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NEC KuliahRepro
NEC KuliahRepro
Reproduction System
2010
OBJECTIVES
Ability to diagnose and treat the signs and
symptoms of NEC
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…….
From UpToDate online, Adapted from Kliegman, RM, Pediatr Res 1993; 34:701.
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:
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 DIC
wall Positive blood cultures
CLINICAL PRESENTATION
Stage IIIa IIb, but more severe, + IIb + peritonitis, Same as IIb
Advanced, Severe NEC combined respiratory & marked distension and
Bowel Intact metabolic acidosis, tenderness
neutropenia, & DIC
Stage IIIb Same as IIb Same as IIIa IIIa +
Advanced Severe NEC pneumoperitoneum
Bowel Perforated
Pneumoperitoneum
free air in the peritoneal cavity secondary to
perforation
falciform ligament may be outlined
“football” sign
surgical emergency
Pneumatosis Intestinalis
http://www.hawaii.edu/medicine/pediatrics/pemxray/v2c14.html
Pneumatosis & Dilated Loops
Pneumatosis
http://www.hawaii.edu/medicine/pediatrics/pemxray/v2c14.html
Dilated loops & Portal Air
Portal Air
Dilated
stomach &
loops of
bowel
http://www.adhb.govt.nz/newborn/TeachingResources/Radiology/AXR/NEC/NECwithPortalGasAP1.jpg
A Bad Case of NEC
Abdomin
Portal Air al free air
Pneumatosis
http://www.medicine.cmu.ac.th/dept/radiology/pedrad/case8ans.html
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
Neonatal NEC Pathology
Pneumatosis
Necrosis
http://phil.cdc.gov/PHIL_Images/02051999/00023/20G0023_lores.jpg
Prevention
Encourage breast feeding
Breast fed babies have lower incidence than
formula fed
No evidence shows that late initiation of
enteral feeding or slow rate of feeding
makes any difference
Maintain high level of suspicion
Feeding babies with NEC worsens the disease
TREATMENT
Stop enteral feeds
re-start or increase IVF
Nasogastric decompression
low intermittent suction
Antibiotics
Medical Treatment
Stage Ia
NPO x 3 days
Stage Ib - IIb/IIIa
NPO
Broad spectrum antibiotics
Cover Gram +, Gram - & Anaerobes
Ib = 3 days, IIa = 7-10 d, IIb & up = 14 d
Follow x-ray for resolution
Resume enteral feeds 10-14 days after radiographic
resolution
May require paracentesis if IIIa
Surgical Treatment
Stage IIIa - IIIb
Laparotomy
Resection of necrotic bowel
Ileostomy with mucous fistula
Subsequent re-anastamosis
May result in strictures requiring further surgery later
Peritoneal drain
Placement in NICU under local anesthetic
Used when infant is too clinically unstable for surgery
May help stabilize pt for subsequent surgery
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
Outcomes
Mortality varies with birth weight:
<1000 g = 40-100%
<1500 g = 10-44%
>2500 g = 0-20%
Morbidity/Mortality vary with severity:
Resection -> Short gut -> FTT, malabsorbtion
Strictures -> further surgery in medical and
surgical NEC
Prolonged NPO status on TPN -> cholestasis &
metabolic abnormalities