NECROTIZING ENTEROCOLITIS

Transcription

1 Necrotising Enterocolitis (NEC) NECROTIZING ENTEROCOLITIS Atan Baas Sinuhaji Department of Childhealth,School of Medicine,University of North Sumatera Medan 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 % >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 Loss of barrier function Ischaemia Milk feeds ors Bacteria Mucus Mucosal disruption Bacterial translocation Macromolecular absorption Toxins Bacterial overgrowth Viruses enterocyt nucleus Goblet cell Mucosal damage NEC 1

2 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 2

3 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 3

4 ABDOMINAL WALL PCM PRUNE BELLY SYNDR. PRUNE BELLY SYNDROME ABDOMINAL OBESITY = EAGLE BARRET SYNDROME = TRIAD SYNDROME DISTENTION ABDOMINAL CONTENT GASES FLUIDS ABD. MASS - DEFICIENT ABDOMINAL MUSCLE - URINARY TRACT ABNORMALITY UROPATHY NON OBSTRUCTIVE - CRYPTORCHIDISM OUT PERFORATION BOWEL : GASES BOWEL PNEUMOPERITONEUM 1. MECHANICAL/PARALYTIC IN MALABSORPTION AEROPHAGIA 2. INCOMPLETE/COMPLETE 3. CONGENITAL/ACQUIRED MECHANICAL SIMPLE STRANGULATION ACUTE SPASMOLYTIC HYPOKALEMIA PNEUMONIA VASCULAR COMPROMISE ILEUS PARALYTIC = ILEUS =INTESTINAL PSEUDO CHRONIC (CHRONIC INTESTINAL PSEUDO ) MUSCLE & NEURON 4

5 ABD. CAVITY ACCUMULATION OF BOWEL CONTENTS OVERGROWTH MICROORG. GUT CIRCULATION ABD.MASS PELVIC MUCOSAL DAMAGE ENTEROCOLITIS SEPSIS RETROPERITONEAL -KIDNEYS : -WILM S TUMOR -NEUROBLASTOMA -CYSTE -PANCREAS OVARIAL CYST IN WORMS > 100 FECAL IMPACTION PELVIC HEMATOCOLPOS TUBOOVARIAN ABSCESS TERATOMA ABD. CAV. GUT OUT TUMOR FOREIGN BODY APP. ABSCESS TUMOR FETUS - KISTA MESENTERIUM ORGANOMEGALY TUMORS OF THE GUT POLYPS OF THE GUT 1.POLYPS 2.HEMANGIOMA 3.LEIOMYOMA 4.CARCINOMA 5.LIMPHOSARCOMA 6.CARCINOID: - CHRONIC DIARRHOEA - VASOMOTOR - BRONCHOCONSTRICTION JUVENILE HAMARTOMA AMPUTATED FAMILIAL ADENOMA PREMALIGNANT 5

6 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 ß LIPOPROTEINEMIA PATHOGENESIS FATTY LIVER HEPATIC STEATOSIS 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 INFLAMATION ALCOHOLIC PROGRESIVE FIBROSIS (10-50 % OF NASH) NON ALCOHOLIC STEATOHEPATITIS (NASH) 8-20 % FIBROSIS (-) NON INFLAMATION (BENIGNA STEATOSIS) NO INCREASED MORTALITY CIRRHOSIS (10% OF NASH) NO INCREASED MORTALITY HEPATIC STEATOSIS FLUIDS NASH ALC. HEPATITIS BOWEL ALT > AST 2 : 1 AST > ALT 2 : 1 IN OUT ALT = SGPT ASCITES ALANINE AMINO TRANSFERASE= SERUM GLUTAMATE PYRUVATE TRANSAMINASSE AST=SGOT ASPARTAT AMINO TRANSFERASE = SERUM GLUTAMIC OXALOACETAT TRANSAMINASE 6

7 PORTAL HYPERTENSION -HEART FAILURE -CIRRHOSIS LOSS - NEPHROTIC SYND. INTAKE - PCM SYNTHESIS - HEPATIC CIRRHOSIS HYDROSTATIC PRESS. ONCOTIC PRESS. ASCITES PERMEABILITY -DHF -PERITONITIS TBC -PERITONEAL TUMOR LYMPH 7