NEC اشرف حامدi

Necrotizing Enterocolitis
(NEC)
Case presentaion
By
Dr. ASHRAF HAMED
prof. Pediatric Surgery
Al Azhar university

Case presentation

MALE saudi baby ,5days old
,preterm(35weeks gestational age)with
history of PROM for >48 hour,referred
from El zulfi general hospital as a case
of sepsis with ?NEC.

There was history of bleeding per rectum
since second day of life and oliguria ,as
the baby passed only 5 ml urine in last 24
hour.

O/E 19-4-24 at 3pm
The baby looks severly ill,dehydrated,toxic facies &
poor perfusion
B W:2.4Kgm
Unstable vital signs:
low BP,pulse:170/min,temp:38.5
The abdomen was severly distended with erythema
of abdominal wall.
Generalized tenderness.
Absent bowel sound (died silent)

Plain x- ray:showed pneumoperitoneum
Blood chemistry:
WBC….1.300/cmm;
platelets…17000/cmm;
HG….9.8gm%,.
PT&PTT>2MIN
ABG……….severe acidosis.

CONT.

 The baby admitted in NICU and
immediately started aggressive
resuscitations with IV fluids and
antibiotics(claforan,flagyl
infusion and vancomycin),NGT
decomression of the stomach

Case presentation

We inserted penrose sheet drain at right lower
quadrant under local anaesthesia which
brought air and faecal matter to give
chance for improvement of general
condition,meanwhile packed rbcs, platelets
and FFP were given with continous IV
fluids resuscitation.

20/4 at 10:00 a.m.
Pt submitted for laparotomy and we
found:
Sever faecal peritonitis and amulgmation of
intestine with pyogenic membrane
covering it.
we discovered oedema and hyperaemia of the
descending colon and big necrotic segment
in the sigmoid colon up to level of
peritoneal reflection over the rectum.

Also there were 2 yellowish dirty,
non viable patches, but not yet
perforated 1st one 15 cm from
DJF and the 2nd 15 cm distal to
the 1st one which were
Imbricated with interrupted
lambert sutures with 5/0 viryl .
Lt hemicolectomy done with
hartman’s procedure closure of
distal stump and the proximal
end as a terminal colostomy .

at 7:30 pm urine output was 5 ml, with
appearance of sclermatous skin changes &
muscle stiffness .
21/4 at 9:00 a.m.
The whole body got oedematous and baby
gained 300 gm postoperatively due to
renal shut down as only 5 ml urine passed.
- Signs of fulminant sepsis in the form of
persistant hypotension, poor perfusion and
scleroderma that carrying out bad
prognosis. C.B.G. also showed mixed
acidosis on high ventilation sitting.

case diagnosed as acute renal failure so,
managed by:-
-Lasix I.V. 5 mg / kg state
- D/C amikine
- Adjust dose of vancomycin and cefotaxim
serum urea 16.7 mmol/l serum.Creatinine
147 mmol.
T .protein 23&albumin 12
albumin 20% 1 gm 1kg over 1 hour given stat
then lasix as before
9:00 pm pt passed 31 cc clear urine after that
ttt with progressive improvement of renal
function and urine output.

2 4/4
Development of purpura fulminans
,ulceration, oral,ETT bleeding with
platelets 10,ooo but pt passed blackish
stool from stoma.
28/4
Sub- cutaneous wound collection without
burst abdomen.
faccal matter coming from the wound with
sluggish instestinal sounds but x-ray
abdomen ----- no pneumoperitoneum so,
2nd laparatomy done

The finding of 2nd laparotomy (29-4-24)
The previous two yellowish dirty non viable
patches in the jejuneum were perforated so,
refreshment of the edges and repair with 5/0
vicryl single layer interrupted for the
proximal one and for the distal one we took its

proximal end as a jejunostomy and the distal
end closed. (jejunostomy at Rt iliac fossa)

Gastrograffin follow
through done and
showed no leakage
of the dye with
healing of the
proximal
perforating.

Then we started oral
feeding through
N.G.T. and every
now and then
correction of
anaemia and
thrombocytopenia.

