Necrotising enterocolitis-a rapid guide

1. NECROTISING ENTEROCOLITIS
Dr. Achumie Victoria. A

2. REFERENCES
• Akhil M, Waldermar AC. Necrotizing Enterocolitis. Nelson textbook of
paediatrics 2016;102:869-871
• Chris AG, Sherin UD. Avery’s diseases of the newborn. 2012; 29:356-357
• El-Dib M, Narang S, Lee E, Massaro AN, Aly H. Red blood cell transfusions,
feeding and necrotizing enterocolitis. J Perinatol. 2011;31:183–187.
• Martin CR, Dammann O, Allred EN, et al. Neurodevelopment of extremely
preterm infants who had necrotizing enterocolitis with or without late
bacteremia. J Pediatr. 2010;157:751–756.
• Schanler RJ, Abrams SA, Kim MS. Clinical features and diagnosis of
necrotizing enterocolitis in newborns(internet). 2016 Nov. Available from:
https://www-uptodate-com.proxy.library.rcsi.ie/contents/clinical features-
and-diagnosis-of-necrotizing-enterocolitis-in-newborns.
• Tracia LG, Douglas CM, Fabien GE. Neonatology management, procedures,
on call problems, diseases and drugs 2013; 113:769-775

3. outline
• Introduction/definition
• Epidemiology
• Pathophysiology
• Risk Factors
• Clinical Presentation
• Staging
• Diagnosis
• Management
• Complications
• Prevention
• prognosis

4. introduction
• Necrotising Enterocolitis (NEC) is an ischaemic
and inflammatory necrosis of the bowel primarily
affecting premature neonates after the initiation
of enteral feeding.
• In term infants it often occurs secondary to an
underlying disease.
• It is the most common life threatening
emergency of the GIT in the neonatal period
• It is characterized by varying degrees of mucosal
and transmural necrosis of the intestine.

5. DEFINITION
• Acquired neonatal disorder representing an
end expression of serious intestinal injury
after a combination of Vascular, mucosal,
metabolic and other unidentified injury to a
relatively immature gut

6. EPIDEMIOLOGY
• A. NEC is predominantly a disorder of preterm
infants, with an incidence of :
– 6-10% in infants weighing <1.5 kg.
– The incidence increases with decreasing gestational
age.
– Seventy to 90% of cases occur in high-risk low birth
weight infants.
– 10-25% occur in full-term newborns.
– Infants with NEC represent 2-5% of neonatal intensive
care unit (NICU) admissions.
• B. NEC occurs sporadically or in epidemic clusters.

7. Pathophysiology.
• No single unifying theory satisfactorily explains it.
• The generally accepted pathophysiologic sequence
of events resulting in overt clinical disease is
thought to involve:
– initial ischemic or toxic mucosal damage
– loss of mucosal integrity.
– substrate enhanced bacterial proliferation
– invasion of the damaged intestinal mucosa by gas-
producing organisims (methane and hydrogen)
– intramural bowel gas (pneumatosis intestinalis).
– transmural necrosis or gangrene
– perforation and peritonitis.

8. GUT ISCHEMIA
• Umbilcal catherisation
• PDA (Left to right shunt)
• Congenital heart disease
• Indomethacin (sphlancnic
vasoconstriction)
• Maternal Cocaine Use,
Hypertension
• Transfusion of packed cells

9. IMPAIRED HOST DEFENSE
Intestinal host defense include- physical barrier, immune
cells and multiple biochemical factors
• Impaired intestinal permeability
• Inadequate intestinal mucus
• Impaired gastric motility
• Compromised immunological factors
• Suppressed biochemical factors essential for gut
maturation (lactoferin, glutamine, growth factors, epo,
gastric acid)
• Impaired intestinal humoral immunity in formula-fed
infants (igA deficiency)

