Neonatal Sepsis

Sehyeon Kim, RN
Kcoc3.medipeace@gmail.com
Medipeace Tanzania team
 Index
Neonates
• Immunity
• Neonatal Immunity
Neonatal Sepsis
• Definition
• Pathophysiology
• Clinical symptoms
• Treatment
• Prevention
Status Analysis

Q&A

Reference
 Immunity
 Overview of the immune system

 Our immune system protects us against viruses, bacteria and parasites

which can cause infectious disease.

 The immune system responds to antigens. An antigen is a substance

that stimulates a specific immune response, especially the production of
antibodies. Basically this involves shape recognition.

 Infectious agents such as viruses and bacteria have unique antigens that
the immune system responds to.
 Immunity
 Types of Immunity

Specific Non-
of specific
adaptive immunity
immunity

Innate
immunity
Immunity
Non-specific immunity
•The first line of defense and generally keeps infectious from entering the
body
•Ex) Skin(physical barrier), mucus, tears, stomach acid

Innate immunity
•The second line of defense
•Certain white cells engulf infectious agents
•They can recognize antigens, but cannot recognize particular pathogens
•Over 90% of infections are controlled by these cells

Specific or adaptive immunity

•The third line of defense
•Lymphocytes(WBC) identify each antigen individually
•This specific response initially takes long to generate (4-7Days) but
results in a memory to the specific antigen
•When an individual is re-infected with the pathogen, this memory
response will remove the infectious agent before it cause disease.
•Ex) Vaccination
Immunity
 Innate immunity

WBC like macrophages and neutrophils,

eat bacteria and damaged cells
 Also kill bacteria through the release of
inflammatory molecules

 Specific immunity

 B lymphocytes (B cells)
; produce antibodies(Ig) which can
neutralize viruses, bacteria or toxic
proteins

 T cells
; develop into killer cells
; prevents the spread of the micro
organism within the body
Neonatal Immunity

Q: What is different about the infant immune system?

Naive

Immature
Neonatal Immunity

 The infants’ immune system is intact but

immature at birth.

Placental The main problem is that it is very naive.

transfer
of IgG ;At the time of birth babies have not been exposed
to any pathogens. This means that babies have to
generate a full immune response to every pathogen
Breast
milk they encounter. (감염 국소화 능력 부족 -> 전신적 반응)

 Each immune response takes about 10 days to

generate. This is where maternal antibody can be
important when present. It will help to protect an
infant if they are exposed to a pathogen in those
Maternal Antibodies
first 10 days.
Definition
 Neonatal sepsis is defined as a clinical syndrome of bacteremia with
systemic signs and symptoms of infection in the first 4 weeks of life.

 When pathogenic bacteria gain access into the blood stream, they may
cause overwhelming infection without much localization (septicemia) or
may get predominantly localized to the lung (pneumonia) or the
meninges (meningitis).

Acquisition of
Early onset microorganisms from
the mother
Neonatal 72
sepsis
Acquired from the
Late onset caregiving
environment
 Pathophysiology
Infection Congenital Infection Neonatal Infection

Timing of
In utero Membrane rupture–day28
transmission

Ascending
Root of infection External
Transplacental Breast milk
transmission from birth environment
canal

Time of Intra or Shortly Month-years

Ante, Intra or immediately after
clinical shortly postpartum –
postpartum delivery
presentation postpartum day 28

Viridans
Toxoplasmosis, Viridans streptococci, Staphylococcus
Common Rubella, CMV, streptococci, Hepatitis B, C,
S agalactiae, aureus, E coli,
pathogens Herpes, HIV
S agalactiae E Coli, Klebsiella spp
Syphilis
Klebsiella spp

Physical or Fetal distress, Liver disease,

Clinical Neonatal sepsis Neonatal sepsis
neurological neonatal sepsis immune-
syndrome syndrome syndrome
abnormalities syndrome deficiency
Pathophysiology
Distal risk factors

• poverty
• poor environment conditions

Proximate risk factors

• prolonged rupture of membranes

• preterm labor
• maternal pyrexia (high fever)
• unhygienic intrapartum/postnatal care
• low birth weight
• prelacteal feeding of contaminated foods and
fluids
Pathophysiology
 The bacteria that cause neonatal sepsis are acquired shortly before,
during, and after delivery.

 They can be obtained directly from mother’s blood, skin, or vaginal tract
before or during delivery or from the environment during and after
delivery.

 Streptococcus agalactiae (Group B streptococcus, GBS)

 Gram-negative bacilli
; E coli, Klebsiella spp, Pseudomonas spp, Acinetobacter spp

 Gram-positive cocci
; Staphylococcus aureus, Staphylococcus epidermidis
 Clinical Symptoms
 General  Cardiovascular system/Respiratory
-Low APGAR - Apnea
-Temperature instability -Tachypnea
-Bulging or sunken fontanels -Labored breathing
-Rash -Pallor or cyanosis
- Axillary temperature ≥37.5 -Bradycardia or Tachycardia
-Axillary temperature <35.5 -Hypotension
-Severe chest indrawing
 Central Nerve System
-Lethargy  Gastrointestinal
-Irritability -Poor feeding
-Focal neurological signs -Vomiting
-Seizure -Diarrhea
-constipation
 Metabolic -bloody stool
-Jaundice
-Hypoglycemia/Hyperglycemia  Urological
-Metabolic acidosis -Decreased urine output
Treatment

