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Nec by Dr Achumie
- 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.
- 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
Notas del editor
- Underlying diseases in term infants include birth asphyxia, downs syndrome, congenital heart disease, rota virus and hirschprungs disease.
- Although NEC is a multifactorial disease primarily associated with intestinal immaturity, the concept of “risk factors” for NEC is controversial. The triad of intestinal ischemia (injury), enteral nutrition (metabolic substrate), and bacterial translocation has classically been linked to NEC
- The generally accepted pathophysiologic sequence of events resulting in overt clinical disease is thought to involve an initial ischemic or toxic mucosal damage resulting in a loss of mucosal integrity. Then, with the availability of suitable substrate provided by enteral feedings, there is bacterial proliferation Followed by invasion of the damaged intestinal mucosa by gas-producing (methane and hydrogen) organisms that cause intramural bowel gas (pneumatosis intestinalis). This sequence of events may then progress to transmural necrosis or gangrene of the bowel and finally to perforation and peritonitis.
- Following stressful condition basal intestinal vascular resistance is is elevated in fetus leading to reduced intestinal blood flow This resitance decreases significantly after birth and allows for rapid increase in intestinal blood flow This change is depends on a balance between dilators and constrictor neurotransmitters and the myogenic response Preterms have abnormal regulation od intestinal circulation which predisposes them to NEC 2. Umbilical catheterisation increaxes portal venous pressure which is transmitted to the illiac and mesenteric vessels 3. Left to right shunt compromises blood flow to the intestines 4. Indomethacin alters intestinal autoregulation 5. Rapid correction of anemia alters intestinal autoregulation
- Physical barriers include mucous membrane, epith tight junctions and mucin Immune cells like PMNL, Macrophages, eosinophils and lymphocytes Impaired int perm allows translocation of ig, proteins and carbs to systemic circ Mucin prevents bacterial and toxin invasion Compromised immun factors- intestinal lymphocytes are decreased in neonates and do not approach adult levels till3-4wks
- Apoptosis of cells Mucosal permeability Bacterial translocation Neutropihl infiltration Infarctive necrosis
- The greatest risk factor for NEC is prematurity. The disorder probably results from an interaction between loss of mucosal integrity due to a variety of factors (ischemia, infection, inflammation) and the host’s response to that injury (circulatory, immunologic, inflammatory), leading to necrosis of the affected area
- Risk factors A. Prematurity. There is an inverse relationship between risk and gestational age. The lower the gestational age, the greater is the risk because of the immaturity of the circulatory, gastrointestinal, and immune systems. B. Asphyxia and acute cardiopulmonary disease lead to low cardiac output and diminished perfusion states, resulting in redistribution of cardiac output away from the mesenteric circulation and causing episodic intestinal ischemia. C. Enteral feedings. NEC is rare in unfed infants. About 90-95% of infants with NEC have received at least one enteral feeding. The explanations for this include the following: 1. Enteral feeding provides necessary substrate for proliferation of enteric pathogens. 2. Hyperosmolar formula or medications cause altered mucosal permeability and direct mucosal damage. 3. There is a loss or lack of immunoprotective factors in commercially prepared formulas and in stored breast milk. 4. Breast-feeding significantly lowers the risk of NEC.
- The onset of NEC is usually in the 2nd or 3rd wk of life but can be as late as 3 mo In VLBW infants. Age of onset is inversely related to gestational age. The first signs of impending disease may be nonspecific, including lethargy and temperature instability, or related to gastrointestinal pathology, such as abdominal distention and gastric retention. Abdominal distention Abdominal tenderness Feeding intolerance Delayed gastric emptying Vomiting Occult/gross blood in stool Change in stool pattern/diarrhea Abdominal mass Erythema of abdominal wall SYSTEMIC Lethargy Apnea/respiratory distress Temperature instability “Not right” Acidosis (metabolic and/or respiratory) Glucose instability Poor perfusion/shock Disseminated intravascular coagulopathy Positive results of blood cultures
- Presence of free air is indicative of intestinal perforation Serial radiographic studies of the abdomen should be obtained every 6-8 hours in the presence of pneumatosis intestinalis or portal venous gas to look for pneumoperitoneum as they are at risk for perforation within 48-72 hours Abd uss can detect portal venous gas not detected on radiographs and should be used in the presence of non specific clinical and radiographic findings.
