necrotizing enterocolitis 1shri.ppt

Definition
Necrotizing enterocolitis
An aquired neonatal acute intestinal
necrosis of unknown etiology.
NEC is neither a uniform nor a well defined
disease entity.

Epidemiology:
Epidemiology
 Incidence: 0.3-2.4 /1000 live births
2.5% of all NICU admissions
5-10% of VLBW infants
 over 90 % of cases occur in preterm babies.
 About 10 % occur in term newborns:essentially
limited to those having some underlying illness or
condition requiring NICU admission.

Epidemiology
 Sporadic or epidemic clusters
 Sex,race,geography,climate,season: no role
 male VLBW infants are at a greater risk of death.
 Black infants: increased Risk of NEC , and its
associated mortality.

 Prematurity is the single greatest risk factor
 The risk is inversely related to birth weight and
gestational age.

 Familial
 Twins
 Gene polymorphism
 VEGF( VASCULAR ENDOTHELIAL GROWTH
FACTOR): VEGF G + 450polymorphism might be
associated with a higher risk of preterm birth and
that VEGF C-2578A polymorphism may participate
in the development of perinatal complications
such as NEC and ARF.

 G-6-PD deficiency
 Indomethacin:
 Metaanalysis 2007 showed that recent exposure
to indomethacin was associated with NEC.
 Indomethacin in early life :associated withSIP.
 DEXAMETHASONE
 H2 BLOCKERS
 Co –amoxiclav
 Acyclovir

 Maternal cocaine abuse:
 It is very potent vasoconstrictor
 Prenatal exposure increase risk of NEC by 2.5 times.
 Greater need for surgical intervention(72%) , higher
incidence of gangrene(54%) , higher mortality(54%) in
infants with prenatal cocaine exposure.

A.Initiation of disease
1. Impaired gut barrier
2. Infectious agent
3. Circulatory instability
B.Progression of disease

A-initiation of disease
1-impaired gut barrier
Preterm GI tract is characterized by
 Immature immunity
 Increase permeability
 Reduce gastric acid secretion
 Reduce proteolytic enzyme
 Decrease motility
 Immaturity of intestinal epithelium and microivilli.

2- infectious agents
 Breast feed infant colonized predominantly with
bifidobacteria (gram+)
 It control growth of (gram -) bacteria
 Formula feed infants colonized with coliforms,
enterococci.

Organism
 E. coli
 Klebsiella pneumoniae
 Proteus mirabilis
 Staph. Aureus
 Staph. Epidermidis
 Enterococci
 Closttridium perfringens
 P. aeruginosa
 Fungal infection

3-Circulatory Instability
 Hypoxic-ischemic injury
Due to
 fetal distress,
 perinatal asphyxia,
 respiratory distress syndrome
 Hypothermia
It causes
 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

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

 On initiation of the pathologic process of NEC ,
cellular communication through inflammatory
mediator result in a multitude of events, cause
end -organ damage seen in NEC.
 Inflammatory mediators involved in development
of bowel injury and sytemic side effects.

1- Epidermal growth factor
 Secreted by salivary glands , brunner gland of
duodenum , breast milk
 It is protective and trophic factor for developing GI
tract
 Reduced levels of EGF found in Premature infant

2- Erythropoietin (Epo)
 Produced by kidney
 Found in breast milk
 Trophic factor in developing GI tract
 Decreased levels found in premature infants
 Intraperitoneal injection of recombinant Epo resulted in
decreased mucosal inflammation and necrosis.

