Neonatal sepsis

Dr.Shireen N. Abed
Board certified in Pediatrics
Palestinian board, Egyptian fellowship
 Objectives

 Definitions
 Etiology
 Clinical manifestations
 Diagnosis
 Differential diagnosis
 Management
 Neonatal meningitis
 Definitions

 Systemic inflammatory response syndrome

(SIRS)
 Sepsis
 Severe sepsis
 Septic shock
 Multisystem organ failure (MSOF)
 SIRS
 Systemic inflammatory response to a variety of
clinical insults,
 manifested by 2 out of 4 criteria, 1 of which must be
abnormal temperature or abnormal leukocyte count:
1) Temperature instability (Core temperature<36 or
>38.5 degree)
2) Tachypnea >2SD above the mean for age
3) HR >2SD above the mean for age
4) Leukocyte count elevated or depressed for age or
>10% immature neutrophils
 Sepsis: SIRS plus suspected or proven evidence of
infection.

 severe sepsis: sepsis combined with organ

dysfunction

 septic shock: severe sepsis plus the persistence of

hypoperfusion or hypotension for >1 hr despite
adequate fluid resuscitation or a requirement for
inotropic agents or vasopressors

 MSOF: Presence of altered organ function such that

homeostasis cannot be maintained without medical
intervention
 HOW CAN BACTERIA
REACH THE FETUS OR
?NEWBORN
1- Maternal blood stream infections: Listeria monocytogenes
and Mycobacterium tuberculosis

2- Bacteria can be acquired from the vagina, cervix, or fecal

contamination of the birth canal through either ruptured or
intact membranes: GBS

3- aspiration of birth canal contents or colonization of mucosal

surfaces during passage through the birth canal, leading to
pneumonia, followed by bacteremia and sepsis after 1 day
or later :Neisseria gonorrhoeae, Escherichia coli, and GBS
 Risk factors of early-onset sepsis

 Prematurity,
 young maternal age,
 prolonged labor,
 prolonged rupture of membranes (≥18 hours),
 internal scalp fetal monitoring,
 urinary tract infections,
 bacterial vaginosis
 Etiologic causes

 Bacteria : gram positive/negative

 Viruses
 Fungi
 Mycoplasma
 protozoa
Bacterial causes  GRAM NEGATIVE
 Bacteroides
 Campylobacter
 GRAM POSITIVE  Citrobacter
 Clostridia  Enterobacter
 Enterococci  Escherichia coli
 Group B streptococcus  Haemophilus influenzae
 Listeria monocytogenes  Klebsiella
 Other streptococci  Neisseria gonorrhoeae
 Staphylococcus aureus  Neisseria meningitidis
 Staphylococcus, coagulase-  Proteus
negative  Pseudomonas
 Streptococcus pneumoniae  Salmonella
 Viridans streptococcus  Serratia

 OTHERS
 Treponema pallidum
 Mycobacterium tuberculosis
 Viruses
 Adenovirus
 Cytomegalovirus
 Enteroviruses
 Parechoviruses
 Hepatitis B virus
 Herpes simplex virus
 Human immunodeficiency virus
 Parvovirus
 Rubella virus
 Varicella-zoster virus
 Others
MYCOPLASMA  
 M .hominis
 Ureaplasma urealyticum

FUNGI
 Candida species
  Malasseziaspecies

PROTOZA  
 Plasmodia
  Toxoplasma gondii
  Trypanosoma cruzi
Sepsis by age of onset
 Clinical manifestations
 General :  GIT:
 Fever, temperature  Abdominal distention
 Vomiting
instability
 Diarrhea
 “Not doing well”
 Poor feeding
Renal: oliguria

Respiratory:
 Tachypnea, retractions
 Flaring, grunting
 Cyanosis
CVS: HEMATOLOGIC:
 Pallor; mottling; cold, clammy skin
 Tachycardia  Jaundice
 Hypotension  Pallor
 Bradycardia
 Petechiae, purpura
CNS:  Bleeding
 Irritability, lethargy
 Tremors, seizures
 Hyporeflexia, hypotonia
 Abnormal Moro reflex
 Irregular respirations
 Full fontanel
 High-pitched cry
 Evaluation
HISTORY (SPECIFIC RISK FACTORS)  
 Maternal infection during gestation or at parturition (type and duration of
antimicrobial therapy):  Urinary tract infection
  Chorioamnionitis
 Gestational age/birthweight
 Multiple birth
 Duration of membrane rupture
 Complicated delivery
 Fetal tachycardia (distress)
  Age at onset (in utero, birth, early postnatal, late)
 Location at onset (hospital, community)
 Medical intervention:  Vascular access,  Endotracheal intubation, Parenteral
nutrition
 Surgery
 EVALUATION

