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NEONATAL SEPSIS

AND
NECROTIZING
ENTEROCOLITIS
C . C . A L C A C H U PA S

NEONATAL
SEPSIS

DEFINITION
CLINICAL syndrome of systemic
illness accompanied by BACTEREMIA
occurring in the FIRST MONTH of
life.

RISK FACTORS
PREMATURITY and LOW BIRTH WEIGHT. Is the most
significant factor correlated with sepsis. The risk increases
in proportion to decrease in birth weight
RUPTURE of MEMBRANES. >18hrs of rupture
MATERNAL PERIPARTUM FEVER (> 38 C/100.4 F) or
INFECTION. Chorioamnionitis, urinary tract infection (UTI),
vaginal colonization with GBS, previous delivery of a
neonate with GBS disease, perineal colonization with E. coli,
and other obstetric complications.
AMNIOTIC FLUID PROBLEMS. Meconium-stained or foulsmelling, cloudy amniotic fluid.

RISK FACTORS
RESUSCITATION AT BIRTH. Infants who had fetal distress,
were born by traumatic delivery, or were severely depressed
at birth and required intubation and resuscitation.
MULTIPLE GESTATION.
INVASIVE PROCEDURES. Invasive monitoring and
respiratory or metabolic support.
INFANTS with GALACTOSEMIA (predisposition to E. coli
sepsis), immune defects, or asplenia.
IRON THERAPY (iron added to serum in vitro enhances the
growth of many organisms).

OTHER FACTORS
SEX
Males are 4 times more affected than females, and the
possibility of a sex-linked genetic basis for host susceptibility is
postulated. Variations in immune function may play a role.
RACE
Sepsis is more common in black than in white infants, but this
may be explained by a higher incidence of premature rupture of
membranes, maternal fever, and low birth weight.
SOCIOECONOMIC
is often reported as an additional risk factor, but again this may
be explained by low birth weight. NICU staff and family
members are often vectors for the spread of microorganisms,
primarily as a result of improper hand washing.

BALANCE OF FACTORS THAT AFFECT


NEONATAL SEPSIS

CLINICAL PRESENTATION
TEMPERATURE IRREGULARITY
CHANGE IN BEHAVIOR
SKIN CHANGES
FEEDING PROBLEMS
CARDIOPULMONARY CHANGES
METABOLIC CHANGES

PATHOPHYSIOLOGY
DEFINED by 3 CLINICAL
situations.
EARLY ONSET
LATE ONSET
VERY LATE ONSET

CHARACTERISTI
CS

Age at onset
Maternal
obstetric
complications
Prematurity
Organism
source
Manifestation

Site

EARLY ONSET

LATE ONSET

VERY LATE
ONSET

Birth to 7 days
usually
<72 hr

7-30 days

>30 days

Common

Uncommon

Varies

Frequent

Varies
Maternal
Genital Tract
Environment

Usual

Maternal
genital tract
Multisystem

Multisystem of
focal

Normal
nursery, NICU,

NICU,

Environment/Co
mmunity
Multisystem of
focal
NICU,

CAUSATIVE AGENTS
PRIMARY SEPSIS
- group B streptococci (GBS) - the most common
- Gram-negative enteric organisms, especially Escherichia coli.
- Other pathogens include Listeria monocytogenes, Staphylococcus, other streptococci
(including the
enterococci), anaerobes, and Haemophilus influenzae.
- Viruses: CMV, HSV, enteroviruses, and HIV.

NOSOCOMIAL SEPSIS
- Coagulase-negative Staphylococci (especially Staphylococcus epidermidis)
- Gram-negative rods (including Pseudomonas, Klebsiella, Serratia, and Proteus) and
fungal organisms predominate.
- Viruses: enteroviruses, CMV, hepatitis A, adenoviruses, influenza, respiratory

syncytial virus (RSV),

rhinovirus, parainfluenza, HSV, and rotavirus.

PREMATURITY AND NEONATAL


INFECTION
MAT E R N A L FA C T O R S

Maternal infections
predispose to preterm labor.
Choriodecidual infections
lead to prostaglandin
release that may trigger
preterm labor.