Algorithm for secondary prevention of early onset GBS disease among newborns (2010 CDC Guideline)
Treatment
Antibiotic Therapy
• should be directed toward the most common causes of neonatal sepsis
• IV ampicillin for GBS and coverage for other organisms (including E col
i and other gram-negative pathogens)
• Early onset : Ampicillin+Gentamicin
• Late onset : Cefotaxime+Aminoglycoside
Diagnostic evaluation
• Blood culture
• CBC count
• CSF analysis (Optional)
• Chest X-ray/CT

Routine clinical care

• Monitoring Vital signs : BP, RR, HR, BT
• Diet
• Monitoring intake/output

Observation
Prevention
Things that we can control

Maternal risk Neonate risk

factors factors

• Prolonged rupture of • Prematurity or low

membranes birth weight neonate
(ROM>18hrs prior to care
delivery) • Care for congenital
• Untreated bacteriuria anomaly that disrupts
during pregnancy skin
• Poor prenatal care • Care for birth asphyxia
• GBS colonization • Invasive procedures
• Intrapartum infection
 Prevention
Vaginal and rectal GBS screening cultures at 35-37 weeks' gestation for ALL
pregnant women (unless patient had GBS bacteriuria during the current
pregnancy or a previous infant with invasive GBS disease)

Intrapartum prophylaxis Intrapartum prophylaxis

indicated
• Previous infant with invasive GBS di
sease
• GBS bacteriuria during current preg
nancy
• Positive GBS screening culture durin
g current pregnancy
• Unknown GBS status (culture not do
ne, incomplete, or results unknown
) and any of the following:
• Delivery at<37weeks' gestation
• Amniotic membrane rupture≥18hrs
• Intrapartum temperature≥38.0℃
not indicated
• Previous pregnancy with a positive
GBS screening culture (unless a cult
ure was also positive during the cur
rent pregnancy)
• Planned C/S performed in the abse
nce of labor or membrane rupture
• Negative vaginal and rectal GBS scr
eening culture in late gestation dur
ing the current pregnancy, regardle
ss of intrapartum risk factors
Prevention

 If ≥37weeks gestation, observation may occur at home after

24hrs if other discharge criteria have been met

 There is ready access to medical care

 A person who is able to comply fully with instructions for home

observation will be present

* If any of these conditions is not met,

the infant should be observed in the hospital for at least 48hrs
and until discharge criteria have been achieved *
Status Analysis
2013 Tanzania
Deaths of newborns(first month of life) due to
(percentage):

Diarrheoea Pneumonia
0.2% 4.9%
Other
5.7%

Congenital
Tetanus 13.8% Preterm
0.9% 24.3%

Sepsis
19.3%

Intrapartum
30.8%

Deaths of newborns(first month of life) due to(%)

Status Analysis
Under-five mortality rate (probability Infant mortality rate (probability of dying
of dying by age 5 per 1000 live births) between birth and age 1 per 1000 live
births)
140
85

90 57

61 41
52 36

1999 2005 2010 2013 1999 2005 2010 2013

Neonatal mortality rate (per 1000 live births)

38

29
23
21

1999 2005 2010 2013

Status Analysis
Use of improved drinking Use of sanitation
water sources(%), 2011 facilities(%), 2011

Rural 44.1 Rural 7.4

Urban 78.7 Urban 24.2

Total 53.3
Total 11.9
Status Analysis
Antenatal care coverage: at Skilled Attendance at
least four visits(%) birth(%), 2010

70
Rural 40
62

43
Urban 83

Total 49

1999 2004-2005 2010

Status Analysis
 5세 미만 아동사망률 및 영아사망률은 큰 폭 감소하였으나 그 중 신생아
사망률이 차지하는 비율은 오히려 증가하였음

 깨끗한 생활용수 공급은 도시 기준 78.7%로 높은 수준이나 탄자니아 전

체 기준 53%에 불과함

 위생시설의 경우 도시 기준 24.2%, 탄자니아 전체 기준 11.9%로 감염예

방 및 가정 내 위생관리와 관련하여 시설 확충이 시급

 4회 이상 산전관리 비율은 오히려 과거보다 감소하였으며 산전관리 횟

수 뿐만 아니라 의료서비스의 질에도 관심을 가져야 함

 도시의 경우 숙련된 전문가의 분만 참여율이 높은 편이나 탄자니아 국가

전체 기준 49%에 불과하며 전문가의 분만 참여율 뿐만 아니라 의료진의 역
량 및 분만과정에 대해서도 평가되어야 함
Reference
1. New Approaches to Preventing, Diagnosing, and Treating Neonatal Sepsis.
Karen Edmond, Anita Zaidi. (Mar, 2010)

2. The infant immune system and immunisation. The university of Auckland

Faculty of Medical and Health Sciences. (Sep, 2006)

3. Clinical Use of 2010 CDC Guidelines to Prevent Early Onset Group B

Streptococcal Sepsis in Neonates. Karen Bockli, MD, Joseph Hageman, MD,
William Mackendrick, MD, AND Michael Caplan, MD. (2010)

4. NICE clinical guideline: antibiotics for the prevention and treatment of early-
onset neonatal infection. Emma Caffrey Osvald, Philippa Prentice. (Feb, 2015)

5. Neonatal Sepsis: pathogenesis and overview of clinical findings. Nick

Baldwin.(June, 2013)

6. Neonatal Sepsis. Ann L Anderson-Berry, Medical Director, NICU, Nebraska

Medical Center. (Feb, 2014)

7. www.who.org

8. www.unicef.org
ASANTE SANA