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Dr. Ufaque Batool Korai
House Officer.
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
OBJECTIVES
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:
NECROTIZING ENTEROCOLITIS
UNKNOWN
CAUSE…….
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
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
RISK FACTORS
Gestational age:
< 30 wks
31-33 wks
> 34 wks
Full term
Age at diagnosis:
20 days
11 days
5.5 days
3 days
CLINICAL PRESENTATION
*Time of onset is inversely related to gestational age/birthweight
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
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
CLINICAL PRESENTATION
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
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
RADIOLOGICAL 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
LABORATORY FINDINGS
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
TREATMENT
Depends on the severity of the illness
Associated with late complications
*strictures
short-gut syndrome
malabsorption
fistulas
abscess
PROGNOSIS
* MOST COMMON
NEC

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NEC

  • 1. Dr. Ufaque Batool Korai House Officer.
  • 2. 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 OBJECTIVES
  • 3. 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
  • 4. 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
  • 5. 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
  • 6. 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
  • 8. 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
  • 9. 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
  • 10. Infectious Agents: usually occurs in clustered epidemics normal intestinal flora E. coli Klebsiella spp. Pseudomonas spp. Clostridium difficile Staph. Epi Viruses RISK FACTORS
  • 11. 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
  • 12. 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
  • 13. 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
  • 14. Enteral Feedings: immature mucosal function malabsorption breast milk may have a protective effect IGA macrophages, lymphocytes complement components lysozyme, lactoferrin acetylhydrolase RISK FACTORS
  • 15. Gestational age: < 30 wks 31-33 wks > 34 wks Full term Age at diagnosis: 20 days 11 days 5.5 days 3 days CLINICAL PRESENTATION *Time of onset is inversely related to gestational age/birthweight
  • 16. 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 CLINICAL PRESENTATION
  • 17. 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 CLINICAL PRESENTATION
  • 18. 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
  • 19. 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
  • 20. 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
  • 21. Pneumoperitoneum free air in the peritoneal cavity secondary to perforation falciform ligament may be outlined “football” sign surgical emergency RADIOLOGICAL FINDINGS
  • 24. Stop enteral feeds re-start or increase IVF Nasogastric decompression low intermittent suction Antibiotics Amp/Gent; Vanc/Cefotaxime Clindamycin suspected or proven perforation TREATMENT
  • 25. 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
  • 26. 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 TREATMENT
  • 27. Depends on the severity of the illness Associated with late complications *strictures short-gut syndrome malabsorption fistulas abscess PROGNOSIS * MOST COMMON