nursing: pa>ent ra>o
4.Avoid overcrowding and excessive workload
5.Readily accessible sinks, an>sep>c solu>ons, soap, and paper towels
6.Handwashing:
•Improve handwashing compliance
•Wash hands before and a`er each pa>ent encounter
Your Date Here Your Footer Here 33 **-

35. •Appropriate use of soap, alcohol-based prepara>ons, or an>sep>c solu>ons
•Alcohol-based an>sep>c solu>on at each pa>ent bedside
•Provide emollients for nursery staU
7.Educa>on and feedback for nursery staU
8.Minimizing risk of CVC contamina>on:
•Maximal sterile barrier precau>ons during CVC inser>on
•Local an>sepsis with chlorhexidine gluconate
•Minimize repeated entry into the line for laboratory tests
•Asep>c technique when entering the line
Your Date Here Your Footer Here 34

36. •Minimize CVC days
•Sterile prepara>on of all Luids to be administered via a CVC
9.Me>culous skin care
10.Encourage early and appropriate advancement of enteral feeding
11.Educa>on and feedback for nursery personnel
12.Con>nuous monitoring and surveillance of nosocomial infec>on rates in the
Neonatal intensive care unit
Your Date Here Your Footer Here 35

37. Your Date Here Your Footer Here 36To minimize the risk of neonatal GBS disease, 2010 guidelines from the Centers for
Disease Control and Preven>on and the American Academy of Pediatrics
recommend maternal intrapartum chemoprophylaxis in the following scenarios:
• A woman with GBS bacteriuria during current pregnancy
• A woman with prior infant with invasive GBS disease, regardless of current GBS
status
• A woman with unknown GBS status and any of the following:
• Preterm labor
• Dura>on of membrane rupture for 18 hours or longer
• Intrapartum temperature ≥ 38°C (100.4°F)
To minimize the risk of neonatal GBS disease, 2010 guidelines from the Centers for
Disease Control and Preven>on and the American Academy of Pediatrics
recommend maternal intrapartum chemoprophylaxis in the following scenarios:
• A woman with GBS bacteriuria during current pregnancy
• A woman with prior infant with invasive GBS disease, regardless of current GBS
status
• A woman with unknown GBS status and any of the following:
• Preterm labor
• Dura>on of membrane rupture for 18 hours or longer
• Intrapartum temperature ≥ 38°C (100.4°F) *
-
->
- -
>
-S
-
-
-- -
X
je9'
"¥
"¥
0
-
->>
"¥
-8
--