The pt became deeply jaundiced with
elevated liver enzymes, ⇑ total and
direct bilirubin and his body weight
decrease to 1.9 kg as stoma extrude
the milk undigested after feeding
through N.G.T., so, at 1st we changed
to N.G.T. drip method.
There is little increase of body weight to
2 kg.
So, we started T.P.N. through Rt
subclavian veiv(cut doun) when all
other substitutes failed. Also, with
little improvement.

CASE PRESENTION
2/6/24
So,we decided to close the jejunostomy.

colostomy became functioning after 2 days
postoperatively . also, we stopped T.P.N.
because of increasing liver enzymes.

Then patient tolerated gradually NGT
feeding and passed post operative
smoothly till discharged at 26/6/24 and 2
months later the patient came for closure
of colostomy

Nectotizing Enterocolitis
Introduction
it is the most common newborn
surgical emergency, with a mortality
rate that far exceeds that of any other
gastrointestinal condition requiring
operation.
It is a syndrome of acute intestinal
necrosis.
NEC is a disease of paradoxes. It
typically affect the preterm infant but

It usually occurs on the tenth day of life,

but it may develop on the first day, several
weeks, or even months after birth.
The disease frequently appears
sporadically but can present in epidemic –
like clusters.
Most patients who develop the disease
were fed enterally, but babies who have
never been fed also are susceptible.

N.E.C. is widely accepted as a
complication of prematurity in which
there is intestinal hypoxia, usually due to
a low perfusion state which results in
mucosal injury and allows translocation
of bacteria into the intestinal wall and
portal venous system.
Two-Thirds of patients respond to
medical management, only about one-
third require surgical intervention.

Epidemiology
I – Incidence
Overall incidence of NEC is 2-5% of all NICU
admissions.

The incidence of NEC is approximately 1-3
cases/1000 live births in the u.s. or about
25,000 new cases of NEC worldwide / year.
The incidence is much higher in premature
(90-93%)and extreme low birth weight
infants.

Epidemiology
 Incidence varies between hospitals
and also within the same institution in
different periods reflecting periodic
epidemics
 It occurs more commonly among
infants fed formula( 9o to 95%
enterely fed)compared to those who
have been fed with breast milk.

Epidemiology
Mean age of onset is 3-4 days for term
infants and 3-4 weeks for infant born at
less than 28 week’s gestation.
Mortality rate varies(30-40%) with a
higher rate in advanced NEC (stage III or
with perforation) and in infants with birth
weight 1000gm or less( >80%).

NECROTIZING
ENTEROCOLITIS

 Pathophysiology:

UNKNOWN
CAUSE…….

CIRCULATORY INSTABILITY
PRIMARY INFECTIOUS AGENTS
Hypoxic-ischemic event
Bacteria, Bacterial toxin, Virus, Fungus Polycythemia

MUCOSAL INJURY

INFLAMMATORY
MEDIATORS ENTERAL FEEDINGS
Inflammatory cells (macrophage) Hypertonic formula or medication
Platelet activating factor (PAF) Malabsorption, gaseous distention
Tumor necrosis factor (TNF) H2 gas production, Endotoxin
Leukotriene C4, Interleukin 1; 6 production

Epidemiology
II Risk Factors
Despite several decades of research the
etiology and pathogenesis remained
elusive.
There is wide controversy about this
topic .

Epidemiology

.Prematurity
The most dominant risk factor for NEC
is the degree of Immaturity.
– 90% of cases are premature infants
– immature gastrointestinal system
 mucosal barrier

 poor motility

– immature immune response
– impaired circulatory dynamics

Epidemiology

2 –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
>20kcal/kg/day

3 – Infant related conditions
A. Perinatal asphyxia & hypoxic
ischaemia
It has more significant role in term and near term
infants.

Epidemiology
B – Umbilical Catheterization
-Embolization of catheters may result in
embolization of mesenteric arteries.
-Infusion of medications such as calcium
may cause vasospasm and frank
intestinal necrosis.
C - Congenital heart disease Especially
PDA and cyanotic heart disease.

Epidemiology

D-– Extreme Low birth weight
It was proved that the incidence of NEC is
higher in those babies with birth
weight 1500 gm or less.