3 -Cytokines
 Proinflammatory cytokines
IL-1, IL-2, IL-6, IL-8, IL-12,
 Anti-inflammatory
IL-4, IL-10, IL-11,
 Produced by intestinal endothelial cells, mucosal fibroblasts,
enterocytes.
 Higher levels of proinflammatory cytokines found in patients
of NEC

4- Nitric Oxide
 Produced from arginine by nitric oxide synthase
Functions of NO
 Maintenance of mucosal integrity
 Regulation of mucosal permeability and blood flow
 Regulation of motility
 Inhibition of leukocytes adhesion and activation

5 -TNF-α
 Proinflammatory effect
 Neutrophil activation
 Induction of leukocytes and endothelial adhesion
molecules
 Induction of other cytokines

6- LPS(endotoxin)
 Bacterial product
 Activation of cytokines
 Produce hypotension, shock and intestinal necrosis
 Mediated by PAF and TNF-α

7- Cyclooxygenase (cox)
 Two forms:
 Constitutive form(cox-1) in GI tract have protective role
 Inducible form(cox-2)

 Onset varies with gestational age
 VLBW – 14-20 days
 Term - first week
 Course of disease
 Fulminant presentation
 Slow, paroxysmal presentation

 Respiratory distress
 Lethargy, irritability
 Temperature instability
 Poor feeding
 Hypotension
 Acidosis
 Oliguria
 Bleeding diathesis

Gastrointestinal:
1. Feeding intolerance
2. Increased gastric residual volume(>70%)
3. Abdominal distention(70 to 98%)
4. Abdominal tenderness
5. Emesis(>70%)
6. Occult/gross blood in stool (79%)
7. Abdominal mass
8. Erythema of abdominal wall

9. Generalized peritonitis
10. Ascites
11. Discolouration of scrotum in males

necrotizing enterocolitis 1shri.ppt

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


stage Systemic signs Intestinal signs Radiological signs
1 suspected
A
Temperature
instability,
bradycardia,apnoea
Elevated gastric
residuals,mild
abdominal
distension,occult
blood in stool
Normal or mild ileus
B
Same as 1A Same as 1A plus gross
blood in stool
same as 1A
2 definite
A mildly ill
same as 1A same as 1A plus
absent bowel sound
and abdominal
tenderness
ileus, pneumotosis
intestinalis

stage Systemic signs Intestinal signs Radiological signs
2
B – moderately
ill
Same as 1 plus
metabolic acidosis
mild
thrombocytopenia
same as1 plus absent
bowel sound,
abdominal
tenderness,abdominal
cellulitis, mass
Same as 2A plus
portal venous gas with
or without ascites
3 advanced
A- severely ill
bowel intact
Same as 2B plus
hypotension,bradycar
dia,metabolic
acidosis,DIC ,
neutropenia
Same as 2 plus
generalized
peritonitis,marked
tenderness,
abdominal distension
Same as 2B plus
Definite ascites
B- severely ill
bowel
perforated
same as 3A same as 3A Same as 2B plus
pneumoperitoneum

 A high index of suspicion is required
 Sometimes cannot be differentiated from sepsis

 No lab test is specifiC for NEC
THE MOST COMMON TRIAD(!)
 Thrombocytopenia
 Persistent metabolic acidosis
 Severe refractory hyponatremia
 WBC-raised / decreased levels
 Hyperkalemia
 Stool:reducing substances, occult blood.

 C-Reactive Protein
 Early indicator of NEC
 Sensitivity- 99%, Specificity- 81%
 Level raises> 10 mg/l within 48 hrs of suspected
diagnosis.
 Failure of CRP to return normal in 10 days is an
indicator of abscess, stricture, septicemia.

Abdominal X- ray:
 AP supine
 Left lateral decubitus
Suggestive findings
1. abnormal gas pattern, ileus
2. Bowel wall oedema
3. Pneumoperitoneum(left lateral decubitus)
4. Intrahepatic portal venous gas(in absence of UVC)
5. fixed configuration of bowel loops over serial
films(every 6 to 8 hour)for 24 to 36 hours.

