NECROTIZING ENTEROCOLITIS Janice Nicklay Catalan M D OBJECTIVES

NECROTIZING ENTEROCOLITIS Janice Nicklay Catalan M. D.

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

NECROTIZING ENTEROCOLITIS • Epidemiology: – most commonly occurring gastrointestinal emergency in preterm infants – leading cause of emergency surgery in neonates – overall incidence: 1 -5% in most NICU’s – most common in VLBW preterm infants • 10% of all cases occur in term infants

NECROTIZING ENTEROCOLITIS • Epidemiology: – 10 x more likely to occur in infants who have been fed – males = females – blacks > whites – mortality rate: 25 -30% – 50% of survivors experience long-term sequelae

NECROTIZING ENTEROCOLITIS • Pathology: – most commonly involved areas: terminal ileum and proximal colon – GROSS: • bowel appears irregularly dilated with hemorrhagic or ischemic areas of frank necrosis – focal or diffuse – MICROSCOPIC: • mucosal edema, hemorrhage and ulceration

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

NECROTIZING ENTEROCOLITIS • Pathophysiology: UNKNOWN CAUSE…….

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 C 4, Interleukin 1; 6 ENTERAL FEEDINGS Hypertonic formula or medication Malabsorption, gaseous distention H 2 gas production, Endotoxin production

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

RISK FACTORS • Infectious Agents: – usually occurs in clustered epidemics – normal intestinal flora • • • E. coli Klebsiella spp. Pseudomonas spp. Clostridium difficile Staph. Epi Viruses

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) LTC 4 Interleukin 1& 6

RISK FACTORS • Circulatory Instability: – Hypoxic-ischemic injury • poor blood flow to the mesenteric vessels • local rebound hyperemia with re-perfusion • production of O 2 radicals – Polycythemia • increased viscosity causing decreased blood flow • exchange transfusion

RISK FACTORS • Enteral Feedings: – > 90% of infants with NEC have been fed – provides a source for H 2 production – hyperosmolar formula/medications – aggressive feedings • too much volume • rate of increase – >20 cc/kg/day

RISK FACTORS • Enteral Feedings: – immature mucosal function • malabsorption – breast milk may have a protective effect • • • IGA macrophages, lymphocytes complement components lysozyme, lactoferrin acetylhydrolase

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

CLINICAL PRESENTATION Gastrointestinal: Systemic Feeding intolerance Abdominal distention Abdominal tenderness Emesis Occult/gross blood in stool Abdominal mass Erythema of abdominal wall Lethargy Apnea/respiratory distress Temperature instability Hypotension Acidosis Glucose instability DIC Positive blood cultures

CLINICAL PRESENTATION Sudden Onset: Insidious Onset: Full term or preterm infants Acute catastrophic deterioration Respiratory decompensation Shock/acidosis Marked abdominal distension Positive blood culture Usually preterm Evolves during 1 -2 days Feeding intolerance Change in stool pattern Intermittent abdominal distention Occult blood in stools

BELL STAGING CRITERIA

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

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

RADIOLOGICAL FINDINGS • Pneumoperitoneum – free air in the peritoneal cavity secondary to perforation • falciform ligament may be outlined – “football” sign – surgical emergency

LABORATORY FINDINGS • CBC – neutropenia/elevated WBC – thrombocytopenia • Acidosis – metabolic • Hyperkalemia – increased secondary to release from necrotic tissue

LABORATORY FINDINGS • DIC • Positive cultures – blood – CSF – urine – stool

TREATMENT • Stop enteral feeds – re-start or increase IVF • Nasogastric decompression – low intermittent suction • Antibiotics – Amp/Gent; Vanc/Cefotaxime – Clindamycin • suspected or proven perforation

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

TREATMENT • Labs: q 6 -8 hrs – CBC, electrolytes, DIC panel, blood gases • X-rays: q 6 -8 hrs – AP, left lateral decubitus or cross-table lateral • Supportive Therapy – fluids, blood products, pressors, mechanical ventilation

PROGNOSIS • Depends on the severity of the illness • Associated with late complications * strictures – short-gut syndrome – malabsorption – fistulas – abscess * MOST COMMON