P R E T ER M FAC T O R S

Dysfunctional preterm
immune system
Decreased RES function
Decreased Complement
Decreased Immunoglobulins

DIAGNOSTICS
L A B OR AT O RY S T U D I E S

CULTURES of Blood and other normally sterile bodily fluid

GRAM STAIN of fluids especially CSF

ADJUNCTIVE STUDIES

WBC and Differential counts


Platelet count
Acute phase reactants

CRP
ESR
Cytokines and Surface Neutrophil
CD11

Miscellaneous tests

R AD I ALO G I C S T U D I E S

A CHEST X-RAY FILM.

URINARY TRACT IMAGING WITH RENAL ULTRASOUND, RENAL


SCAN OR CYSTOURETHROGRAPHY.

MANAGEMENT
P R E V E N T I ON

Group B streptococcus
Prophylaxis
Standard Precautions

C UR E

A Penicillin + an
Aminoglycoside
Continuation of therapy is
based on culture and
sensitivity results, and other
serial laboratories.

INDICATIONS FOR STARTING ANTIBIOTICS:


The indications for starting antibiotics

in neonates at risk of EOS include any


one of the following:
(a) presence of >3 risk factors for early
onset sepsis (see right table)
(b) presence of foul smelling amniotic
fluid
(c) presence of >2 antenatal risk factor(s)
and a positive septic screen and
(d) strong clinical suspicion of sepsis.

* Presence of foul smelling liquor or three of the


above mentioned risk factors warrant initiation of
antibiotic treatment. Infants with two risk factors
should be investigated and then treated
Source:accordingly.
http://www.newbornwhocc.org/neonatalsepsis20

The indications for starting antibiotics in


LOS include:
(a) positive septic screen and/or
(b) strong clinical suspicion of sepsis.

The following risk factors seem to be associated


with an increased risk of early onset sepsis:
1. Low birth weight (<2500 grams) or prematurity
2. Febrile illness in the mother with evidence of
bacterial infection within 2 weeks prior to delivery
3. Foul smelling and/or meconium stained amniotic
fluid
4. Rupture of membranes >24 hours
5. Single unclean or > 3 sterile vaginal
examination(s) during labor
6. Prolonged labor (sum of 1st and 2nd stage of
labor > 24 hrs)
7. Perinatal asphyxia (Apgar score <4 at 1 minute)

SCLEREMA
NEONATORUM

ETIOLOGY/ PATHOGENESIS
The cause remains unknown.
Four Theories proposed:
1. Hardening of the subcutaneous fat due to a decrease in body temperature
as a consequence
of circulatory shock
II. Defect in lipolytic enzymes or in lipid transport
III. Association with an underlying severe disease
IV. Special form of edema affecting the connective tissue that supports the
adipocytes

CLINICAL MANIFESTATIONS
Usually manifests in preterm, gravely ill infants as:
as diffuse, yellowish white woody induration of the skin
stony in consistency, cold, and non-pitting
face assumes a mask-like expression,
joint mobility may be compromised because of inflexibility of the skin

TREATMENT
Almost always associated with serious illness, such as sepsis,
congenital heart disease, multiple congenital anomalies, or
hypothermia.
The appearance of sclerema in a sick infant should be regarded as
an ominous prognostic sign.

The outcome depends on the response of the underlying


disorder to treatment.

NECROTIZING
ENTEROCOLITIS

DEFINITION
is an ACQUIRED neonatal disorder
representing an end expression of SERIOUS
INTESTINAL INJURY after a combination of
VASCULAR, MUCOSAL, AND METABOLIC
(and other unidentified) insults to a relatively
immature gut.

EPIDEMIOLOGY
NEC is predominantly A DISORDER OF PRETERM INFANTS.
Incidence is INVERSELY CORRELATED WITH BIRTH
WEIGHT, with the greatest incidence occurring in INFANTS
<1.5 KGMS.
70%-90% of cases occur in HIGH RISK, LOW BIRTH WEIGHT
INFANTS.

