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Necrotizing enterocolitis

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Necrotizing enterocolitis



  1. Definitions
  2. Epidemiology
  3. Risk Factors
  4. Pathogenesis
  5. Pathophysiology
  6. Clinical Presentation
  7. Diagnosis
  8. Management
  9. Prognosis
  10. Prevention

Definitions


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

Definitions



Isolated spontaneous intestinal perforation 

(SIP): ill-defined clinical syndrome of undetermined cause resembling NEC with less systemic involvement and a less severe clinical course. It may present a variant of classical NEC

The National Institute of Child Health and Human Development Neonatal Network (NICHD): intestinal perforation without evidence of pneumatosis since


Definitions




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 not.

Includes:

  • NEC
  • SIP
  • Viral enteritis of infancy
  • Cow’s milk protein allergy

Epidemiology



Incidence: 0.3-2.4 / 1000 live births

  • 2-5 % of all NICU admissions
  • 5-10 % of VLBW infants


Over 90 % of cases occur in preterm babies

About 10 % occur in term newborns: 

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


Epidemiology



Sporadic or epidemic clusters

Sex, race, geography, climate, season: No role

  • Male VLBW infants are at greater risk of death
  • Black infants: increased risk of NEC, and its associated mortality


Risk Factors: Prematurity



Prematurity is the single greatest risk factor

The risk is inversely related to birth weight and gestational age


Risk Factors: Genetics



Familial:

There are report a consanguineous Jewish Ashkenazi family in which three of four children died within a few weeks after birth from severe enterocolitis

Also a Lebanese consanguineous family where three  term sibs presented with severe early and lethal enterocolitis, all with delayed meconium passage

a multicenter retrospective study of 450 twin pairs born at < or =32 weeks of gestation, showed that intraventricular hemorrhage, 

necrotizing enterocolitis, and bronchopulmonary dysplasia are familial in origin


Risk Factors: G-6-PD deficiency



G6PD deficiency was significantly higher (27.8%) in infants with NEC compared with the 5.3% prevalence 

among NICU admissions (odds ratio = 6.9; 95% confidence interval = 2 to 23.5)

G6PD deficiency also was found to be a marker for more severe NEC

G6PD deficiency should be considered a risk factor for  NEC


Risk Factors: Cocaine


Maternal cocaine abuse increases the risk by 2.5 folds (95% CI = 1.17 to 5.32, P = 0.02)



Risk Factors: Indomethacin



Indomethacin for Tocolysis: Metaanalysis 2007

Recent exposure (within 48 hours of delivery) to antenatal indomethacin was associated with 

necrotizing enterocolitis (OR, 2.2; 95% CI; 1.1-4.2).


Risk Factors: Indomethacin



Indomethacin in Early Life:

Associated with SIP3

Prolonged versus Short Course of Indomethacinfor the treatment of PDA in preterm infants: Systematic Review

  • The reduction of transient renal impairment does not outweigh the increased risk of NEC associated with the prolonged course.
  • Based on these results, a prolonged course of indomethacin cannot be recommended for the routine treatment of PDA in preterm infants

Risk Factors: Dexamethasone



Combined use of  indomethacin and dexamethasone increases the risk of SIP in VLBW neonates


Risk Factors: H2-blockers



Antecedent H2-blocker use was associated with an increased incidence of
  NEC (OR 1.71, 95% CI 1.34-2.19, P < .0001)

Risk Factors: Co-amoxiclav



Co-amoxiclav should be avoided in women at risk of preterm delivery because of the increased risk of neonatal necrotizing enterocolitis (RR 4.60, 95% CI 1.98 to 10.72)

Risk Factors: Acyclovir



Term baby, developed NEC after receiving prophylactic acyclovir.

Mother had herpes genitalis and pROM at 32 wks of GA, treated with acyclovir until vaginal delivery

Acyclovir treatment in uteroand after birth is discussed as a possible cause of necrotizing enterocolitis in the infant.


