NECROTIZING

ENTEROCOLITIS
Atan Baas Sinuhaji

Department of Childhealth,School of
Medicine,University of North Sumatera
Medan

Necrotising Enterocolitis (NEC)

Affects 0.5 to 1 per 1000 live births
Incidence 3-10% in infants < 1500 g
Incidence increase with decreasing
birthweigh and gestational age
Usually affects terminal ileum and colon to
a
variable extent
NEC rarely occus before the initiation of
enteral
feeding

Incidence of NEC related to gestational age

no IUGR

IUGR

10
8

6
4
2
0
26 27 28 29 30 31 32 33 34 35 36 >37

gestational age

NECROTIZING
ENTEROCOLITIS
An Acute Intestinal Necrosis Syndrome Resulting From
Complex Interaction :
= Gut Ischemia
= Poor Mucosal Integrity
= Microbial Infection
= Enteral Nutrition

MUCOSAL INJURY

INTESTINAL PERFORATION

Immaturity

Ischaemia
Milk feeds

Loss of barrier function

Mucosal disruption

Bacterial translocation
Macromolecular absorption

Mucosal damage

Toxins

Bacterial overgrowth
Viruses

NEC

ors
Bacteria
Mucus

enterocyt
Goblet cell

nucleus

ENTERAL FEEDING
1.PROVIDES SUBSTRATE FOR
PROLIFERATION OF
ENTERAL
PATHOGENS
2.HYPEROSMOLAR FORMULA
MUCOSAL
DAMAGE
3.LACK OF IMMUNOPROTECTIVE FACTORS
4.AGGRESSIVE ENTERAL FEEDING
5.BREASTFEEDING
LOWERS THE RISK
OF NEC

Necrotising Enterocolitis (NEC)

Clinical features
Usually occurs in the first two weeks of life
Child is lethargic and apathetic with vomiting and
increasing
abdominal distension
Bloody diarrhoea is a late feature
Progression may be rapid from to mild to severe
after 72 hours
Abdominal examination may show peritonitis or a
mass

Abdominal x-ray may show

Distended bowel with mucosa edema
Intramural gas ( = pneumatosis

intestinalis )
Portal venous gas or free intraperitoneal
gas

Abdominal x-ray

AA

Abdominal x-ray

Treatment
A. Medical

No definitive

treatment

B. Surgical

1. Perforation
2.Fixed dilated loop on serial x-ray
3.Abdominal wall cellulitis
4.Progressive deterioration despite
maximal medical
support

Medical
1.Preventing futher injury

a. Cessation of feeding
b. Decompression
c. IntraVenous Fluid Drip ( IVFD )
2.Supportive
a. Respiration status
b. Coagulation profile
c. Electrolyte and Acid base balance
d. Antibiotics

PREVENTION
1. EXCLUSIVELY BREAST-FED
2. MINIMAL ENTERAL FEEDS FOLLOWED BY
JUDICIOUS VOLUME ADVANCEMENT
3. PROBIOTIC

ABDOMINAL DISTENTION
OR
MASSES
Atan Baas Sinuhaji

Department of ChildHealth
School of Medicine,University Of Sumatera Utara
Medan

PCM
ABDOMINAL
WALL

PRUNE BELLY
SYNDR.

OBESITY

ABDOMINAL
DISTENTION

GASES
ABDOMINAL
CONTENT

FLUIDS
ABD. MASS

PRUNE BELLY SYNDROME

= EAGLE BARRET SYNDROME
= TRIAD SYNDROME

- DEFICIENT ABDOMINAL MUSCLE

- URINARY TRACT ABNORMALITY

UROPATHY NON OBSTRUCTIVE

- CRYPTORCHIDISM

OUT

GASES

PERFORATION

PNEUMOPERITONEUM

BOWEL
OBSTRUCTION

IN

MALABSORPTION

AEROPHAGIA

BOWEL OBSTRUCTION :

1. MECHANICAL/PARALYTIC

2. INCOMPLETE/COMPLETE
3. CONGENITAL/ACQUIRED

MECHANICAL

SIMPLE
STRANGULATION

OBSTRUCTION

VASCULAR
COMPROMISE

PARALYTIC
= ILEUS
=INTESTINAL PSEUDOOBSTRUCTION

SPASMOLYTIC

ACUTE

HYPOKALEMIA
PNEUMONIA

ILEUS

CHRONIC

MUSCLE & NEURON

(CHRONIC INTESTINAL PSEUDO

OBSTRUCTION)

OBSTRUCTION
ACCUMULATION OF
BOWEL CONTENTS
OVERGROWTH
MICROORG.

