NICU NEC.pptx
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This document provides information about necrotizing enterocolitis (NEC) for physicians. It covers the objectives, risk factors, pathogenesis, clinical presentation, diagnosis, treatment and prognosis of NEC. NEC is a disease that primarily affects premature infants and causes necrosis of the intestinal tissue. The main risk factors are prematurity, formula feeding and circulatory instability. Clinically, infants may present with feeding intolerance and abdominal distension. Diagnosis involves radiological evidence of pneumatosis intestinalis or portal venous gas. Treatment involves bowel rest, antibiotics and surgery for severe or perforated cases. Outcomes depend on severity but mortality can be over 50% for cases involving perforation.
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NICU NEC.pptx
- 1. NECROTIZING ENTEROCOLITIS Dr. Yvonne N. Nyatundo NICU – Kijabe Hospital 29/08/22
- 2. OBJECTIVES • Ability to diagnose and treat the signs and symptoms of NEC • Ability to evaluate radiographs for the classic findings of NEC • List several long-term complications associated with NEC
- 3. NECROTIZING ENTEROCOLITIS • a disorder characterized by ischemic necrosis of the intestinal mucosa, which is associated with severe inflammation, invasion of enteric gas forming organisms, and dissection of gas into the bowel wall and portal venous system • Time of onset is inversely related to gestational age/birthweight
- 4. NECROTIZING ENTEROCOLITIS • Epidemiology: – most common gastrointestinal emergency in preterm infants(>90% in <1500g at <32 GA) – leading cause of emergency surgery in neonates – overall incidence: 2-7.5% in most NICU’s – Incidence decreases with incr. GA and BW • 10% of all cases occur in term infants
- 5. NECROTIZING ENTEROCOLITIS • Epidemiology: – 10x more likely to occur in infants who have been fed – Incidence incr. 5-fold in ELBW preterms – males = females – blacks > whites – mortality rate: >50% Depending on severity – 50% of survivors experience long-term sequelae
- 6. NEC- RISK FACTORS • Prematurity • VLBW <1500g • Sepsis • Enteral feeds • Bovine milk formula • non-human milk feeding – MPA, FPIES • Circulatory instability – HIE , CHDs, perinatal asphyxia, FGR • Early Atbc Rx in preterms within 1st 14DOL or >5d
- 7. RISK FACTORS • Prematurity: * primary risk factor – 90% of cases are premature infants – immature gastrointestinal system • mucosal barrier • poor motility – immature immune response – impaired circulatory dynamics
- 8. RISK FACTORS • Infectious Agents: – usually occurs in clustered epidemics – normal intestinal flora • E. coli • Klebsiella spp. • Pseudomonas spp. • Clostridium difficile • Staph. Epi • Viruses
- 9. RISK FACTORS • Inflammatory Mediators: – involved in the development of intestinal injury and systemic side effects • neutropenia, thrombocytopenia, acidosis, hypotension – primary factors • Tumor necrosis factor (TNF) • Platelet activating factor (PAF) • LTC4 • Interleukin 1& 6
- 10. RISK FACTORS • Circulatory Instability: – Hypoxic-ischemic injury • poor blood flow to the mesenteric vessels • local rebound hyperemia with re-perfusion • production of O2 radicals – Polycythemia • increased viscosity causing decreased blood flow • exchange transfusion
- 11. RISK FACTORS • Enteral Feedings: – > 90% of infants with NEC have been fed – provides a source for H2 production – hyperosmolar formula/medications – aggressive feedings • too much volume • rate of increase – >20cc/kg/day
- 12. RISK FACTORS • Enteral Feedings: – immature mucosal function • malabsorption – breast milk may have a protective effect • IGA • macrophages, lymphocytes • complement components • lysozyme, lactoferrin • acetylhydrolase
- 13. QUESTION • WHAT ARE OTHER PROTECTIVE FACTORS IN NEC?
- 14. NECROTIZING ENTEROCOLITIS • Pathology: • primarily due to changes from severe intestinal inflammation and infarction • specific findings vary ranging from mucosal injury to full-thickness bowel necrosis and perforation
- 15. NECROTIZING ENTEROCOLITIS • Pathology: – most commonly involved: terminal ileum and proximal colon, entire GI affected in severe cases – GROSS: • bowel appears irregularly dilated with hemorrhagic or ischemic areas of frank necrosis – focal or diffuse – MICROSCOPIC: • mucosal edema, hemorrhage and ulceration
- 17. NECROTIZING ENTEROCOLITIS • MICROSCOPIC: – minimal inflammation during the acute phase • increases during revascularization – granulation tissue and fibrosis develop • stricture formation – microthrombi in mesenteric arterioles and venules
- 18. NECROTIZING ENTEROCOLITIS • MICROSCOPIC: • The major histologic findings are: • mucosal edema, hemorrhage, and transmural bland necrosis. • Others; acute inflammation, secondary bacterial infiltration, and subserosal collections of gas along the mesenteric border. • Vascular thrombi are rare.