Risk Factors: Kayexalate



Necrotizing enterocolitis in a 850 gram infant receiving sorbitol-free sodium polystyrene sulfonate

Their case report shows that Kayexalateper se, and not necessarily suspended in sorbitol, can lead to 

gastrointestinal tract complications and NEC in preterm infants.


Risk Factors: UAC


UAC cause a decrease in mesenteric blood flow

Therefore, their use in hemodynamically unstable neonates or in those with gastrointestinal disease should be very carefully Considered

High vs. low UAC: necrotising enterokolitis are not more frequent with high compared to low catheters

Preprandial SMA BFV and postprandial SMA BFV responses to minimal enteral feedings were not affected by the presence of a UAC


Risk Factors: UVC


Compared long-term (up to 28 days) and short-term (7-10 days) use of umbilical venous catheters in premature infants with birth weights of less than 1251 grams

There were no differences in time to full feedings or to regain birth weight or in the incidence of necrotizing enterocolitis or death


Risk Factors: PDA



No association between significant PDA and NEC

The age at starting feed and full enteral feed was significantly delayed in infants with significant PDA


Risk Factors: in Term babies



Limited to those that have some underlying illness or condition requiring NICU admission.2

  • Congenital Heart Disease
  • Intrauterine growth restriction
  • Polycythemia
  • Hypoxic-ischemic events

Risk Factors: Exchange transfusion


There is no evidence of long-term benefit from partial exchange in polycythaemic infants

The incidence of gastrointestinal injury is increased NEC (RR 8.68; 95% CI 1.06 to 71.1)




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Pathophysiology



Hypoxic-Ischemic insult

Enteral Feeding

Microbiologic Flora

Cytokines and Inflammatory Mediators


Hypoxic-ischemic insult



Hypoxia-Reoxygenation.
 

Ischemia-Reperfusion.
 

Intramural microcirculation.

Balance between Endothelin-1 and Nitric Oxide.26


Enteral feeding



Formula vs. Donor Breast Milk

Formula is associated with higher risk of NEC


Enteral feeding



Disadvantages of Formula:

  Higher osmolality ±
 

  Lack of immunoprotective factors
 

  Lack of growth factors
 

  Altering intestinal flora


Microbiome and Infection



  • Microbiome and Infection
  • Several organisms have been accused, but non has been proven to be causative:
  • Enterobacteriaceae
  • Enterobacter sakazakii
  • Coagulase-negative staphylococci: SIP
  • Closrtidium perfringens
  • Candida species: SIP
  • Cytomegalovirus
  • Torovirus
  • HIV
  • Mucormycosis

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Cytokines and Inflammatory Mediators



Platelet Activating Factor (PAF)

Tumor Necrosis Factor (TNF)

High-mobility group box 1 protein (HMGB 1)

Interferon-gamma (INF-gamma)

Interleukins (ILs)

Matrix metalloproteinases (MMPs)

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Clinical presentation



Onset varies with gestational age

  • VLBW   14 – 20 days
  • Term   first week

Course of the disease

  • Fulminant presentation
  • Slow, paroxysmal presentation

Clinical presentation



Systemic signs: 

  • Respiratory distress, apnea, bradycardia
  • Lethargy, irritability
  • Temp. instability
  • Poor feeding
  • Hypotension
  • Acidosis
  • Oligurea
  • Bleeding diathesis

Clinical presentation



Abdominal (enteric) signs:

  • Distension
  • Tenderness
  • Gastric aspirate, vomiting
  • Ileus
  • Abdominal wall erythema, induration
  • Ascites
  • Abdominal mass
  • Bloody stool

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Diagnosis



A high index of suspicionis required Sometimes cannot be differentiated from sepsis

Diagnosis, laboratory studies



No lab test is specific for NEC

The most common triad(!): 

  • Thrombocytopenia
  • Persistent metabolic acidosis
  • Severe refractory hyponatremia

↑ WBC, ↓ WBC, ↓ PMN

Hyperkalemia

Stool: reducing substances, occult blood


Diagnosis, radiologic studies



Abdominal X-ray:

  • Abnormal gas pattern, ileus
  • Bowel wall edema
  • Pneumatosis intestinalis
  • Fixed position loop
  • Intrahepaticportal venous gas (in the absence of  UVC)
  • Pneumoperitonium, left lateral decubitus or cross-table lateral views

Diagnosis, radiologic studies



Pneumatosis intestinalis. 