E -Drugs
I) Theophylline→ toxic oxygen radicles
II) Oral Vitamin E→interfere with killing of
bacteria
III) Indomethacin→vasoconstriction→↓
mesenteric blood flow

Epidemiology
F. Infection
- Although no specific single organism
was implicated in the disease
G. Hypotension & Shock
H. Polycythemia
I Exchange Transfusion
J Thrombocytosis
K Anaemia
L RDS

Epidemiology
4. Maternal Risk Factors

1) Pre-eclampsia
2) Placental insufficiency
3) Prolonged PROM
4) Drugs as Heroin

34

Pathogenesis
 Most investigators suggested that NEC
resulted from intestinal mucosal injury
from low - Flow states, or hypoxia, with
secondary bacterial invasion.
 These factors may initiate the disease
process by injuring the protective barriers
of the intestine (The mucosa). The injury
can be direct or indirect.
 Direct injuries are caused by bacteria
or by exposure to hypertonic solution.

Pathogenesis
Indirect injuries are the result of mucosal
cell hypoxia from low flow states:
 .Shock
 .Hyperviscosity
 .Vascular obstruction
 Or generalized hypoxia
⇒ birth asphyoxia
→lung or heart disease

Pathogenesis
* Once the mucosa has been injured,
bacteria in the lumen can breach the gut barrier
And initiate an inflammatory cascade, causing
further damage and eventual intestinal
necrosis.
 The presence of substrate provided by
Feedings, bowel stasis and reduction in
defences of the local gut Mucosa ⇒ All
facilitate bacterial proliferation.

Pathology
NEC may be
I. FOCAL(Isolated) disease
When a single area of bowel is
necrotic or perforated
II.MULTIFOCAL Multi –
segmental disease (> 50%
viable.)
.The most common site of NEC is
the terminal ileum, the second
most common site in the left
colon.
.The disease can occur anywhere
from the stomach to the rectum.

Pathology
Involvement of both the
large and small
intestine occurs in
44% of cases.
III. Pan – Involvement
(NEC totalis)
 Account for 19% of the
cases
 Characterized by
necrosis of at least 75%
of the gut.

Macroscopic Features

 Grossly distended loops of the intestine
with spotty intramural haemorrhagl and
areas of necrosis with serosal gas
collection.
 The diseased bowel wall may be thinned
with fibrinous exudate covering the serosal
surface.
 Mucosal ulceration with associated
epithelial sloughing may be extensive.

Microscopic Features

 The essential feature are haemorrhage and
necrosis (coagulation necrosis).
 Mucosal oedema followed with formation
of a pseudo-membrane of fibrinous
exudates and necrotic cellular debris.
 The necrosis may progressively involve all
layers of the bowel to the serosa.

Complications
Short Term

1 – Perforation.

2 – Septicaema.

3 – Metabolic and electrolyte
distubance.

4 – Prolonged need for artificial
ventilation with its hazards.

II – Long Term
1. Strictures
 - It is the most common long term GIT complication
of NEC, occuring in (10-35%) of all survivors.

2 – Short bowel syndrome
 The most important determinant of future
GIT function is the absence or presence of
ileocecal valve, regardless of the length of gut
resected.
 The syndrome refers to malabsorption and
under nutrition after extensive bowel
resection.

3.FULMINANT SEPSIS

4.TPN related complications:

Cholestasis;Thrombosis;Infection

5. Complications related to stoma:
Retraction,Prolapse&Parastomal hernia
6. adverse neurodevelopmental outcomes
Delays in “locomotor,” “hearing and speech,”
“intellectual performance” and “personal and
social” skills.[

6. Wound complications
Infection, Dehiscence
or Enterocutaneous fistula
7. Recurrence
Occurred in 10% (Rennie and Roberton
2002)
8. Others:
Chronic anaemia & malabsorption
Eye complication
Abscess & Fistula formation

CLINICAL PRESENTATION

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

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

Modified Bell Stages
Stage Stage Systemic Intestinal Radiolog
Signs Signs ical Sign

I IA Temperature −⇑Gastric .Intestinal
Suspected instability aspirate .mild dilutation
NEC Apnea abdominal .Mild ileus
Bradycardic distension
Lethergy .Emesis
.Faecal occult Blood