- 20. NECROTIZING ENTEROCOLITIS • Pathophysiology: • available evidence supports a multifactorial mechanism that requires the concurrent presence of an immature GI tract and immune system (incr. susceptibility), triggers that lead to dysbiosis (disruption of the normal intestinal bacterial flora, resulting in incr. growth of potentially pathogenic bacteria), and an exaggerated inflammatory host response with release of cytokines and chemokines in the presence of R/Fs
- 23. 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
- 24. CLINICAL PRESENTATION Gestational age: < 30 wks 31-33 wks > 34 wks Full term Age at diagnosis: 20 days 11 days 5.5 days 3 days *Time of onset is inversely related to gestational age/birthweight
- 25. CLINICAL PRESENTATION Gastrointestinal: Feeding intolerance Abdominal distention Abdominal tenderness Emesis Occult/gross blood in stool Abdominal mass Erythema of abdominal wall Systemic Lethargy Apnea/respiratory distress Temperature instability Hypotension Acidosis Glucose instability DIC Positive blood cultures
- 26. CLINICAL PRESENTATION Sudden Onset: Full term or preterm infants Acute catastrophic deterioration Respiratory decompensation Shock/acidosis Marked abdominal distension Positive blood culture Insidious Onset: Usually preterm Evolves during 1-2 days Feeding intolerance Change in stool pattern Intermittent abdominal distention Occult blood in stools
- 27. NEC • While gastric residuals are often seen in early NEC, there is no evidence that routine measurement of gastric residual volumes in asymptomatic infants is a useful guide to prevent or detect the onset of NEC, or help to advance feeds
- 28. BELL STAGING CRITERIA STAGE CLINICAL X-RAY TREATMENT I. Suspect NEC Mild abdominal distention Poor feeding Emesis Mild ileus Medical Work up for Sepsis II. Definite NEC The above, plus Marked abdominal distention GI bleeding Significant Ileus Pneumatosis Intestinalis PVG Medical III. Advanced NEC The above, plus Unstable vital signs Septic Shock Pneumo- Peritoneum Surgical
- 29. BELL STAGING CRITERIA STAGE CLINICAL X-RAY TREATMENT I. Suspect NEC Mild abdominal distention Poor feeding Emesis Mild ileus Medical Work up for Sepsis II. Definite NEC The above, plus Marked abdominal distention GI bleeding Significant Ileus Pneumatosis Intestinalis PVG Medical III. Advanced NEC The above, plus Unstable vital signs Septic Shock Pneumo- Peritoneum Surgical
- 30. RADIOLOGICAL FINDINGS • Pneumatosis Intestinalis – hydrogen gas within the bowel wall • product of bacterial metabolism a. linear streaking pattern • more diagnostic b. bubbly pattern • appears like retained meconium • less specific
- 31. RADIOLOGICAL FINDINGS • Portal Venous Gas – extension of pneumatosis intestinalis into the portal venous circulation • linear branching lucencies overlying the liver and extending to the periphery • associated with severe disease and high mortality- no evidence supporting this
- 32. RADIOLOGICAL FINDINGS • Pneumoperitoneum – free air in the peritoneal cavity secondary to perforation • falciform ligament may be outlined – “football” sign – surgical emergency
- 33. RADIOLOGICAL FINDINGS • Sentinel bowel loops • Doppler ultrasonography is increasingly used to diagnosis NEC especially when there are equivocal findings on abdominal radiography. • Contrast enema: Contraindicated — Contrast enemas are not recommended if NEC is suspected, as it may result in bowel perforation with extravasation of contrast material into the peritoneum.