Very obvious case. 

Tremendous amount of air in bowel walls


Diagnosis, radiologic studies



Pneumatosis intestinalis. Note the air visible in 

the bowel wall. The air dissects the bowel wall 

giving it a double lined appearance (ie., ailroad 

tracks without the ties)



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Diagnosis, radiologic studies



Abdominal ultrasound:

Thick-walled loops of bowel with hypomotility.

Intraperitoneal fluid is often present

Intramural gas can be identified in early-stage NEC

In the presence of pneumatosis intestinalis, gas is identified in the portal venous irculation within the liver

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


Diagnosis, radiologic studies



Abdominal Doppler ultrasound:

neonates with high resistance patterns of blood flow velocity in the superior mesenteric artery on the first day of life are at increased risk of developing necrotizing enterocolitis


Modified Bell’s Staging Criteria


Stage I : Suspected NEC

Clinical signs and symptoms

No diagnostic radiograph


Modified Bell’s Staging Criteria


Stage II : Definite (confirmed) NEC
 

A.Mild NEC

  • Sign & symptoms, absent B/S, gross blood in stool
  • AXR: ileus, focal areas of pneumatosis intestinalis
  •  
  • A.Moderate NEC
  • Systemically ill
  • AXR: extensive pneumatosis intestinalis, early ascites, possible intrahepatic portal venous gas




Modified Bell’s Staging Criteria



A:
Severe NEC without perforation
 

  • Critically ill
  • Abdominal wall induration, extensive erythema
  • AXR: prominent ascites, paucity of bowel gas, persistent fixed loop

B: Severe NEC with perforation

Differential diagnosis



Systemic infection: sepsis, pneumonia
 

Surgical abdominal catastrophes
 

Infectious enterocolitis
 

Allergic collitis
 

Feeding intolerance


Management



The main principle of management of confirmed NEC is to treat it as an acute abdomen with impending or septic peritonitis

Isolation: cohort isolation in case of epidemic clusters


Management, medical



Basic NEC protocol: for all stages

NPO

  • NGT with low pressure suction
  • Close monitoring of vital signs & abdominal girth
  • Remove UAC and UVC
  • Septic workup: blood, urine, and stool cultures
  • LP and CSF culture: controversial
  • Antibiotics: ampicillin + gentamicin or cefotaxime
  • add Metronidazole or clindamycin if peritonitis or 
  • perforation is suspected


Management, medical


Basic NEC protocol       
…..continued
 

  • Monitor for GI bleeding
  • Fluid balance: maintain urine output 1-3 ml/kg/hr
  • Lab.: CBC, PLT, electrolytes q 8-12 hrs
  • PT, PTT, as indicated CR 
  • Radiology: serial AXR q 6-8 hrs in the first 2-3 days
  • Family support

Management, medical


Stage I

Basic NEC protocol

If all cultures are negative, the infant improved clinically, and AXR is normal, antibiotics can be stopped after 2-3 days and feeding can be resumed.


Management, medical



Stage II

Basic NEC protocol

  • NPO for 14 days
  • TPN, 90-110 kcal/kg/day
  • Antibiotics for 14 days
  • Respiratory support
  • ± Inotropic support
  • Surgical consultation


Management, medical



Stage III

  • As stage II
  • Inotropic support
  • Treat anemia, thrombocytopenia, coagulopathy
  • Surgical intervention

Management, surgical



Early Surgical Consultation

Indications for surgery:

  • Perforation: 20-30 % of cases
  • 12-48 hrs after onset
  • Full-thickness necrosis
  • Deterioration despite aggressive medical treatment

Management, surgical



Surgical Approach:

Exploratory laparotomy
 

Peritoneal drainage


Management, surgical



Exploratory laparotomy:

The most commonly used approach
 

Intestinal resection with enterostomy
 

Primary anastomosis


Management, surgical

Peritoneal drainage:
 

More conservative approach, Started in 1977
 

Insertion of a peritoneal drainelocal anaesthesia
 

Initially, used for very sick premature babies, with weight ≤ 1000 g
 

Now, it is used more commonly with larger and more stable babies
 

It is used as a definite treatment in some centers






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Management, surgical


Laparoscopy:

use of laparoscopy on day 30 of life in the treatment of a VLBW infant (900 g)

with perforated NEC

Needlescopic diagnosis is feasible and appears to be safe, even in 

critically ill micropremmies less than 1000 g. The technique can provide useful information for surgical decision-making and allows for precise placement of a microlaparotomy incision over the site of perforation, thus minimizing the trauma from open surgery in this special group of patients


Prognosis and Outcome

NEC with perforation: mortality   20-40 %

Recurrent NEC : rare complication,  4%

Subacute or intermittent symptoms of bowel obstruction: strictures,   10-35 %

Short-gut syndrome: FTT, high mortality

The type of operation (peritoneal drain vs. laparotomy) performed for erforated NEC does not influence survival or other clinically important early outcomes in preterm infants


Neurodevelopmental Outcome



Preterm infants who develop NEC are at a significantly higher risk for developing neurodevelopmental disability

Neurodevelopmental Outcome



NEC is associated with significantly worse neurodevelopmental outcome than prematurity alone. 

Presence of advanced NEC and need for surgery increase the risk of neurological impairment

Survivors of stage II or higher NEC are at risk for long-term neurodevelopmental impairment, especially if they require surgery for the illness





Prevention



  • Breast milk
  • Antenatal Steroid therapy
  • Oral immunoglobulins
  • Oral antibiotics
  • Probiotics (Lactobacillus, Bifidobacterium)
  • Feeding strategies
  • Oral PAF antagonists
  • Glutamine
  • Arginine
  • Polyunsaturated fatty acids (PUFA)
  • Lactoferin
  • Pentoxifylline


Prevention: breast milk



Formula vs. Donor Breast Milk:

Breast milk is associated with lower risk of NEC slower growth in the early postnatal period ¨


Prevention: Antenatal steroids



Antenatal corticosteroids for women at risk of preterm birth: Systematic Review

Decreased risk of NEC

RR 0.46, 95% CI 0.29 to 0.74, eight studies, 1675 infants


Prevention: Oral imunoglobulin



The evidence does not support the administration of oral immunoglobulin for the prevention of NEC. There are no randomised controlled trials of oral IgA alone for the prevention of NEC

Prevention: Probiotics



Probiotics might reduce the risk of necrotising enterocolitis in preterm neonates with less than 33 weeks' gestation (relative risk 0.36, 95% CI 0.20-0.65) the short-term and long-term safety of probiotics needs to be assessed in large trials Unanswered questions include the dose, duration, and type of probioticagents (species, strain, single or combined, live or killed) used for supplementation

Prevention: Feeding strategie




Probiotics might reduce the risk of necrotising enterocolitis in preterm neonates with less than 33 weeks' gestation (relative risk 0.36, 95% CI 0.20-0.65)

the short-term and long-term safety of probiotics needs to be assessed in large trials

Unanswered questions include the dose, duration, and type of probioticagents (species, strain, single or combined, live or killed) used for supplementation


Prevention: Glutamine


The available data from good quality randomised controlled trials suggest that glutamine supplementation does not confer clinically significant benefits for preterm infants 

The narrow confidence intervals for the effect size estimates suggest that a further trial of this intervention is not a research priority


Prevention: Arginine

The data are insufficient at present to support a practice recommendation. A multicentre randomized controlled study of arginine supplementation in preterm neonates is needed, focusing on the incidence of NEC, particularly the more severe stages (2 or 3)