I IB Same as IA Bright red blood per Same as IA
Suspected rectum
NEC

Stage Stage Systemic Intestinal Radiologic
Signs Signs al Sign

II II A Same as IA Same as IB + •Intestinal
Definite (mildly ill) .absent bowel dilatation
NEC sound •Ileus
.Abd. Tenderness •Pneumatosis
intestinalis

II II B Same as II A plus: Same as II A plus Same as II A
Definite (moderat *Metabolic Acidosis *Defenite Abd. plus
NEC ely Ill) *Mild Distension +portal vein
Thrombocytopenia +Abd. Celluitis gas
+ Lower Abd. + Ascites
Quadrant mass
*Absent bowel
sound

Stage Stage Systemic Signs Intestinal Radiologi
Signs cal Sign
III III A Same as II B plus Same as II B Same as II B
Advanced (Severely Ill) * Hypotension plus plus
NEC * Bradycardia *Generalized * Definite
* Severe Apnea Peritonitis Ascites
* Combined respiratory *Marked
&metabolic acidosis Abd.Tenderness
* DIC *Abd.
* Neutropenia and Distension
* Anuria *abd Wall
Erythema

III III B Same as III A plus Same as III A Same as III A
Advanced (Severely ill sudden perforation plus plus
& bowel Increased pneumoperito
perforation) Distension neum

IMAGING
The cornerstone of the diagnosis of
NEC is plain anteroposterior and
left lateral decubitus radiography.
1. Bowel distension
It is the earliest and most common
radiologic finding in patients with
NEC (55% to 100% of cases)
2. Pneumatosis intestinalis
• It is intramural gas (mainly
hydrogen)
• The frequency ranges from
19% to 98%.

Pneumatosis Intestinalis

hydrogen gas within the bowel wall
 A by-product of bacterial metabolism

a. linear streaking pattern
 represents subserosal air
 more diagnostic

b. bubbly (cystic form)pattern
o More common
o . represent submucosal air
o appears like retained meconium
o less specific

3. Portal venous gas
• It appears as linear
branching arborizing pattern
of air over the liver shadow.
• It may be fleeting and
accounting for 9% to 20%.
Portal vein gas is associated
with poor prognosis.
4. Pneumoperitoneum
• It is best noted in left lateral
decubitus
• Pneumoperitoneum may
occur without intestinal
perforetion (barotraume).

5. Intraperitoneal fluid

• It is assoicated with high mortality rate.

• Amenable to paracentesis

6. Persistent dilated loops

* When a single loop or sevseral loops of
dilated bowel remained unchanged in
position and configuration for 24 to 36
hours usually occurs in full-thickness
necrosis.

Contrast Study
 It may be used in patients with equivocal
radiologic signs
 Barrium should never be used

 Newer water – soluble agents as isotonic
metrizamide which produce excellent
specification of the gut.

Ultra- Sonography
It has been used to identify

a. Necrotic bowel
b. Intraperitoneal fluid
c. Portal venous gas

• It is the most applicable tool in patient
with gasless abdomen and to localize
intra-abdominal fluid for paracentesis.

MANAGEMENT
Non-operative
The mainstay of treatment for NEC is non-operative
therapy.

1. NPO & gastric suction ⇒ 10 – 14 days

2. Cultures:- Blood culture is essential

- CSF, Urine, Other Sites cultured as indicated.
3. Antibiotics:- Vancomycin
Aminoglycoside
Flagyl Infusion for at least
Cephalosposine 2 weeks

4. Intravenous fluids: 150 – 250 ml / kg
5. TPN
6. Blood and Blood products: as needed for
correction of anaemia and coagulopathy.

7. Close Clinical observation ⇒ consists of:

a.Frequent physical examination
b.Abdominal radiography every 8 hours
c.C.B.C. Blood gas analysis, serum
electrolyte & serum platelet

Indications for operation
1. Pneumoperitoneum
• This is the only absolute indication for
surgery.
• Relative indication:
2. clinical deterioration despite adequate
therapy:
a. Erythema and oedema of abdominal
wall
b. Abdominal mass
c. Signs of peritonitis on physical
examination
d. Increasing acidosis and
e. Persistent and progressive
thrombocytopenia.

