NEONATAL NECROTIZING ENTEROCOLITIS

By :Rasha AlqdiAlwehda hospital

◦ 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 1–10% of infants in NICU.

◦ Although rare, the disease does occur in term infants (10%)

◦ The mortality rates vary from 10% to 50% .

Birth weight

Incidence, Fatality

Gestational age(less than 28 weeks of gestation)

◦Necrotizing Enterocolitis In The Beginning

◦ NEC was unknown as a disease before the 1950’s

◦ First described in 1950’s by Schmid and Quaiser

◦ – Case reports describing neonates who died from necrotizing lesions

of their GI tracts.

NEC became recognized as a clinical entity in 1960’s and 1970’s

◦ – At this time NEC’s mortality exceeded 70%

◦ – NEC was initially described as idiopathic gastrointestinal perforations

So what is NEC ?

Def. of NEC

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.

Risk factors◦ Prematurity. The lower the gestational age the greater the risk of the NEC, because of the

immaturity of the circulatory, gastrointestinal, and immune systems.

◦ Asphyxia and acute cardiopulmonary collapse, as they lead to low cardiac output and

diminished intestinal perfusion.

◦ Enteral feeding: NEC is rare in unfed infants. About 90-95% of infants with NEC received at least

one enteral feeding.

◦ Enteral feeding provides a substrate for proliferation of enteric pathogens.

◦ Hyperosmolar formula may cause direct damage to intestinal mucosa.

◦ Lack of the immuno-protective factors in commercially prepared formula.

◦ Breast-feeding significantly lowers the risk of NEC ( suggesting that breast milk factors, including growth

factors, antibodies, and cellular immune factors, might be protective).

◦ Polycythymia and hyperviscosity syndrome.

◦ Exchange transfusion.

◦ Large feeding volumes and rapid advancement of enteral feedings.

◦ Enteric pathogenic organisms comprising bacterial and viral pathogens. These include E.coli,

Klebsiella, salmonella, rotaviruses, and enteroviruses.

Why Exchange transfusion is a risk factor for NEC ?

Answer :◦By using Umbilical Catheter for

Exchange transfusion , increase in

portal venous pressure that can result

in decrease in ilial and colonic blood

flow

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.

PATHOLOGY AND PATHOGENESIS:

Intestinal ischemia (injury)

Enteral nutrition Pathogenic

(metabolic substrate) organisms

What is the most common site of NEC?

◦A. Stomach

◦B. Jejunum

◦C. Ileum

◦D. Colon

Terminal ileum/

Proximal Colon

In fatal cases, gangrene may extend from the stomach to the rectum.

PATHOLOGY AND PATHOGENESIS: contd..◦ 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.

◦ 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.

Question :◦Why drugs like theophylline , sodium

bicarbonate and calcium supplements ,

increase the risk of NEC ?

Answer :

◦All the previouse medications increase

the osmolarityof the stomach and

intestine .

Why the Preterm Gut is Different

◦Decreased IgA

◦Decreased Intestinal T lymphocytes

◦Poor Antibody Response

◦Higher Membrane Permeability of GI Epithelial

Lining

◦Lower Gastric Motility

◦More Scant and More Permeable Mucin Blanket

Intestinal Archetecture

Keep in mind we will be

looking at a small slice of an

enormous organ that has

multiple layers of complexity…

Platlate activating factor

Tumer necrosis factor

CLINICAL MANIFESTATIONS: ◦ Onset can be insidious or rapid.

◦ Onset time: The onset of NEC varies; in very low birth weight (VLBW)

infants, NEC is usually diagnosed between 14-20 days of life. In full-term

infants, the age of onset is usually during the first week of life.

◦ 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.

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.

What do we use to determine severity

and medical management in NEC?

◦Modified Bell’s Staging

True or False:Gastroschisis carries

anincreased risk of

developing NEC…

Diagnosis of NEC◦ 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.

4. Blood studies:

Thrombocytopenia

COMMON TRIAD

OF SIGNS

Persistent Severe Refractory

Metabolic Acidosis Hyponatremia

Pneumoperitoneum

“football” sign

◦ The median umbilical ligament and falciform ligamentare sometimes included in the description of this sign

Portal vein gas

Pneumoperitoneum/scrotum

◦ Intestinal perforation.

◦ Abdominal Xray in NEC demonstrates marked distention and massive

pneumoperitoneum

Free air below the anterior abdominal wall.

◦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.

◦ 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.

◦ 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.

◦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.

◦ 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.

◦ 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.

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.

◦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.

◦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.