Definitive finding-
Pneumatosis Intestinalis(50-75%)
 Most common in RLQ
 More frequently when infant have been fed(84%)
than unfed(14%).
 Hydrogen gas within the bowel wall
 Product of bacterial metabolism

portal venous gas (PVG)
• linear branching lucencies over liver
• more peripheral than biliary gas
• It represent the gas dispersed through
fine radicals of the portal venous system
• In 10 to 30% of cases
• Associated with poor prognosis
• 61% in pan necrosis

Pneumoperitoneum
 free air in the peritoneal cavity secondary to
perforation
 In 12% to 30% of cases
 Best noted in left lateral view
 Air on both sides of bowel wall(rigler sign or double wall
sign)
 Outline of falciform ligament(football sign)
 Surgical emergency

Intraperitoneal fluid
 Grossly distended abdomen devoid of gas
 Gas filled loops in center surrounded by opacity in
flanks
 Increase haziness within the abdomen
 Separation of bowel loops
 In 11% cases
 Associated with high mortality

DIAGNOSIS,RADIOLOGICAL STUDIES
ABDOMINAL Ultrasonography-
 Used in case of distended and gasless abdomen
1. Thickened bowel loops
2. Increased or decreased vascularity
3. Intraperitoneal fluid
4. Portal venous air
5. Hypoechoic ring with central echogenic focus (target sign )
suggests abnormal bowel loop
6. Pericholecystic hyperechogenecity

CT scan
 Not typically used for diagnosis
1. Bowel wall thickened with increased or decreased bowel
wall enhancement.
2. Pneumatosis, free air, PVG, ascites

Contrast studies
 Upper GI contrast study
 Use water soluble contrast agent
 Barium should never be used
 Contrast enema should never be performed –risk of
rectosigmoid perforation.
Finding
1. Bowel loops separated by edematous wall
2. An irregular mucosa with ill defined margins
3. Mucosal ulceration
4. Bowel wall spiculations
5. Pnuematosis intestinalis

Gross
 Bowel is markedly distended with patchy areas of
thining.
 Serosal surface red to gray
 With frank gangrene serosal surface is black
 Subserosal gas collection
 Mucosal surface is ulcerated with areas of
epithelial sloughing

Resected portion of necrotic bowel

Microscopic
 Acute and chronic inflammatory changes coexist in 60% of
cases
 Coagulative necrosis of mucosa(89%)
 Edema and hemorrhage of submucosa
 Pneumatosis intestinalis in submucosa and muscularis and
subserosa later.

 Bacteria in bowel lumen and wall in 40% of cases
 Transmural necrosis in advancd cases
 Granulation tissue with mucosal and submucosal
fibrosis
 Small vessel thrombosis

Non operative
 In the absence of necrosis or perforation the mainstay of
treatment is supportive.
 Feedings are stopped (NPO)
 Nasogastric tube decompression
 i.v fluid
 Central venous access for parenteral nutrition
 Broad spectrum antibiotics for 7 to 14 days

 Ampicillin(50mg/kg/day), gentamicin
(5mg/kg/day)and clindamycin(10mg/kg/day)
 vancomycin (15mg/kg/day),third generation
cephalosporin (100mg/kg/day)with
metro(15mg/kg/day)
Close clinical observation
 Frequent physical examination
 Abdominal x-ray every 6 to 8 hour

 Enteral feeding withheld for 10 to 14 days after
radiological evidence of disease has abated.
 After resumption of feeding stools are tested for occult
blood and reducing substances
 Feeding discontinued if result is positive
 Feeding volume increase slowly

Surgical treatment
Operative intervention require in 50% of
infants with NEC
Principles
 Removal of gangrenous bowel
 Preserve intestinal length

Indications of surgery
A- best indicator
 1- pneumoperitoneum
 2- positive paracentesis
 3- portal venous gas
 Specificity and positive predictive value about 100%
 Aspiration of >o.5 ml brown or yellow fluids defined as
positive paracentesis

B- good indicator
 1- fixed intestinal loop
 2- erythema of abdominal wall
 3- palpable abdominal mass
 4- pneumatosis intestinalis
 Specificity and PPV <100%

C-Poor indicator
 1- clinical deterioration
 2- platelet count <100,000/mm3
 3- Abdominal tenderness