GUT CIRCULATION

MUCOSAL DAMAGE
ENTEROCOLITIS

SEPSIS

ABD. CAVITY

ABD.MASS

PELVIC

RETROPERITONEAL
-KIDNEYS :

-WILMS TUMOR
-NEUROBLASTOMA
-CYSTE

-PANCREAS

OVARIAL CYST

HEMATOCOLPOS

PELVIC

TUBOOVARIAN ABSCESS

TERATOMA

FETUS

IN

WORMS > 100

FECAL IMPACTION
TUMOR

FOREIGN BODY

ABD. CAV.

GUT

APP. ABSCESS

OUT
TUMOR

- KISTA MESENTERIUM

ORGANOMEGALY

TUMORS OF THE GUT

1.POLYPS
2.HEMANGIOMA
3.LEIOMYOMA
4.CARCINOMA

5.LIMPHOSARCOMA
6.CARCINOID:
- CHRONIC DIARRHOEA
- VASOMOTOR
- BRONCHOCONSTRICTION

POLYPS OF THE GUT

JUVENILE

HAMARTOMA

AMPUTATED

FAMILIAL

ADENOMA

PREMALIGNANT

HEPATOMEGALY
1. INFLAMMATION

HEPATITIS

2. CONGESTION : DECOMPENSATION,

CONTRICTIVE PERICARDITIS
3. BLOOD DISORDERS :
HEMOLYSIS

: THALASSEMIA

MALIGNANCY : LEUKEMIA
4. TUMORS :CHOLEDOCHAL CYST
HEPATOMA
5. METABOLIC DISORDERS : FATTY LIVER

FATTY LIVER
1. NUTRITIONAL : OBESITY, KWASHIORKOR
2. DRUGS : ESTROGEN, STEROID
3. INTOXICATION : ALCOHOL
4. ALTERATION OF GI ANATOMY :
JEJUNOILEAL BY PASS
5. OCCUPATIONAL EXPOSURE :
HYDROCARBON
6. METABOLISM : A LIPOPROTEINEMIA

PATHOGENESIS

1.PERIPHERAL
MOBILIZ. OF
FATTY ACID

2. HEPATIC SYNTHESIS
OF FATTY ACID

4. IMPAIRED SYNTHESIS
& EXCRETION VLDL (
VERY LOW DENSITY
LIPOPROTEIN) FROM
THE LIVER
3. HEPATIC CATABOLISM OF
FATTY ACID

FATTY LIVER
HEPATIC STEATOSIS
INFLAMATION

NON INFLAMATION
(BENIGNA STEATOSIS)

ALCOHOLIC
NON ALCOHOLIC
STEATOHEPATITIS
(NASH)
8-20 %

PROGRESIVE FIBROSIS
(10-50 % OF NASH)

CIRRHOSIS (10% OF NASH)

NO INCREASED
MORTALITY

FIBROSIS (-)

NO INCREASED MORTALITY

HEPATIC STEATOSIS

NASH

ALC. HEPATITIS

ALT > AST

AST > ALT

2:1

2:1
ALT = SGPT

ALANINE AMINO TRANSFERASE= SERUM GLUTAMATE PYRUVATE TRANSAMINASSE

AST=SGOT
ASPARTAT AMINO TRANSFERASE = SERUM GLUTAMIC OXALOACETAT
TRANSAMINASE

FLUIDS
BOWEL
IN

OBSTRUCTION

OUT

ASCITES

INTAKE

PORTAL HYPERTENSION
-HEART FAILURE

- PCM

LOSS
- NEPHROTIC SYND.

SYNTHESIS
- HEPATIC CIRRHOSIS

-CIRRHOSIS

HYDROSTATIC PRESS.
ONCOTIC PRESS.

ASCITES
PERMEABILITY
-DHF
-PERITONITIS TBC

-PERITONEAL TUMOR

LYMPH
OBSTRUCTION