Download NEONATAL CONSIDERATIONS Part 1

1. Neonatal Infections
DR. MAHMOUD MOHAMED OSMAN
MBBCh, MSc (Pedia), MRCPCH (UK), FRCP (Edinburgh)
Consultant Pediatrician & Neonatologist
Al Yammamah Hospital , MOH
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Learning Objectives:
1. Definition of Neonatal sepsis
2. Early-onset infections
3. Late-onset infections
4. Clinical Presentations
5. Investigations for Neonatal sepsis
6. Management of Neonatal sepsis
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I- Neonatal Infections
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1. Definition of Neonatal Sepsis:
It is a clinical syndrome of systemic
illness accompanied by bacteremia or
septicemia occurring in the first month of
life.
2. Clinical Situations :
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Early- Onset Disease
Late - Onset Disease
Very late - Onset Disease
 Infection can present in many different ways and may
involve almost any system in the body.
 Infection must be considered in almost every differential
diagnosis of any condition.
 Infection poses a significant risk of mortality and is
associated with major morbidity.
3- Incidence:
 The incidence of infection is approximately
. 5 /1000 live births.
 It is more common in premature infants;
. 13-27/1000 for infants weighing <1500 gm.
 Mortality rate is high (13-25%); and higher rates
are seen in premature infants and in those with
early fulminant disease
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Early-onset
(Perinatal) Infection
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1- INTRODUCTION:
 Neonatal infections were originally divided arbitrarily
into infections occurring before and after 1 wk of life.
 It is more useful to separate early-onset and late-onset
infections according to peripartum pathogenesis.
 Early-onset infections are acquired before or during
delivery (vertical mother-to-child transmission).
 Late-onset infections develop after delivery from
organisms acquired in the hospital or the community.
 Very-late-onset infections develop after 1 month of
life in VLBW preterm or term infants requiring
prolonged intensive care.
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 The age at onset depends on the timing of
exposure and virulence of the organism.
 A newborn infant with early-onset infection
may be initially asymptomatic or has any of
the clinical signs and symptoms of infection.
2. RISK FACTORS:
 The presence of a number of maternal and
neonatal risk factors significantly increases
the risk of infection in the newborn period.
A - Maternal risk factors for early-onset infection:
• Maternal features of sepsis or chorioamnionitis:
Fever ≥38°C,
High white cell count,
Tender uterus,
Offensive or purulent liquor
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Preterm labour <37 weeks’ gestation
Membranes ruptured for more than 18–24 hs
Prolonged labour beyond 12 hs
Frequent vaginal examinations
Group B streptococcus (GBS) colonization
Bacteriuria in current pregnancy
Previous infant with early-onset GBS disease
• Amniotic fluid problems.
Meconium-stained or foul-smelling amniotic fluid.
B - Neonatal risk factors for early-onset infection:
Prematurity and low birth weight
Resuscitation at birth.
Infants who had fetal distress, were born by traumatic
delivery or were severely depressed at birth and required
intubation and resuscitation.
Invasive procedures.
Invasive monitoring and respiratory or metabolic support.
Other factors.
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Males are 4 times more affected than females.
More common in black than in white infants.
Variations in immune function may play a role.
NICU staff and family members are often vectors for the spread
of microorganisms, as a result of improper hand washing
3.Clinical Presentation:
 Initial diagnosis of sepsis is, by necessity, a clinical
one because it is imperative to begin treatment
before the results of cultures are available.
 Clinical Presentation of sepsis are nonspecific, and
the differential diagnosis is broad.
 Common Clinical Presentation of sepsis include:
Temperature irregularity.
Hypo- or hyperthermia.
2. Change in behavior.
Lethargy, irritability, crying or change in tone.
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Skin.
Poor peripheral perfusion, cyanosis, mottling, pallor,
petechiae, rashes, sclerema, or jaundice.
Feeding problems.
Feeding intolerance, vomiting, diarrhea (watery loose
stool), or abdominal distention with or without visible
bowel loops.
Cardiopulmonary.
Tachypnea, respiratory distress (grunting, flaring, and
retractions), apnea , tachycardia, or hypotension,
which tends to be late sign.
Metabolic.
Hypo- or hyperglycemia or metabolic acidosis.
Summary of Clinical signs of neonatal sepsis
4. Differential Diagnosis
1. Respiratory distress syndrome (RDS)
2. Metabolic diseases
3. Hematologic disease
4. CNS disease
5. Cardiac disease
6. Other infectious processes
(TORCH infections)
5- Investigations:
1.