- Typical abdominal radiographic appearance of intestinal pneumatosis seen in necrotizing enterocolitis: dark concentric rings around the bowel loops in the right upper quadrant
- This radiograph displays the presence of portal gas, which is seen as linear dark streaks within the hepatic density.
- Start ampicillin and gentamicin or cefotaxime intravenously. Add anaerobic coverage (clindamycin or metronidazole [Flagyl]) if peritonitis or perforation is suspected
- Start ampicillin and gentamicin or cefotaxime intravenously. Add anaerobic coverage (clindamycin or metronidazole [Flagyl]) if peritonitis or perforation is suspected
- Indications for surgery include evidence of perforation on abdominal x-ray (pneumoperitoneum) or positive result of abdominal paracentesis (stool or organism on Gram stain preparation from peritoneal fluid). Failure of medical management, a single fixed bowel loop on radiographs, abdominal wall erythema, and a palpable mass are relative indications for exploratory laparotomy. Ideally, surgery should be performed after intestinal necrosis develops but before perforation and peritonitis occur. In unstable premature infants with perforated NEC, peritoneal drainage can be cautiously considered as an alternative to exploratory laparotomy, although the best surgical approach in these infants remains unresolved. The type of surgical operation did not
- . Early postoperative complications include wound infection, dehiscence, and stomal problems (prolapse, necrosis). Later complications include intestinal strictures, which develop at the site of the necrotizing lesion in approximately 10% of surgically or medically managed patients. Resection of the obstructing stricture is curative. After massive intestinal resection, complications from postoperative NEC include shortbowel syndrome (malabsorption, growth failure, malnutrition), complications related to central venous catheters (sepsis, thrombosis), and cholestatic jaundice. Preterm infants with NEC who require surgical intervention or who have concomitant bacteremia are at increased risk for adverse growth and neurodevelopmental outcome.
- Idiopathic focal intestinal perforation can occur spontaneously or after the early use of postnatal steroids and indomethacin. Pneumoperitoneum develops in such patients, but they are usually less ill than those with NEC. Patients with isolated intestinal perforation (not related to NEC) tend to have a lower birthweight, are less likely to be receiving oral feeding, and are prone to perforation at an earlier postnatal age than are patients with perforation related to NEC. In many patients with isolated intestinal perforation treated by drainage, no further surgical procedure is needed; a small subgroup may require later surgery to repair an intestinal stricture or fistula.
- Newborns exclusively breastfed have a reduced risk of NEC. There have been concerns about early and aggressive increase in feeding volumes in raising the risk of NEC in VLBW infants, although a safe feeding regimen remains unknown. Gut stimulation protocols consisting of minimal enteral feeds followed by judicious volume advancement decreased the incidence of NEC in smaller study cohorts, but significant benefits were not detected in a meta-analysis of all randomized studies. In other studies, slow advancement or delayed introduction of enteral feedings did not protect against NEC. Emerging evidence indicates that the use of inhibitors of gastric acid secretion (H2-receptor blockers, proton pump inhibitors) or prolonged empirical antibiotics in early neonatal period is associated with increased risk of NEC. Prophylactic enteral antibiotics reduced the risk of NEC in a study but although concerns about adverse outcomes persist, particularly related to the development of resistant bacteria. Extensive data and metaanalyses show that probiotic preparations decrease the incidence of severe NEC (stage II or higher) and mortality in preterm infants but an FDA-approved preparation is not available.
- Medical management fails in approximately 20-40% of patients with pneumatosis intestinalis at diagnosis; of these, 10-30% die. Early postoperative complications include wound infection, dehiscence, and stomal problems (prolapse, necrosis). Later complications include intestinal strictures, which develop at the site of the necrotizing lesion in approximately 10% of surgically or medically managed patients. Resection of the obstructing stricture is curative. After massive intestinal resection, complications from postoperative NEC include shortbowel syndrome (malabsorption, growth failure, malnutrition), complications related to central venous catheters (sepsis, thrombosis), and cholestatic jaundice. Preterm infants with NEC who require surgical intervention or who have concomitant bacteremia are at increased risk for adverse growth and neurodevelopmental outcome.