3. Fixed dilated intestinal loop.
4. Ascites
• 43% of patient’s ascites will have
bowel necrosis.
• The demonstration of ascites
mandates paracentesis .

Paracentesis

5. Positive Paracentesis
– Indicated for infants with
extensive pneumatosis
intestinalis or who have failed to
improve on medical
management
– This is defined as free flowing
aspiration of more than 0.5 ml
of brown or yellow brown fluid
that contains bacteria on gram
stain.

6.Portal Venous Gas

Operative Management

bed-side Peritoneal drainage
* It is insertion of a penrose drain
through a right lower quadrant
incision under local anaesthesia for
extremely ill infants with bowel
perforation.

Laparoscopy
�Clarckand Mackinaly reported the use of laparoscopy
in the treatment of a VLBW infant (900 g) with
perforated NEC.
Tan et al.:4 babies (500-1000 g)

 Needlescopic diagnosis is feasible and appears to be safe, even
in critically ill baby less than 1000 g. The technique can provide
useful information for surgical decision-making and allows for
precise placement of the incision over the site of perforation,
thus minimizing the trauma from open surgery in this special
group of patients.

 Clark C, MackinlayGA. Laparoscopy as an adjunct to peritoneal drainage in perforated
necrotizing enterocolitis. J Laparoendosc Adv Surg Tech A. 2006 Aug;16(4):411-3.39 Tan HL
et al. The role of diagnostic laparoscopy in micropremmieswith suspected necrotizing
enterocolitis. Surg Endosc. 2007 Mar;21(3):485-7.

II. Principles of Resection
A. When a single area of bowel is necrotic or
perforated only limited resection is
necessary.
• A proximal ostomy and distal mucus
fistula are created
B. Resection with primary anastomosis in
these conditions
i) a sharply localized (proximal)segment of
disease
ii) undamaged appearance of the
remaining intestine.
iii) good general condition.

Segmental NEC
Contrast study
Segmenal necrosis Multiple segments necrotic
of one segment but >50%viable bowel

Resection of Resection of
necrotic segment necrotic segments

Primary
stoma Proximal stoma
anastomosis!?

Muliple anastomoses
of distal
Contrast defunctionalized bowel
study

Stoma closure 4-6 weeks

III. Multi – segmental disease( > 50%
viable)
A. Excision of each diseased segment and
creates multiple stomas.
B. “Patch, drain, and wait” procedure; which
include
- Transverse single layer suture
approximation of perforations (patch).
- Insertion of two penrose drains (drain)
- Long-term TPN (wait)

C. “Clip and drop-back” Technique
• Obviously necrotic bowel is removed.

• The cut ends are closed with titanium clips.

• Re-exploration is done 48 to 72 hours later
⇒ All segments are re-anastomosed without
any stoma.

Pan – Involvement = Nec Totalis
Operation
1.high stoma in proximal viable bowel
2.irrigate distal bowel
Perforated No
segments perforations

No resection
Mucus fistula of distal bowel
Limited
resections

Mucs fistula Muliple Stent deteriorate stable
distal bowel stomas Muliple segmnts
over silastic cather

TPN for 6-8 weeks
Contrast study

Multiple resections of scarred segments ananastomosis.
Proximal stoma remains

Proximal stoma
closure in 6 weeks

IV. Pan – Involvement = Nec Totalis
The Treatment options

1. Simple closure of the abdomen
2. Resection of all necrotic bowel
3. Proximal diversion without bowel
resection…..second-look operation after 6-
8weeks.

Prevention

 �Breast milk
 �Antenatal Steroid therapy
 �Oral immunoglobulins
 �Oral antibiotics
 �Probiotics(Lactobacillus, Bifidobacterium)
 �Feeding strategies
 �Glutamine
 �Arginine
 �Polyunsaturated fatty acids (PUFA)
 �Lactoferin
 �Pentoxifylline

Take Home Messages

 Go slow!!!!!

 Breast is best!!!

NEC اشرف حامدi

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