Operative methods
1- primary peritoneal drainage
 For unstable patients >1500g
 Use in patients <1500g with perforation
 It allow resuscitation and stabilization before definitive
laparotomy.
 Performed at bedside with local anesthesia
 Placement of drain in right lower quadrant

2- laparotomy
 Incision- Rt transverse supraumblical
 Sample of peritoneal fluid may be taken for culture.
Assess
 extent of disease
 Focal, multifocal (>50% viable) , pan necrosis(<25% viable)
 Viability of bowel

1 – focal disease
 When a single area of bowel is necrotic or perforated
 Proximal enterostomy and distal mucus fistula
 Perforation repair
 Resection and primary anastomosis in carefully selected
patients
 A sharply localized disease
 Undamaged remaining intestine
 A good overall patient condition

2- multifocal disease
 A -Resection and anastomosis
 B – a proximal jejunostomy created and distal bowel
spliced together
 C – Moore described ‘ patch, drain and wait procedure
in 1989.
This involves-
 Transverse single layer suture approximation of
perforation(patch)
 Insertion of two drains in lower quadrant.
 Long term parenteral nutrition

D-’clip and drop method’
 Described by Vaughan et al.
 Necrotic bowel removed and the cut ends are closed with
titanium clips or staples.
 Re-exploration is performed 48 to 72 hour later
 Clips removed and all segments are reanastomosed without
any stoma.

3 – pan involvement (NEC totalis)
 In 19% of patients
A- resection of all necrotic bowel with proximal or multiple
stomas.
B – proximal diversion without bowel resection with second
look procedure after 6 to 8 weeks.

Stoma closure
 There is neither an ideal weight nor age for stoma
closure.
 Enterostomy may be safely closed anytime after 4
weeks since last operation.
 Before closure patency of distal end should be
confirmed by contrast study.

Complication
 Liver hemorrhage
 Wound infection
 Wound dehiscence
 Stoma stenosis
 Incisional hernia
 Parastomal hernia
 Prolapse
 Intussusception
 Small bowel obstruction

Long term Complication of NEC
Occurs in 50% of cases
1 – intestinal strictures
 9% to 36% incidence
 More frequent after nonoperative treatment
 Colon (80%)
 Terminal ileum(15%)
 Splenic flexure – most common site.
 Multiple strictures- 21%
 Failure to thrive, rectal bleeding bowel obstruction after non
operative treatment suggest stricture

2 – malabsorption and short bowel syndrome
-Occur in 23% cases
Due to
 Decreased bowel length
 Decreased mucosal area
 Enzyme depletion
 Gut hypermotility
 Hypersecretion of gastric acid
 Decreased intestinal transit time
 Bacterial overgrowth
 Vit. B 12 deficiency

3 – cholestatic liver disease
4 – recurrent NEC-4% to 6% incidence
5 – anastomotic ulceration
 Lower GI bleeding
 Diagnosed by colonoscopy
 Treatment-Ulcer resection

Prevention
1 – infection control measures in nursery
 Proper hand washing
 Use of gloves and long sleeved gown
 Separate diaper and laundry bag for each patient
 Isolation of confirmed cases

2 – oral immunoglobulins
 IgA deficient in premature gut
 It act as an antiseptic paint by binding the bacteria and
prevent attachment to the intestinal mucosa
 Enteral administration of IgA preparation decreases the
incidence of NEC

3 – breast milk
 breast milk may have a protective effect
 IgA
 macrophages, lymphocytes
 complement components
 lysozyme, lactoferrin
 Acetylhydrolase
 Interferon
 EGF
 Erytheropietin
 Probiotics

4 - Maternal glucocorticoid
 Accelerate mucosal cell maturation
 improve gut barrier function
 Down regulation of inflammatory response
5 – feeding practices
 For premature infants given a hypocaloric formula at a
slow rate

6 – administration of probiotics
 ‘ live microbial supplements that colonize the gut to provide
benefit to host
 Use of probiotics (bifidobactetria) decrease the incidence of
NEC
.

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