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Introduction:
NEC is the most common life-threatening emergency of the
gastrointestinal tract in the newborn.
Various degrees of mucosal or transmural necrosis of the
intestine occurs.
The incidence of NEC is 1–5% of infants in NICU.
Although rare, the disease does occur in term infants (10%)
Birth weight
Incidence, Fatality
Gestational age
3. Dr.Padmesh. V
ETIOLOGY:
Etiology of NEC is unclear; May be multifactorial.
Prematurity is the single greatest risk factor.
Infants exposed to cocaine have a 2.5 times increased risk of
developing NEC.
The mean gestational age of infants with NEC is 30 to 32 weeks,
and the infants generally are weight appropriate for gestational
age.
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PATHOLOGY AND PATHOGENESIS:
Intestinal ischemia (injury)
Enteral nutrition Pathogenic
(metabolic substrate) organisms
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PATHOLOGY AND PATHOGENESIS:
Distal part of the ileum
Involved most frequently
Proximal segment of colon
In fatal cases, gangrene may extend from the stomach to the
rectum.
NEC probably results from an interaction between loss of
mucosal integrity due to factors like
ischemia, infection, inflammation,
and the host's response to that injury like
circulatory, immunologic, inflammatory responses resulting in
necrosis of the affected area.
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PATHOLOGY AND PATHOGENESIS: contd..
Various bacterial and viral agents, including Escherichia coli,
Klebsiella, Clostridium perfringens, Staphylococcus epidermidis,
and rotavirus, have been recovered from cultures.
However, in most situations, no pathogen is identified.
NEC rarely occurs before the initiation of enteral feeding and is
much less common in infants fed human milk.
Aggressive enteral feeding may predispose to the
development of NEC.
Coagulation necrosis is the characteristic histologic finding of
intestinal specimens.
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CLINICAL MANIFESTATIONS:
Onset can be insidious or rapid.
The onset of NEC usually occurs in the 1st 2 weeks of life (with
a mean age at onset of 12 days) but can be as late as 3 months
of age in VLBW infants.
The postnatal age at onset is inversely related to birth weight
and gestational age.
It is unusual for the disease to progress from mild to severe after
72 hr.
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CLINICAL MANIFESTATIONS:
The 1st signs of impending disease may be
-Nonspecific including lethargy and temperature instability
or
-Related to gastrointestinal pathology such as abdominal
distention and gastric retention.
Obvious bloody stools are seen in 25% of patients.
The spectrum of illness is broad and ranges from
-Mild disease with only guaiac-positive stools to
-Severe illness with bowel perforation, peritonitis, systemic
inflammatory response syndrome, shock, and death.
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MODIFIED BELL’S STAGING OF NEC:
Based on:
1. Systemic Signs
2. Intestinal Signs
3. Radiological Signs
Classified into:
I. Suspected:
A
B
II. Definite :
A (Mildly ill) ,
B (Moderately ill)
III. Advanced:
A (Severely ill,bowel intact),
B (Severely ill,bowel perforated)
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DIAGNOSIS:
Very high index of suspicion.
1. Plain abdominal x-rays :
Pneumatosis intestinalis (air in the bowel wall) is diagnostic;
Portal venous gas is a sign of severe disease, and
Pneumoperitoneum indicates a perforation.
2. Hepatic ultrasonography:
May detect portal venous gas despite normal abdominal Xray.
3. Analysis of stool for blood and carbohydrate
Carbohydrate malabsorption - positive stool Clinitest
result, can be a frequent and early indicator of NEC.
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DIAGNOSIS: contd…
4. Blood studies:
Thrombocytopenia
COMMON TRIAD
OF SIGNS
Persistent Severe Refractory
Metabolic Acidosis Hyponatremia
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Intestinal perforation.
Abdominal Xray in NEC demonstrates marked distention and massive pneumoperitoneum
Free air below the anterior abdominal wall.
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Differential diagnosis of NEC :
Specific infections (systemic or intestinal)- Pneumonia, Sepsis.
Gastrointestinal obstruction, volvulus, malrotation,
Isolated intestinal perforation.
Severe Inherited Metabolic disorders. (e.g., galactosemia with
Escherichia coli sepsis)
Feeding intolerance
Severe allergic colitis
Idiopathic focal intestinal perforation can occur spontaneously
or after the early use of postnatal steroids and indomethacin.
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TREATMENT:
Rapid initiation of therapy is required for suspected as well as
proven NEC cases.
There is no definitive treatment for established NEC and,
therapy is directed at supportive care and preventing further
injury with
-Cessation of feeding,
-Nasogastric decompression, and
-Administration of intravenous fluids.
Once blood has been drawn for culture, systemic antibiotics
(with broad coverage for gram-positive, gram-negative, and
anaerobic organisms) should be started immediately.
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TREATMENT: Contd..
Umbilical catheters if present should be removed.
Ventilation should be assisted as required.
Intravascular volume replacement with crystalloid or blood
products.
Cardiovascular support with volume and/or inotropes.
Correction of hematologic, metabolic, and electrolyte
abnormalities.
Careful attention to respiratory status, coagulation profile, and
acid-base and electrolyte balance are important.
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MONITORING:
Sequential anteroposterior and cross-table lateral or lateral
decubitus abdominal x-rays to detect intestinal perforation;
Serial determination of hematologic status,
Serial determination of electrolyte status, and
Serial determination of acid-base status.
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Indications for surgery :
Absolute indications:
Evidence of perforation on abdominal roentgenograms
(pneumoperitoneum) or
Positive abdominal paracentesis (stool or organism on Gram
stain from peritoneal fluid).
Relative indications:
Failure of medical management,
Single fixed bowel loop on roentgenograms,
Abdominal wall erythema, or
A palpable mass.
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Ideally, surgery should be performed after
intestinal necrosis develops, but before
perforation and peritonitis occurs.
Peritoneal drainage may be helpful for patients
with peritonitis who are too unstable to undergo
surgery. Peritoneal drainage is more successful in
patients with isolated intestinal perforation.
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PROGNOSIS.:
Medical management fails in about 20–40% of patients with
pneumatosis intestinalis at diagnosis; of these, 10–30% die.
Early postoperative complications : Wound infection,
dehiscence, and stomal problems (prolapse, necrosis).
Later complications : Intestinal strictures develop at the site of
the necrotizing lesion in about 10% of surgically or medically
managed patients.
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PROGNOSIS….
After massive intestinal resection,
-Complications from postoperative NEC include short-
bowel syndrome (malabsorption, growth failure, malnutrition),
Premature infants with NEC who require surgical intervention
or who have concomitant bacteremia are at increased risk for
adverse growth and neurodevelopmental outcome.
The overall mortality is 9% to 28% regardless of surgical or
medical intervention.
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PREVENTION:
Always better than cure!
Newborns exclusively breast-fed have a reduced risk of NEC.
Early initiation of aggressive feeding may increase the risk of NEC in
VLBW infants.
Gut stimulation protocol of minimal enteral feeds followed by judicious
volume advancement may decrease the risk.
Probiotic preparations have also decreased the incidence of NEC. .
Induction of GI maturation.
Incidence of NEC is significantly reduced after prenatal steroid therapy.
Alteration of the immunologic status of the intestine using
immunoglobulin A (IgA) and immunoglobulin G (IgG) supplementation.