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    Necrotizing Enterocolitis: Janice Nicklay Catalan M.D

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    rianurjanah
    Necrotizing enterocolitis (NEC) is a leading cause of emergency surgery in neonates, most commonly affecting very low birth weight preterm infants. It involves inflammation and necrosis of the intestinal tissue. Clinical presentation includes feeding intolerance, abdominal distension, and systemic signs. Diagnosis is suggested on x-ray findings like pneumatosis intestinalis or portal venous gas. Treatment involves stopping feeds, antibiotics, and possible surgery for severe or worsening cases. Long term complications can include strictures and short gut syndrome.

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    Necrotizing Enterocolitis: Janice Nicklay Catalan M.D

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    rianurjanah
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    Necrotizing enterocolitis (NEC) is a leading cause of emergency surgery in neonates, most commonly affecting very low birth weight preterm infants. It involves inflammation and necrosis of the intestinal tissue. Clinical presentation includes feeding intolerance, abdominal distension, and systemic signs. Diagnosis is suggested on x-ray findings like pneumatosis intestinalis or portal venous gas. Treatment involves stopping feeds, antibiotics, and possible surgery for severe or worsening cases. Long term complications can include strictures and short gut syndrome.

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    Necrotizing enterocolitis (NEC) is a leading cause of emergency surgery in neonates, most commonly affecting very low birth weight preterm infants. It involves inflammation and necrosis of the intestinal tissue. Clinical presentation includes feeding intolerance, abdominal distension, and systemic signs. Diagnosis is suggested on x-ray findings like pneumatosis intestinalis or portal venous gas. Treatment involves stopping feeds, antibiotics, and possible surgery for severe or worsening cases. Long term complications can include strictures and short gut syndrome.

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    Download as pptx, pdf, or txt
    50 views27 pages

    Necrotizing Enterocolitis: Janice Nicklay Catalan M.D

    Uploaded by

    rianurjanah
    Necrotizing enterocolitis (NEC) is a leading cause of emergency surgery in neonates, most commonly affecting very low birth weight preterm infants. It involves inflammation and necrosis of the intestinal tissue. Clinical presentation includes feeding intolerance, abdominal distension, and systemic signs. Diagnosis is suggested on x-ray findings like pneumatosis intestinalis or portal venous gas. Treatment involves stopping feeds, antibiotics, and possible surgery for severe or worsening cases. Long term complications can include strictures and short gut syndrome.

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    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:
    – 10x 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…….
    CIRCULATORY INSTABILITY
    PRIMARY INFECTIOUS AGENTS
    Hypoxic-ischemic event
    Bacteria, Bacterial toxin, Virus, Fungus Polycythemia

    MUCOSAL INJURY

    INFLAMMATORY MEDIATORS
    Inflammatory cells (macrophage) ENTERAL FEEDINGS
    Platelet activating factor (PAF) Hypertonic formula or medication
    Tumor necrosis factor (TNF) Malabsorption, gaseous distention
    Leukotriene C4, Interleukin 1; 6 H2 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)
    • LTC4
    • 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 O2 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 H2 production
    – hyperosmolar formula/medications
    – aggressive feedings
    • too much volume
    • rate of increase
    – >20cc/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: Age at diagnosis:

    < 30 wks 20 days


    31-33 wks 11 days
    > 34 wks 5.5 days
    Full term 3 days

    *Time of onset is inversely related to gestational age/birthweight


    CLINICAL PRESENTATION
    Gastrointestinal: Systemic
    Feeding intolerance Lethargy
    Abdominal distention Apnea/respiratory distress
    Abdominal tenderness Temperature instability
    Emesis Hypotension
    Occult/gross blood in stool Acidosis
    Abdominal mass Glucose instability
    Erythema of abdominal wall DIC
    Positive blood cultures
    CLINICAL PRESENTATION
    Sudden Onset: Insidious Onset:
    Full term or preterm infants Usually preterm
    Acute catastrophic deterioration Evolves during 1-2 days
    Respiratory decompensation Feeding intolerance
    Shock/acidosis Change in stool pattern
    Marked abdominal distension Intermittent abdominal
    Positive blood culture distention
    Occult blood in stools
    BELL STAGING CRITERIA
    STAGE CLINICAL X-RAY TREATMENT

    I. Suspect Mild abdominal Mild ileus Medical


    distention Work up for
    NEC Poor feeding Sepsis
    Emesis

    II. Definite The above, plus Significant Medical


    Marked abdominal Ileus
    NEC distention Pneumatosis
    GI bleeding Intestinalis
    PVG

    III. Advanced The above, plus Pneumo- Surgical


    Unstable vital signs Peritoneum
    NEC Septic Shock
    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: q6-8hrs
    – CBC, electrolytes, DIC panel, blood gases
    • X-rays: q6-8hrs
    – 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

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