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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.
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
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
ADJUNCTIVE STUDIES
CRP
ESR
Cytokines and Surface Neutrophil
CD11
Miscellaneous tests
R AD I ALO G I C S T U D I E S
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.
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.
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
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
Extensive
Pneumatosis, early
ascites,
Intrahepatic/portal
venous gas
SYSTEMIC SIGNS
Thrombocytopenia
CLINICAL PRESENTATION
STAGE III (ADVANCED)
IIIA Severely Ill, Bowel
Intact
SYSTEMIC SIGNS
INTESTINAL FINDINGS
RADIOGRAPHY
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.
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).
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
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
Stage IIIA
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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