10. ENTERAL FEEDING
• Osmolar stress
• By-product synthesis of toxic short chain FAs
• Intestinal Distention

11. BACTERIAL COLONISATION
• Gut of healthy term nursing infants rich with
bifidobacteria and lactobacillus enhanced by presence
of oligosaccharides
• Immature gut flora stimulates pro-inflammatory
response following formula feeding, ischemic stress
• Normally prevents against bacterial invasion
• Overzealous pro-inflammatory response and
inadequate anti-inflammatory signaling leads to
intestinal inflammation and necrosis and bacterial
translocation
• Preterms are more prone to pro-inflammatory
signaling

12. AETIO-PATHOGENESIS
• Ischemic or toxic mucosal damage
• Loss of mucosal integrity
• Substrate enhanced bacterial proliferation
• Invasion of damaged intestinal mucosa by gas
producing organisms
• Intramural bowel gas
• Transmural necrosis or gangrene
• Perforation and peritonitis

13. Risk FactorsFactors
• Prematurity
• Asphyxia and acute cardiopulmonary disease
• Enteral feedings.
• Polycythemia and hyperviscosity syndromes.
• Blood transfusions.
• Feeding volumes: timing of enteral feeding, and rapid
advancement in enteral feedings.
• Enteric pathogenic microorganisms. Bacterial and viral
pathogens, eg E coli, Klebsiella, Enterobacter, clostridium
perfringes, Staphylococcus epidermidis, astrovirus,
norovirus, rotavirus etc
• Drugs- Indomethacin
• Maternal cigarette smoking

14. CLINICAL FEATURES
• Onset in 2nd or 3rd week of life
• Systemic clinical features include
• Lethargy
• Apnea
• Respiratory distress
• Temperature instability
• “not right”
• Acidosis(metabolic and or respiratory)
• Glucose instability
• Poor perfusion/shock
• DIC
• *positive results of blood culture

15. Clinical features
• GI symptoms and signs include
• Abdominal distention
• Abdominal tenderness
• Feeding intolerance
• Delayed gastric emptying
• Vomiting
• Occult to gross blood in stool
• Change in stool pattern/diarrhea
• Abdominal mass
• Erythema of abdominal wall

16. Modified bells staging
• The modified bells staging criteria classifies NEC
according to clinical and radiographic
presentation.
• A, stage1-suspected NEC
• 1. systemic signs-non specific including apnea,
bradycardia, lethargy and temperature instability
• 2. intestinal findings-Feeding intolerance,
recurrent gastric residuals and abdominal
distension.
• 3. Radiographic findings- Normal or non specific

17. • Stage 2: PROVEN NEC
• 1. Systemic signs: Include stage 1 +
abdominal tenderness and thrombocytopenia
• 2. Intestinal finding: Prominent abdominal
distension, tenderness, bowel wall edema,
absent bowel sounds and grossly bloody
stools
• 3. Radiologic Findings: Pneumatosis with or
without portal venous gas

18. • Stage 3: Advanced NEC
• 1. Systemic signs-Respiratory and metabolic
acidosis, respiratory failure, hypotension,
decreased urine output, shock, neutropenia
and DIC
• 2. Intestinal finding-Tense discoloured
abdomen with spreading abdominal wall
edema, induration and discouloration
• 3. Radiographic findings-Pneumoperitoneum

21. Laboratory studiesLaboratory studies
• The following should be performed as baseline studies
• 1. Full blood cell count (FBC) with differential. The white blood cell
(WBC) may be normal but is more frequently either elevated, with a
shift to the left, or low (leukopenia).
• 2. Platelet count. Thrombocytopenia is seen. 50% of patients with
proven NEC have platelet counts <50,000/uL.
• 3. Blood culture for aerobes, anaerobes, and fungi (Candida sp).
• 4. Stool screening for occult blood.
• 5. Arterial blood gas measurements. Metabolic or combined acidosis
or hypoxia may be seen.
• 6. Electrolyte panel. hypo- or hypernatremia, and hyperkalemia are
common.
• 7. Stool cultures for rotaviruses and enteroviruses
• 8. C-RP
• 9. Coagulation studies. Including PT, PTT, fibrinogen and fibrin
degradation products

22. Imaging
• Plain abdominal X-ray
• Lateral decubitus and cross table lateral
studies of the abdomen
• Abdominal USS

23. • Supportive for NEC. : Abnormal bowel gas
patterns, ileus, a fixed sentinel loop of bowel, or
areas suspicious for pneumatosis intestinalis.
• Confirmatory of NEC (1) intramural bowel gas
(pneumatosis intestinalis) and (2) intrahepatic
portal venous gas (in the absence of an umbilical
venous catheter).
• 2. Lateral decubitus and cross-table lateral
studies of the abdomen. These studies are more
likely to demonstrate a pneumoperitoneum.