A blood culture (>1mL):
Should be collected before antibiotics commenced.
2.
A complete blood count (CBC):
Abnormal findings can include:
Increased white cell count or neutropenia,
Increased numbers of immature neutrophils
( Bands, blasts, myelocytes, metamyelocytes, [shift to the left] )
Increased immature : mature/ total neutrophil ratios.
Toxic granulation, vacuolation, Dohle bodies, intracellular
organisms
Thrombocytopenia.
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Mature neutrophil
Band cell
Toxic granulation
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3. An elevated C-reactive protein (CRP):
May be a marker of infection.
4. Lumbar puncture:
Should be considered and is essential if
the blood culture becomes positive or if the
baby has signs or symptoms of meningitis.
5. Imaging studies:
X-rays, US, CT, or isotopic imaging.
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6 - COMMENEST AGENTS IN EARLY-ONSET:
1- Group B β-haemolytic streptococcus
2- Escherichia coli
3- Listeria monocytogenes
4- Herpes simplex virus (HSV)
5- Chlamydia trachomatis
6- Other agents
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1-Early-onset group B β-haemolytic streptococcus:
• Group B β-haemolytic streptococcus (GBS) is the
most common cause of early-onset sepsis.
• Although the prognosis has improved, it is still fatal in
10–20% of cases depending on gestational age and
age of onset.
• Vaginal or rectal colonization with GBS is found in
15–30% of pregnant women depending on the local
population, and 10–20% of infants born to colonized
women will be colonized.
• Early-onset GBS infection in the neonate
occurs in only 1% of colonized women.
• In areas that are known to have high rates of
colonization (e.g. USA), routine screening for
GBS in pregnancy is often undertaken.
• Intrapartum antibiotics prophylaxis for women
with risk factors significantly reduces the risk
of early-onset infection, but does not
eliminate it.
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Early neonatal sepsis with multi-organs failure
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2- Escherichia coli
 E.coli (particularly K1 strain), is associated with
perinatal infection.
 E.coli may cause septicemia or meningitis.
 The incidence of E.coli infection appears
to be increasing, due to the increasing use of
antibiotics aimed at preventing GBS.
 The sensitivity of E.coli to antibiotics is variable.
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3- Listeria monocytogenes
• This is a not uncommon perinatal pathogen and
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may invade the fetus through intact membranes.
Characteristically, infected infants pass meconium
in utero, and if this is seen in premature infants
listeria should be strongly suspected.
The organism has a predilection for the lungs and
brain.
Hydrocephalus is a common sequel to listeria
meningitis.
The organism is usually sensitive to Ampicillin.
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4- Herpes simplex virus (HSV)
• Neonatal herpes simplex infection is a rare but
devastating condition. It occurs as a result of HSV type
1 and 2 in equal proportion.
• In most babies with neonatal HSV, there is no history
of genital herpes and their mothers are asymptomatic
• Caesarean section reduces the risk of infection if there
is active maternal shedding of HSV.
• The virus enters the baby through skin, eye or mouth
and may disseminate to the brain or other organs.
• The risk of an infant being infected from a parent, nurse
or midwife with cold sores is small, but not negligible.
Neonatal HSV presents in one of three ways:
• Systemic symptoms.
In the first few days of life with signs of major overwhelming illness including shock, respiratory failure and
often severe hepatitis and coagulation disorders.
• Neurological symptoms.
Approximately one third of babies present with
encephalopathic signs of meningoencephalitis, most
commonly at 10–14 days.
• Cutaneous symptoms.
Include rash and keratoconjunctivitis. These babies
present in the second week of life; and rarely become
seriously ill.
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5- Chlamydia trachomatis
• Chlamydia is found in the vagina of 4% of pregnant
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women.
Up to 70% of infants born through an infected cervix
will acquire chlamydia, but with no symptoms.
Chlamydia conjunctivitis and, less commonly,
pneumonia occur in a small proportion of infants.
The conjunctivitis is purulent and is indistinguishable
from that of gonococcal ophthalmia.
Specific culture media are necessary for this organism
Diagnosis can be made by detecting DNA with PCR.
Infants should be treated with tetracycline eye ointment
and oral erythromycin.
6- Other Agents:
• Pneumococcus, Haemophilus influenzae:
are probably haematogenously spread from
maternal septicaemia .
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They may cause profound shock in the
infant, indistinguishable clinically from Group
B β-haemolytic streptococcus (GBS) .