RISK FACTORS
Prematurity greatest risk factor
Asphyxia and acute cardiopulmonary disease
Causes low cardiac output and decreased perfusion with
shunting of blood away from the peripheral and splanchnic
circulation to the central
Polycythaemia and Hyperviscosity syndromes
Leads to diminished perfusion and intestinal ischemia in
watershed areas

Enteral feedings
Substrate for proliferation of pathogens
Hyperosmolar feedings can cause altered mucosal
permeability and can cause direct mucosal damage
Lack of immunoprotective factors
Breast feeding significantly decreases risk

Exchange transfusions
Probably due to intestinal ischemia as a result of wide
variations in venous or arterial perfusion pressures
Enteric pathogenic microorganisms
Bacterial and viral pathogens, including Escherichia coli,
Klebsiella, Enterobacter, Pseudomonas, Salmonella,
Staphylococcus epidermidis, Clostridium sp, coronaviruses,
rotaviruses, and enteroviruses, have been implicated, either
directly or indirectly,by blood, stool, or peritoneal space
cultures.

CLINICAL PRESENTATION
MODIFIED BELLS STAGING CRITERIA FOR NEC
STAGE 1
(SUSPECTED)

STAGE II (DEFINITE)
IIA - (Mild)

STAGE II (DEFINITE)
IIB - (Moderate)

Nonspecific: Apnea,
Bradycardia,
Lethargy,
Temperature instability

Similar to stage I

Stage I plus mild


acidosis and

INTESTINAL FINDINGS

Feeding intolerance,
recurrent gastric
residuals, Guaiacpositive stools

Prominent distention w/
or w/o tenderness, absent
bowel sounds, gross
hematochesia

Increasing distention
Abdominal wall edema
Tenderness w/ or w/o
palpable mass

RADIOGRAPHY

Normal or nonspecific

Ileus, dilated bowel loops


Pneumatosis
Intestinalis

Extensive
Pneumatosis, early
ascites,
Intrahepatic/portal
venous gas

SYSTEMIC SIGNS

Thrombocytopenia

CLINICAL PRESENTATION
STAGE III (ADVANCED)
IIIA Severely Ill, Bowel
Intact

STAGE III (ADVANCED)


IIIB Severely Ill, Bowel
Perforated

SYSTEMIC SIGNS

Respiratory and metabolic


acidosis, assisted ventilation
for apnea,
Decreasing blood pressure and
urine output, neutropenia, and
coagulopathy.

Generalized edema, deteriorating


vital signs and laboratory indices,
Refractory hypotension, shock
syndrome, disseminated
intravascular coagulation (DIC),
and Electrolyte imbalance.

INTESTINAL FINDINGS

Spreading edema, erythema or Tense, discolored abdomen and


discoloration, and induration of ascites
the
Abdominal wall.

RADIOGRAPHY

Prominent ascites, paucity of Absent bowel gas and often


bowel gas, or presence of a
evidence of intraperitoneal
sentinel loop
free air.

DIAGNOSIS
A HIGH INDEX OF SUSPICION
should be entertained in any infant that
displays a COMBINATION OF THE RISK
FACTORS for NEC

CLINICAL DIAGNOSIS
TRIAD OF:
Feeding intolerance
Abdominal distention
Grossly bloody stools
Note:
This will should make NEC the tentative diagnosis
The earliest signs are usually identical to neonatal sepsis

LABORATORY STUDIES
1.Complete blood cell count (CBC) with differential.
1. The white blood cell (WBC) may be normal but is more frequently either
elevated, or low (leukopenia).

2.Platelet count.
1. Thrombocytopenia is seen. Fifty percent of patients with proven NEC
have platelet counts <50,000/uL.

3.Blood culture
1. for aerobes, anaerobes, and fungi (Candida sp).

4.Stool screening
1. for occult blood. Routine testing of stools for occult blood does not
identify a population at greater risk for NEC. In suspect patients, the
presence of occult blood may influence management but may not be
helpful in making a diagnosis of NEC.