- 34. LABORATORY FINDINGS • CBC – neutropenia/elevated WBC – Thrombocytopenia, anemia • Acidosis - BGA – metabolic • Hyperkalemia – increased secondary to release from necrotic tissue
- 35. LABORATORY FINDINGS • DIC • Positive cultures – Blood – 20% +ve – CSF – urine – Stool diagnostic abdominal paracentesis
- 36. DDX • INFECTIOUS ENTERITIS • SIP –bluish disc. Of abd wall, absent P. I • ANATOMIC –Hirschsprung, ileal atresia, volvulus • ANAL FISSURES • Cow’s milk protein allergy • Neonatal appendicitis – laparotomy • FPIES- leukocytosis, thrombocytosis, eosinophilia
- 37. TREATMENT • Supportive care – bowel rest, gastric decompression, nutrition, cvs and resp support • Empiric antibiotic therapy – bcx first, antibiogram guided • Serial examinations and close lab and radiologic monitoring
- 38. TREATMENT • Stop enteral feeds – re-start or increase IVF • Nasogastric decompression • Antibiotics – Amp/Gent(amikacin)+metronidazole/clindamyc in; Amp+Cefotaxime/cefepime +metronidazole; monoRx: piptaz; meropenem; Vanc- MRSA; Fungal – Fluc/Amph B – Clindamycin • suspected or proven perforation
- 39. TREATMENT • Bells stage 1 – may choose to stop atbcs early and resume feeds depending on course of d’se • Bells stage 2 or > - complete 10-14 days even with neg cx unless complicated by abdominal abscess formation
- 40. TREATMENT • Surgical Consult – suspected or proven NEC – indications for surgery: • portal venous gas; pneumoperitoneum • clinical deterioration – despite medical management • positive paracentesis • fixed intestinal loop on serial x-rays • erythema of abdominal wall
- 41. TREATMENT • Labs: q12-24hrs – CBC, electrolytes, DIC panel, blood gases • X-rays: 12-24hrs – AP, left lateral decubitus or cross-table lateral, supine • Supportive Therapy – fluids, blood products, pressors, mechanical ventilation
- 42. PROGNOSIS • Depends on the severity of the illness • Mortality 12.5%, perforation 20-4-% • Associated with late complications * Colonicstrictures – short-gut syndrome – Malabsorption, delayed growth – fistulas – Abscess – PNALD- parenteral nutrition assoc LD * MOST COMMON
- 43. CASES • DOL 18 Prem male BGA 28 wks CGA 30+3wks BWT 920g PWT 880g CWT 850g • spiked fever overnight 38.8 , had 1 episode of vomiting in the morning with abdominal distension
- 44. CASES • Attempted gastric aspirate revealed same EBM-12cc that had been fed 3 hours earlier • *** • Was passing non bloody stool • Bowel sounds heard , abdomen soft, distended
- 46. CASES • plan keep NPO for 48hrs ct IVF • Babygram xray CBC CRP K+ BCX Full septic w/up UA/UCX, CSF analysis start piptaz 100mg/kg/dose 92mg TDS +amikacin 18mg/kg/dose 16mg q48h while awaiting CSF
- 52. THANK YOU
Editor's Notes
- In retrospective studies, term infants who develop NEC typically receive non-human milk feeding and have a preexisting illness
- Typically occurs in the second to third week of life in premature, formula-fed infants, is characterized by variable damage to the intestinal tract, ranging from mucosal injury to full-thickness necrosis and perforation NEC affects close to 10% of infants who weigh less than 1500 g, with mortality rates of 50% or more depending on severity,
- Non-human milk feedings and rarely components in human milk may trigger a sensitivity or allergic response (eg, food protein-induced enterocolitis syndrome or milk protein allergy) FPIES
- 6 weeks after preterm birth, a female infant who was being treated in the neonatal intensive care unit was found to have severe abdominal distention. She had been born at 23 weeks of gestation by emergency cesarean section because of premature rupture of membranes; her weight was 520 g at birth. She had been growing well with a combination of enteral feeding and parenteral nutrition. At the time that the abdominal distention developed, plain radiography showed dilated loops of small bowel, and abdominal ultrasonography indicated possible perforation. Exploratory laparotomy was performed, and a diagnosis of necrotizing enterocolitis was made. Necrotizing enterocolitis is characterized by inflammation of the intestinal mucosa and can result in bowel necrosis and perforation; it remains an important cause of complications and death in neonates, especially among preterm infants. The affected bowel segment was resected, and an ileostomy was performed. Four months later, the patient underwent ileostomy reversal and was able to feed fully by mouth at the time of discharge. At the 2-year follow-up, she was growing well.
- multifactorial
- multifactorial
- Commensal bacteria play a symbiotic role with the intestine through toll-like receptors by regulating the expression of genes involved in intestinal maturation, and function (eg, barrier, digestion, angiogenesis, and production of IgA), and protection against more pathologic organisms
- Age of onset inversely related to gestational age at birth. In term infants, the reported median age of onset is 1-3 days, but onset may occur as late as age 1 month. It remains uncertain why there is an inverse relationship between GA and timing of the presentation of NEC. Proposed explanations include that very preterm infants take longer to begin enteral feeding and therefore longer to reach a critical amount of feeding mass needed for the development of NEC and that changes with development and exposures make an infant more prone to intestinal inflammation or immune dysregulation as they mature (eg, exposure to broad-spectrum antibiotics) resulting in microbial dysbiosis.
- In a single-center study of 141 infants, 74 were randomized to undergo gastric residual checks while the other half did not have residuals checked. The no residual group were able to achieve faster feeding rates and had consumed more feedings at weeks 5 and 6. This group had higher mean weights and were discharged earlier than the residual check group. In addition, there were no differences in risk for NEC, late-onset sepsis, or death