Necrotizing Enterocolitis

Necrotizing enterocolitis

- DrRaghavendra Babu S

DNB year II

JLNHampRC

Necrotizing Enterocolitis 1048766an acquired neonatal acute intestinal necrosis of unknown etiology1048766NEC is neither a uniform nor a well-defined disease entity

Acquired neonatal intestinal diseases (ANIDs)

Wider umbrella includes different pathologies affecting gastrointestinal tract in preterm and term infants Some which do lead to the common final pathology of NEC and some which do not1048766Includes1048766NEC1048766SIP (isolated spontaneous intestinal perforation)1048766Viral enteritis of infancy1048766Cowrsquos milk protein allergy

Epidemiology

Incidence 03-24 1000 live births2-5 of all NICU admissions5-10 of VLBW infants Over 90 of cases occur in preterm babiesAbout 10 occur in term newborns essentially limited to those that have some underlying illness or condition requiring NICU admission Sex race geography climate has no role in

determining the incidence of NEC Prematurity is the single greatest risk factor

Intestinal ischemia (injury)

Enteral nutrition Pathogenic

organisms

Risk Factors for NEC - Triad

Risk factors influencing NEC prediposition

bull Prematurity inflamatory propensity of the immature gut Decreases intestinal barrier function Decreased gut motility and abberent vascular regulation

bull Enteral feeding Aggressive advancement of feeding Non human milk feeding

bull Abnormal bacterial colonization Prolonged emperical antibiotic therapy Decreased commensal flora Increased pathogenic bacteria

Maternal cocaine abuse ndash 25 times increases risk

Risk Factors in Term Babies

Limited to those that have some underlying illness or condition requiring NICU admission

bull Congenital Heart Diseasebull Intrauterine growth restrictionbull Polycythemiabull Hypoxic-ischemic events

bull The mean gestational age of infants with NEC is 30 to 32 weeks and the infants generally are weight appropriate for gestational age

bull Postnatal age at onset is inversely related to birth weight and gestational age with mean age at onset of 12 days

PRIMARY INFECTIOUS AGENTS

Bacteria Bacterial toxin Virus Fungus

CIRCULATORY INSTABILITY

Hypoxic-ischemic event Polycythemia

MUCOSAL INJURY

ENTERAL FEEDINGS

Hypertonic formula or medication Malabsorption gaseous distention H2 gas production Endotoxin production

INFLAMMATORY MEDIATORS

Inflammatory cells (macrophage) Platelet activating factor (PAF) Tumor necrosis factor (TNF) Leukotriene C4 Interleukin 1 6

pathogenesis

Microbiologic Flora and Infection

Several organisms have been accused but non has been proven to be causativendash Enterobacteriaceaendash Enterobactersakazakiindash Coagulase-negative staphylococci SIPndash Closrtidium perfringensndash Candida species SIPndash Cytomegalovirusndash Torovirusndash HIVndash Mucormycosis

Cytokines and Inflammatory Mediators

ndash Platelet Activating Factor (PAF)ndash Tumor Necrosis Factor (TNF)ndash High-mobility group box 1 protein (HMGB 1)ndash Interferon-gamma (INF-gamma)ndash Interleukins (ILs)ndash Matrix metalloproteinases(MMPs)

Clinical Presentation

bull Course of the diseaseFulminant presentation

Slow paroxysmal presentationbull 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

bull 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

bull 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

bull Abdominal (enteric) signsndash Distensionndash Tendernessndash Gastric aspirate

vomitingndash Ileusndash Abdominal wall

erythema indurationndash Ascitesndash Abdominal massndash Bloody stool

bull Systemic signs ndash Respiratory distress

apnea bradycardiandash Lethargy irritabilityndash Temp instabilityndash Poor feedingndash Hypotensionndash Acidosisndash Oligureandash Bleeding diathesis

Laboratory featuresbull No lab test is specific for NECbull The most common triad

ndash Thrombocytopeniandash Persistent metabolic acidosisndash Severe refractory hyponatremia

Serial measurements of CRP ndash diagnostic and prognostic

bull uarrWBC darrWBC darrPMNbull Hyperkalemiabull Stool reducing substances occult blood

Blood studies

Thrombocytopenia

COMMON TRIAD

OF SIGNS

Persistent Severe Refractory

Hyponatremia Metabolic Acidosis

HAT

Radiology studies

bull Abdominal X-raybull Abnormal gas pattern ileusbull Bowel wall edemabull Pneumatosis intestinalisbull Fixed position loopbull Intra hepatic-portal venous gas ( in the absence of

UVC)bull Pneumoperitonium - left lateral decubitus or cross-

table lateral views

bull Intestinal perforation bull Abdominal Xray in NEC demonstrates marked distention and massive

pneumoperitoneum

Free air below the anterior abdominal wall

NEC

bull Abdominal ultrasoundndash Thick-walled loops of bowel with hypomotilityndash Intraperitonealfluid is often presentndash Intramural gas can be identified in early-stage NEC ndash In the presence of pneumatosisintestinalis gas is

identified in the portal venous circulation within the liver

ndash Color Doppler US is more accurate than abdominal radiography in depicting bowel necrosis in NEC

bull Differential diagnosis of NEC bull Specific infections (systemic or intestinal)- Pneumonia