24. PNEUMATOSIS INTESTINALIS

25. PORTAL VENOUS GAS

26. PNEUMO-PERITONEUM

27. RADIOLOGICAL FINDINGS IN NEC
• Pneumatosis Intestinalis
• Portal venous Gas
• Pneumo-peritoneum

28. MANAGEMENT
The goal is to prevent progression of disease, intestinal
perforation, and shock:
• 1. Nothing by mouth to allow gastrointestinal rest.
• 2. Use of a nasogastric tube (on low intermittent suction) to keep the
bowel decompressed.
• 3. Close monitoring of vital signs and abdominal circumference.
• 4. Removal of the umbilical catheter
• 5. Antibiotics.
• 6. Monitoring for gastrointestinal bleeding. Check all gastric aspirates and
stools for blood.
• 7. Strict monitoring of fluid intake and output. Try to maintain urine output
of 1-3 mL/kg/h.
• 8. Removal of potassium from intravenous fluids in the presence of
hyperkalemia or anuria.
• 9. Laboratory monitoring. Check FBC, platelet count, and electrolyte panel
every 12-24 h until stable, PCT.
• 10. Septic workup.
• 11. Radiologic studies

29. ManagementMANAGEMENT
Stage 1:
• If all cultures are negative and the infant has improved
clinically, antibiotics can be stopped after 3 days. The infant
may also be fed after 3 days if clinically improved.
Stages IIA and B
1. Basic NEC protocol, including antibiotics for 10 days
2. NPO for 2 weeks. Oral feedings may be started 7-10 days
after radiographic resolution of pneumatosis.
3. Continue and advance TPN to achieve a caloric intake of 90-
110 kcal/ kg/day.
4. Respiratory support.
5. Fluid and electrolyte management.
6. Surgical consultation is required.
7. Low-dose dopamine infusion.

30. Management
• Stage III
• 1. Basic NEC protocol.
• 2. Plus stage II management.
• 3. Blood pressure support. Refractory hypotension is
common and multifactorial in origin.
• Treatment includes replacement of ongoing fluid losses,
volume expansion with colloids and vasopressors such as
dopamine
• The goal is to maintain adequate mean blood pressure
and urine output (1-3 mL/kg/h).
• 4. Progressive leukopenia, granulocytopenia, and
thrombocytopenia usually parallel . Blood and platelet
transfusions are frequently needed.

31. INDICATIONS FOR SURGERY
• Pneumoperitoneum(absolute)
• Positive result of abdominal paracentesis
• Failure of medical management
• Fixed dilated bowel loop on Serial Xray
• Abdominal wall erythema
• Palpable abdominal mass

32. COMPLICATIONS
• Bowel perforation
• Dyselectrolytemia
• Hypo/hyperglycemia
• Anemia
• DIC
• Sepsis
• Post-op complications
• Intestinal strictures
• Short bowel syndrome
• Recurrence of NEC(5% of cases)
• Death

33. DIFFERENTIAL DIAGNOSIS
• Sepsis
• Infectious Enteritis
• Intestinal Obstruction
• Isolated intestinal perforation

34. PREVENTION
• Exclusive breastfeeding
• Early Trophic feeding in pre-terms
• Probiotics
• Antibiotic prophylaxis
• Avoid prolonged empiric antibiotic use.

35. PROGNOSIS
• Medical management fails in about 20-40%
• 20-30% die
• 50% will require surgery
• 10% develop long term complications

36. CONCLUSION
• NEC is a common multifactorial acquired life
threatening emergency in newborns which
may require a multi-disciplinary approach
• High index of suspicion is necessary for early
diagnosis and prevention of complications

37. THANK YOU FOR YOUR TIME