LABORATORY STUDIES
1.Arterial blood gas measurements.
1. Metabolic or combined acidosis or hypoxia may be seen.

2.Electrolyte panel.
1. Electrolyte imbalances, particularly hypo- or hypernatremia,
and hyperkalemia are common.

3.Stool cultures for rotaviruses and enteroviruses


1. should be obtained if diarrhea is an epidemic in the nursery.

RADIOLOGIC STUDIES
Flat plate x-ray studies of the abdomen
Supportive for NEC.
Look for abnormal bowel gas patterns, ileus, a fixed sentinel loop of
bowel, or areas suspicious for pneumatosis intestinalis.

Confirmatory of NEC.
Look for (1) intramural bowel gas (pneumatosis intestinalis) and (2)
intrahepatic portal venous gas (in the absence of an umbilical venous
catheter).

Lateral decubitus and cross-table lateral studies


of the abdomen.
These studies are more likely to demonstrate a

NECROTIZING
ENTEROCOLITIS

A kidney-ureter-bladder film
demonstrates abdominal distention,
hepatic portal venous gas (arrow), and a
bubbly appearance of pneumatosis
intestinalis (arrowhead; right lower
quadrant). The latter two signs are
thought to be pathognomonic for
neonatal necrotizing enterocolitis

Submucosal gas
*Arrows are pointing to gas along the wall

Football sign free air outlines the


whole abdomen
Triangle sign seen between
three loops
Portal venous air
Double walling/Rigler sign
-normally you can only see the
outline of the inner intestinal wall
due to presence of gas inside -outer
wall is seen here (pic) due to free
air

Refers to a
segment of the
intestine that
becomes
paralyzed and
dilated as it lies
next to an
inflammed area

SENTINEL
LOOP

INTESTINAL
P E R F O R AT I O N .

A cross-table
abdominal
roentgenogram in a
patient with a
neonatal necrotizing
enterocolitis
demonstrates
marked distention
and massive
pneumoperitoneum
as evidenced by the
free air below the
anterior abdominal
wall.

NOTE
Perforation commonly occurs within 48-72 h after
pneumatosis or portal venous gas. In the presence of
pneumatosis intestinalis or portal venous gas, flat plate and
left lateral decubitus or cross-table lateral x-ray studies of
the abdomen should be obtained every 6-8 h to check for
the development of pneumoperitoneum, signaling intestinal
perforation. Serial x-ray studies may be discontinued with
clinical improvement, usually after 48-72 h.

MANAGEMENT
NO DEFINITIVE TREATMENT

Supportive care:
NPO
Nasogastric decompression
IV fluid administration

Careful attention
Respiratory status
Coagulation profile APTT, Protime

MANAGEMENT
SYSTEMIC ANTIBIOTICS - gram-positive, gram-negative and
anaerobic organisms in the particular NICU
CLOSE MONITORING, Frequent PE, Sequential AP and lateral
decubitus abdominal radiographs, Serial determination of
hematologic, electrolyte and acid-base status
SURGERY
Indications: perforation, (+) abdominat paracentesis
Performed after intestinal necrosis develops but before perforation
and peritonitis
Unstable neonates Peritoneal drainage

MANAGEMENT BY STAGE
STAGE

MANAGEMENT

Stage IA and IB

NPO, IV fluids, Parenteral nutrition


Antibiotics for 3 DAYS

Stage IIA and


IIB

RESPIRATORY AND CARDIOVASCULAR SUPPORT


Surgical consultation
After stabilizations, TPN is provided while on NPO

Stage IIIA

NPO with TPN for 14 days


Support Measures: Fluid resuscitation, Inotropic
support, Ventilator support
Surgical consultation

Stage IIIB

SURGICAL INTERVENTION

PROGNOSIS
Medical management fails in about 20-40% of patients with
pneumatosis intestinalis, of these, 10-30% die
Post-op complications
Wound infection
Dehiscence
Stomal problems
Short-bowel syndrome (malabsorption, growth failure,
malnutrition)

PREVENTION
Breastfeeding
Gut Stimulation protocols
Prophylactic enteral antibiotics
Probiotics

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