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Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
Necrotizing Enterocolitis
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Necrotizing Enterocolitis

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prepared from clohorty …

prepared from clohorty
some slides were taken from dr. Padmesh Vadakepat presentation

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  • Clinical decision algorithm
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    • 1. Necrotizing enterocolitis - Dr.Raghavendra Babu S DNB year II JLNH&RC
    • 2. Necrotizing Enterocolitis: 􀂾 an acquired neonatal acute intestinal necrosis of unknown etiology 􀂾 NEC 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 not. 􀂾 Includes: 􀂾 NEC 􀂾 SIP (isolated spontaneous intestinal perforation) 􀂾 Viral enteritis of infancy 􀂾 Cow’s milk protein allergy
    • 3. 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  Sex, race, geography, climate has no role in determining the incidence of NEC  Prematurity is the single greatest risk factor
    • 4. Intestinal ischemia (injury) Enteral nutrition Pathogenic organisms
    • 5. Risk factors influencing NEC prediposition • Prematurity:  inflamatory propensity of the immature gut.  Decreases intestinal barrier function.  Decreased gut motility and abberent vascular regulation. • Enteral feeding:  Aggressive advancement of feeding.  Non human milk feeding • Abnormal bacterial colonization:  Prolonged emperical antibiotic therapy  Decreased commensal flora  Increased pathogenic bacteria Maternal cocaine abuse – 2.5 times increases risk
    • 6. Risk Factors: in Term Babies Limited to those that have some underlying illness or condition requiring NICU admission. • Congenital Heart Disease • Intrauterine growth restriction • Polycythemia • Hypoxic-ischemic events • The mean gestational age of infants with NEC is 30 to 32 weeks, and the infants generally are weight appropriate for gestational age. • Postnatal age at onset is inversely related to birth weight and gestational age with mean age at onset of 12 days
    • 7. PRIMARY INFECTIOUS AGENTS Bacteria, Bacterial toxin, Virus, Fungus CIRCULATORY INSTABILITY Hypoxic-ischemic event Polycythemia MUCOSAL INJURY INFLAMMATORY MEDIATORS Inflammatory cells (macrophage) Platelet activating factor (PAF) Tumor necrosis factor (TNF) Leukotriene C4, Interleukin 1; 6 ENTERAL FEEDINGS Hypertonic formula or medication Malabsorption, gaseous distention H2 gas production, Endotoxin production
    • 8. pathogenesis
    • 9. Microbiologic Flora and Infection Several organisms have been accused, but non has been proven to be causative: – Enterobacteriaceae – Enterobactersakazakii – Coagulase-negative staphylococci: SIP – Closrtidium perfringens – Candida species: SIP – Cytomegalovirus – Torovirus – HIV – Mucormycosis
    • 10. 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)
    • 11. Clinical Presentation • Course of the disease Fulminant presentation Slow, paroxysmal presentation • 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
    • 12. • 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.
    • 13. • Abdominal (enteric) signs: – Distension – Tenderness – Gastric aspirate, vomiting – Ileus – Abdominal wall erythema, induration – Ascites – Abdominal mass – Bloody stool • Systemic signs: – Respiratory distress, apnea, bradycardia – Lethargy, irritability – Temp. instability – Poor feeding – Hypotension – Acidosis – Oligurea – Bleeding diathesis
    • 14. Laboratory features • No lab test is specific for NEC • The most common triad: – Thrombocytopenia – Persistent metabolic acidosis – Severe refractory hyponatremia Serial measurements of CRP – diagnostic and prognostic • ↑WBC, ↓WBC, ↓PMN • Hyperkalemia • Stool: reducing substances, occult blood
    • 15. Blood studies: Thrombocytopenia COMMON TRIAD OF SIGNS Persistent Hyponatremia Severe Refractory Metabolic Acidosis
    • 16. Radiology studies • Abdominal X-ray: • • • • • Abnormal gas pattern, ileus Bowel wall edema Pneumatosis intestinalis Fixed position loop Intra hepatic-portal venous gas ( in the absence of UVC) • Pneumoperitonium - left lateral decubitus or crosstable lateral views
    • 17. • • Intestinal perforation. Abdominal Xray in NEC demonstrates marked distention and massive pneumoperitoneum Free air below the anterior abdominal wall.
    • 18. • Abdominal ultrasound: – Thick-walled loops of bowel with hypomotility. – Intraperitonealfluid is often present. – Intramural gas can be identified in early-stage NEC – In the presence of pneumatosisintestinalis, gas is identified in the portal venous circulation within the liver. – Color Doppler US is more accurate than abdominal radiography in depicting bowel necrosis in NEC.
    • 19. • 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.
    • 20. • MODIFIED BELL’S 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 ill,bowel intact), B (Severely ill,bowel perforated)
    • 21. • 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, gramnegative, and anaerobic organisms) should be started immediately.
    • 22. • 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.
    • 23. • MONITORING: • Sequential abdominal grith measuremet • 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.
    • 24. • 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.
    • 25. • 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.
    • 26. Initial signs of possible NEC (bell’s stage I ) •NPO •GI decompression- low constant sucton, replace output with electrolytes •CBC with differentials, blood culture, CRP, S.Electrolytes •Abdominal radiograph •Begin antibiotics Mild to Moderate (Bell’s stage II) Advanced (Bell’s Stage III) •Serial abdominal radiographs •Serial abdominal radiographs •Broad spectrum antibiotics for 7- 10 days •Broad spectrum antibiotics for 7- 10 days •NPO for 5-10 days, parentaral nutrition •NPO for 10-14 days, parentaral nutrition •Monitor electrolytes •Monitor electrolytes •Serial CBCs every 12h to 24h for 2-3 days •Serial CBCs every 12h to 24h for 2-3 days •Co-mangement with paediatric surgeon •Hemodynamic support •Monitor coagulation abnormalities and correct Indications for surgery •Intestinal perforation •Fixed adynamic loop – necrotic gut •Signs suggestive of necrotic gut –persistent severe thrombocytopenia, severe metabolic acidosis
    • 27. • 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.
    • 28. • 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.
    • 29. • 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.

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