Sepsis

bull Gastrointestinal obstruction volvulus malrotation

bull Isolated intestinal perforation

bull Severe Inherited Metabolic disorders (eg galactosemia with Escherichia coli sepsis)

bull Feeding intolerance

bull Severe allergic colitis

bull Idiopathic focal intestinal perforation can occur spontaneously or after the early use of postnatal steroids and indomethacin

bull MODIFIED BELLrsquoS STAGING OF NEC Based on

1 Systemic Signs

2 Intestinal Signs

3 Radiological Signs

Classified into

I Suspected

II Definite

A (Mildly ill)

B (Moderately ill)

III Advanced

A (Severely illbowel intact)

B (Severely illbowel perforated)

SIR

bull TREATMENTbull Rapid initiation of therapy is required for suspected as well

as proven NEC cases

bull 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

bull Once blood has been drawn for culture systemic antibiotics (with broad coverage for gram-positive gram-negative and anaerobic organisms) should be started immediately

bull TREATMENT Contdbull Umbilical catheters if present should be removed

bull Ventilation should be assisted as required

bull Intravascular volume replacement with crystalloid or blood products

bull Cardiovascular support with volume andor inotropes

bull Correction of hematologic metabolic and electrolyte abnormalities

bull Careful attention to respiratory status coagulation profile and acid-base and electrolyte balance are important

bull MONITORING

bull Sequential abdominal grith measuremet

bull Sequential anteroposterior and cross-table lateral or lateral decubitus abdominal x-rays to detect intestinal perforation

bull Serial determination of hematologic status

bull Serial determination of electrolyte status and

bull Serial determination of acid-base status

bull Indications for surgery bull Absolute indicationsbull Evidence of perforation on abdominal roentgenograms

(pneumoperitoneum) or bull Positive abdominal paracentesis (stool or organism on

Gram stain from peritoneal fluid)

bull Relative indicationsbull Failure of medical management bull Single fixed bowel loop on roentgenograms bull Abdominal wall erythema or bull A palpable mass

bull Ideally surgery should be performed after intestinal necrosis develops but before perforation and peritonitis occurs

bull 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

Initial signs of possible NEC (bellrsquos stage I )

bullNPObullGI decompression- low constant sucton replace output with electrolytesbullCBC with differentials blood culture CRP SElectrolytesbullAbdominal radiographbullBegin antibiotics

Mild to Moderate (Bellrsquos stage II)bullSerial abdominal radiographsbullBroad spectrum antibiotics for 7- 10 daysbullNPO for 5-10 days parentaral nutritionbullMonitor electrolytesbullSerial CBCs every 12h to 24h for 2-3 days

Advanced (Bellrsquos Stage III)bullSerial abdominal radiographsbullBroad spectrum antibiotics for 7- 10 daysbullNPO for 10-14 days parentaral nutritionbullMonitor electrolytesbullSerial CBCs every 12h to 24h for 2-3 daysbullCo-mangement with paediatric surgeonbullHemodynamic supportbullMonitor coagulation abnormalities and correct Indications for surgery

bullIntestinal perforationbullFixed adynamic loop ndash necrotic gutbullSigns suggestive of necrotic gut ndashpersistent severe thrombocytopenia severe metabolic acidosis

bull PROGNOSIS

bull Medical management fails in about 20ndash40 of patients with pneumatosis intestinalis at diagnosis of these 10ndash30 die

bull Early postoperative complications Wound infection dehiscence and stomal problems (prolapse necrosis)

bull Later complications Intestinal strictures develop at the site of the necrotizing lesion in about 10 of surgically or medically managed patients

bull PROGNOSIShellip

bull After massive intestinal resection

-Complications from postoperative NEC include short-bowel syndrome (malabsorption growth failure malnutrition)

bull Premature infants with NEC who require surgical

intervention or who have concomitant bacteremia are at increased risk for adverse growth and neurodevelopmental outcome

bull The overall mortality is 9 to 28 regardless of surgical or medical intervention

bull PREVENTION bull Always better than curebull Newborns exclusively breast-fed have a reduced risk of NEC

bull Early initiation of aggressive feeding may increase the risk of NEC in VLBW infants

bull Gut stimulation protocol of minimal enteral feeds followed by judicious volume advancement may decrease the risk

bull Probiotic preparations have also decreased the incidence of NEC Induction of GI maturation

bull Incidence of NEC is significantly reduced after prenatal steroid therapy

bull Alteration of the immunologic status of the intestine using immunoglobulin A (IgA) and immunoglobulin G (IgG) supplementation

Thank You