• Anaerobes: are contracted from the birth
canal and require special culture media.
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IV. Late-onset
(Postnatal) Infection
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1. The definition of late-onset infection:
The most common definition is “signs of infection
developing at least 7 days after birth”.
2. The risk factors of nosocomial infection:
• Direct contamination by the hands of medical
staff or parents.
• Frequently performed procedures.
• Cross-infection.
3.Clinical features
- There are no pathognomonic signs of infection
or any totally reliable way to make an early
diagnosis in the laboratory.
- The doctor must have a high level of suspicion
for infection and not be too reliant on blood tests
to make the diagnosis.
- If in doubt, treat the baby
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4. Commenest agents in late-onset:
• Late-onset group B β-haemolytic
streptococcus infection
• Coagulase-negative staphylococci
• Staphylococcus aureus
• Others include: Pseudomonas, Proteus,
Klebsiella, Serratia, and Candida.
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5. Common presentation:
• Meningitis.
• Lower respiratory tract infection.
• Urinary tract infection.
• Conjunctivitis (‘sticky eyes’).
• Infection of the skin and subcutaneous
tissues.
• Gastroenteritis.
• Systemic candidiasis.
Late-onset GBS Septicemia, and Meningitis with Convulsion
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Late Onset Neonatal Sepsis Pneumoccoci
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Management
of Neonatal Infections
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1.GBS prophylaxis:
- The most common cause of early-onset sepsis
- Incidence of infection has been estimated at 1-5 /1000
live births (unchanged for the past three decades).
- Case fatality rate ranges from 5—15%
The guidelines recommended one of two approaches:
1- The prenatal screening approach:
(screening all pregnant women for GBS infection at
35-37 weeks gestation and treatment of women with
positive cultures)
2- Identifying women who present with risk factors:
and treating them during labor.
2. Initial therapy:
 Treatment is most often begun before a definite
causative agent is identified.
 Penicillin, usually Ampicillin, plus an
Aminoglycoside are commonly used.
 In nosocomial sepsis:
Flora of the NICU must be considered. However,
staphylococcal coverage with Vancomycin plus
a 3rd Generation cephalosporin are commonly
used.
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3. Continuing therapy:
 It is based on culture and sensitivity results,
clinical course, and other serial lab studies (CRP).
 Monitoring of antibiotic levels and toxicity are
important.
 When GBS is documented as the causative agent.
Penicillin is the DOC Aminoglycoside is often
given as well because of documented synergism.
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4. Supportive Therapy & Complications:
RESPIRATORY:
Ensure adequate oxygenation with blood gas monitoring
and initiate O2 therapy or ventilator support if needed
2. CARDIOVASCULAR:
Support BP and perfusion to prevent shock.
- Use volume expanders, 10-20 mL/kg (normal saline,
albumin, and blood), and
- Monitor the intake of fluids and output of urine.
- Pressor agents such as dopamine or dobutamine may
be needed.
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3. Hematologic:
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b)
DIC: Generalized bleeding at puncture sites,
gastrointestinal tract, or CNS sites.
- In the skin, large vessel thrombosis  gangrene.
- Lab. parameters consistent with DIC include :
thrombocytopenia, prolonged PT, and PTT.
- Measures include: treating the underlying disease;
fresh-frozen plasma, 10 mL/kg; vitamin K; platelet
infusion; and possible exchange transfusion.
Neutropenia: Studies suggest the use of recombinant
human granulocyte colony-stimulating factor (rhG-CSF)
or recombinant human granulocyte-macrophage
colony-stimulating factor (rhGM-CSF) can reduce
morbidity and mortality.
4. CNS
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Implement seizure control measures 
Phenobarbital, 20 mg/kg loading dose
Monitor for the syndrome of inappropriate antidiuretic
hormone (SIADH) :
i.
Decreased urine output,
ii.
Hyponatremia,
iii.
Decreased serum osmolarity, and
iv.
Increased urine specific gravity and osmolarity.
METABOLIC
Monitor for and treat hypo- or hyperglycemia.
Metabolic acidosis may accompany sepsis and is
treated with bicarbonate and fluid replacement.
IN SUMMARY
 Infection is a commonl problem in neonatal medicine.
It has significant morbidity and mortality.
 Signs and symptoms may be present at or shortly after
birth or may occur at any time during admission.
 Staff looking after neonates must have a high suspicion
index of infection, as prompt treatment is required.
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A number of measures have been proven to decrease
the risk of nosocomial infection with the most important
being careful hand-washing.
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