EVIDENCE OF OTHER DISEASES: Congenital

malformations

EVIDENCE OF FOCAL OR SYSTEMIC DISEASE  

 appearance,
 neurologic status
 Abnormal vital signs
 Organ system disease
 Feeding, stools, urine output,
 extremity movement
 Laboratory studies

Evidence  of Infection 

 culture from a normally sterile site (blood, CSF, urine)
 Demonstration of a microorganism in tissue or fluid

Evidence of Inflammation  
 Leukocytosis, increased immature/total neutrophil
count ratio
 Acute-phase reactants: C-reactive protein, erythrocyte
sedimentation rate
  
Evidence of Multiorgan System
Disease  function:
 ABG
 Renal function
 Hepatic injury/function: LFT
 Bone marrow function: neutropenia, anemia,
thrombocytopenia
 Differential diagnosis
 CARDIAC : CHD 

 GASTROINTESTINAL  : NEC

 HEMATOLOGIC:  Neonatal purpura
fulminans. Immune-mediated thrombocytopenia,
Immune-mediated. Neutropenia.Severe anemia
Malignancies (congenital leukemia)
Hereditary clotting disorders
 Differential diagnosis
 METABOLIC:  Hypoglycemia, Adrenal disorders

 Inborn errors of metabolism

 NEUROLOGIC:  Intracranial hemorrhage:
  Hypoxic-ischemic encephalopathy
  Neonatal seizures
  
 RESPIRATORY:  Respiratory distress syndrome
  Aspiration pneumonia, TTN
  
Prophylaxis
Prophylaxis
Prophylaxis
 Treatment
 Empiric therapy for early-onset sepsis generally consists of
combinations of antibiotics effective against grampositive
and gram-negative

 The two most commonly used combinations are

(1) ampicillin with an aminoglycoside,usually gentamicin,
(2) ampicillin with a third-generation

 Therapy for most bloodstream infections should be

continued for a total of 7-10 days, or for at least 5-7 days
after a clinical response has occurred.
NEONATAL BACTERIAL
MENINGITIS
 ETIOLOGY

 GBS and E. coli accounting for approximately

70% of all cases,
 L. monocytogenes accounting for an additional
5% in the first week of life.
 Streptococcus pneumoniae and Haemophilus
influenzae,
 in infants who are older than 1 week residing
in NICU, coagulase-negative staphylococci are
the most common isolates.
 Clinical manifestations

 The signs and symptoms of neonatal

meningitis are not easy to distinguish from
those of sepsis.
 The most common presenting symptoms are
lethargy, feeding problems, instability of
temperature regulation, vomiting, respiratory
distress, and apnea.
 A bulging fontanel (late)
 Seizures.
 Diagnosis
 The gold standard for diagnosis of meningitis is the
analysis of the cerebrospinal fluid, including the WBC
count,glucose and protein levels, Gram stain, and culture.

 1% to 10% of infants with proven meningitis have

normal results of CSF .

 Other investigations (like in sepsis)

 20-30% of infants with meningitis have negative blood
cultures
 Treatment
 In many intensive care units, ampicillin and
gentamicin are recommended for the initial
therapy for neonatal meningitis.
 An alternative regimen of ampicillin and
cefotaxime

 In general, continue therapy for 2 weeks after

sterilization of the cerebrospinal fluid, or a
minimum of 2 weeks for gram-positive and a
minimum of 3 weeks for gram-negative meningitis.
 Complications of neonatal
meningitis
 Early: electrolyte imbalance, seizures
 Brain abscess,
 communicating or noncommunicating
hydrocephalus,
 subdural effusions, ventriculitis, deafness, and
blindness
 Follow up

 Infants who survive neonatal meningitis

should have regular audiology, language, and
neurologic evaluations until they enter school

(Edwards et al, 1985;Stevens et al, 2003).

 Prognosis
 Approximately 40% to 50% of survivors have some
evidence of neurologic damage, with severe damage
being obvious in 11%.

 GBS meningitis has a mortality approaching 30%

and a morbidity of 50%

 Mortality rates for neonatal E. coli meningitis

vary from 20% to 30% in some centers and 50% to
60% in others.
 Conclusion

 Definitions
 Etiology
 Clinical manifestations
 Diagnosis
 Differential diagnosis
 Management
 Neonatal meningitis
Thank you