nec kuliahrepro

7/28/2019 NEC KuliahRepro

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NECROTIZING

ENTEROCOLITIS

Reproduction System

2010


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OBJECTIVES

Ability to diagnose and treat the signs and

symptoms ofNEC

Ability to evaluate radiographs for the

classic findings ofNEC

List several long-term complications

associated with NEC


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NECROTIZING

ENTEROCOLITIS Epidemiology:

most commonly occurring gastrointestinal

emergency in preterm infants

leading cause of emergency surgery in neonates

overall incidence: 1-5% in most NICUs

most common in VLBW preterm infants

10% of all cases occur in term infants


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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


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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


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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


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NECROTIZING

ENTEROCOLITIS

Pathophysiology:

UNKNOWNCAUSE.


8/39From UpToDate online, Adapted from Kliegman, RM, Pediatr Res 1993; 34:701.


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RISK FACTORS

Prematurity:

* primary risk factor

90% of cases are premature infants

immature gastrointestinal system

mucosal barrier

poor motilityimmature immune response

impaired circulatory dynamics


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RISK FACTORS

Infectious Agents:

usually occurs in clustered epidemics

normal intestinal flora E. coli

Klebsiella spp.

Pseudomonas spp.

Clostridium difficile

Staph. Epi

Viruses


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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


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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


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RISK FACTORS

Enteral Feedings:

> 90% of infants withNEChave been fed

provides a source for H2 productionhyperosmolar formula/medications

aggressive feedings

too much volume

rate of increase

>20cc/kg/day


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RISK FACTORS

Enteral Feedings:

immature mucosal function

malabsorption

breast milk may have a protective effect

IGA

macrophages, lymphocytes complement components

lysozyme, lactoferrin

acetylhydrolase


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CLINICAL PRESENTATION

Gestational age:

< 30 wks31-33 wks

> 34 wks

Full term

Age at diagnosis:

20 days11 days

5.5 days

3 days

*Time of onset is inversely related to gestational age/birthweight


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Gastrointestinal:Feeding intolerance

Abdominal distentionAbdominal tenderness

Emesis

Occult/gross blood in stool

Abdominal mass

Erythema of abdominal wall

SystemicLethargy

Apnea/respiratory distressTemperature instability

Hypotension

Acidosis

Glucose instability

DIC

Positive blood cultures


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Sudden Onset:Full term or preterm infants

Acute catastrophic deterioration

Respiratory decompensation

Shock/acidosis

Marked abdominal distension

Positive blood culture

Insidious Onset:Usually preterm

Evolves during 1-2 days

Feeding intolerance

Change in stool pattern

Intermittent abdominal

distentionOccult blood in stools


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Modified Bell Staging for NEC

Stage &

Severity

Systemic Signs Abdominal Signs Radiographic Signs

Stage Ia

Suspected NEC

Temp changes, apnea,

bradycardia, lethargy

Distension, gastric

retention, emesis, heme

positive stool

Normal, or intestinal

dilation

Mild ileus

Stage Ib

Suspected NEC

Same as Ia Ia + grossly bloody

stool

Same as Ia

Stage IIa

Definite Mild NEC

Same as Ia Ib + absent bowel

sounds +/- abdominal

tenderness

Intestinal dilation,

ileus, pneumatosis

intestinalis

Stage IIb

Definite Moderate NEC

Ia + mild metabolic

acidosis,

thrombocytopenia

IIa + definite

tenderness, +/- abd

cellulitis, RLQ mass

IIa + ascites

Stage IIIa

Advanced, Severe NEC

Bowel Intact

IIb, but more severe, +

combined respiratory &

metabolic acidosis,

neutropenia, & DIC

IIb + peritonitis,

marked distension and

tenderness

Same as IIb

Stage IIIb

Advanced Severe NEC

Bowel Perforated

Same as IIb Same as IIIa IIIa +

pneumoperitoneum

Adapted from sources showing Bell Staging


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BELL STAGING CRITERIA

STAGE CLINICAL X-RAY TREATMENT

I. Suspect

NEC

Mild abdominal

distention

Poor feedingEmesis

Mild ileus Medical

Work up for

Sepsis

II. Definite

NEC

The above, plus

Marked abdominal

distention

GI bleeding

Significant

Ileus

Pneumatosis

IntestinalisPVG

Medical

III. Advanced

NEC

The above, plus

Unstable vital signs

Septic Shock

Pneumo-

Peritoneum

Surgical


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RADIOLOGICAL FINDINGS

Pneumatosis Intestinalis

hydrogen gas within the bowel wall

product of bacterial metabolism

a. linear streaking pattern

more diagnostic

b. bubbly pattern appears like retained meconium

less specific


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Abdominal Distension


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Severe Abdominal Distension


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Image from LearningRadiology.com


24/39


Portal Venous Gas

extension of pneumatosis intestinalis into the

portal venous circulation

linear branching lucencies overlying the liver and

extending to the periphery

associated with severe disease and high mortality


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Pneumoperitoneum

free air in the peritoneal cavity secondary toperforation

falciform ligament may be outlined

football sign

surgical emergency


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http://www.hawaii.edu/medicine/pediatrics/pemxray/v2c14.html


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Pneumatosis & Dilated Loops

Pneumatosis

http://www.hawaii.edu/medicine/pediatrics/pemxray/v2c14.html


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Dilated loops & Portal Air

Portal Air

Dilated

stomach &

loops ofbowel

http://www.adhb.govt.nz/newborn/TeachingResources/Radiology/AXR/NEC/NECwithPortalGasAP1.jpg


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A Bad Case of NEC

Pneumatosis

Portal Air

Abdomin

al free air

http://www.medicine.cmu.ac.th/dept/radiology/pedrad/case8ans.html


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LABORATORY FINDINGS

CBC

neutropenia/elevated WBC

thrombocytopenia Acidosis

metabolic

Hyperkalemiaincreased secondary to release from necrotic

tissue


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LABORATORY FINDINGS

DIC

Positive cultures

blood

CSF

urine

stool


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Neonatal NEC Pathology

Pneumatosis

Necrosis

http://phil.cdc.gov/PHIL_Images/02051999/00023/20G0023_lores.jpg


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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 feedingmakes any difference

Maintain high level of suspicion

Feeding babies with NEC worsens the disease


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TREATMENT

Stop enteral feeds

re-start or increaseIVF

Nasogastric decompressionlow intermittent suction

Antibiotics


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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


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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


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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


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PROGNOSIS

Depends on the severity of the illness

Associated with late complications

* strictures

short-gut syndrome

malabsorption

fistulas

abscess

* MOST COMMON


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Outcomes

Mortality varies with birth weight: Short gut -> FTT, malabsorbtion

Strictures -> further surgery in medical and surgical

NEC

Prolonged NPO status on TPN -> cholestasis &

metabolic abnormalities

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