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ENTEROCOLITIS
By : Irwan Subekti
NECROTIZING
ENTEROCOLITIS
Epidemiology:
Paling sering terjadi pada bayi prematur
kegawatan GI
Penyebab utama bedah emergensi pada neonatus
Kebanyakan incidence: 1-5% di NICU
Paling sering terjadi pada bayi prematur BBLSR
10% of all cases occur in term infants
NECROTIZING
ENTEROCOLITIS
Epidemiology:
10x sangat mungkin terjadi pada bayi yang
telah diberi makanan
males = females
blacks > whites
mortality rate: 25-30%
50% dari pasien mengalami gejala sisa jangka
lama
FROM: Necrotizing Enterocolitis in Full-Term Infants: CaseControl Study and Review of the Literature
Ayala Maayan-Metzger, Amir Itzchak, Ram Mazkereth and Jacob Kuint
NECROTIZING
ENTEROCOLITIS
Pathology:
Area yang paling sering terlibat: terminal ileum
and proximal colon
MAKROSKOPIS:
Usus mengalami dilatasi tak beraturan dengan
perdarahan/area ischemic pada frank necrosis
focal or diffuse
MICROSCOPIC:
mucosal edema, hemorrhage and ulceration
NECROTIZING
ENTEROCOLITIS
MICROSCOPIC:
Inflamasi minimal selama fase akut
Meningkat selama revaskularisasi
Jaringan granulasi dan fibrosis berkembang
Pembentukan striktur
Microthrombi di arteriol mesenterika dan
venula
CIRCULATORY INSTABILITY
Hypoxic-ischemic event
Polycythemia
UNKNOWN CAUSE
MUCOSAL INJURY
INFLAMMATORY MEDIATORS
Inflammatory cells (macrophage)
Platelet activating factor (PAF)
Tumor necrosis factor (TNF)
Leukotriene C4, Interleukin 1; 6
ENTERAL FEEDINGS
Hypertonic formula or medication
Malabsorption, gaseous distention
H2 gas production, Endotoxin
production
RISK FACTORS
Infectious Agents:
usually occurs in
clustered epidemics
normal intestinal flora
Prematurity:
mucosal barrier
poor motility
immature
response
impaired
dynamics
immune
circulatory
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
E. coli
Klebsiella spp.
Pseudomonas spp.
Clostridium difficile
Staph. Epi
Viruses
Inflammatory Mediators:
neutropenia, thrombocytopenia,
acidosis, hypotension
primary factors
RISK FACTORS
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
>20cc/kg/day
Enteral Feedings:
immature mucosal function
malabsorption
IGA
macrophages, lymphocytes
complement components
lysozyme, lactoferrin
acetylhydrolase
CLINICAL PRESENTATION
Gestational age:
< 30 wks
31-33 wks
> 34 wks
Full term
Age at diagnosis:
20 days
11 days
5.5 days
3 days
CLINICAL PRESENTATION
Gastrointestinal:
Systemic
Feeding intolerance
Abdominal distention
Abdominal tenderness
Emesis
Occult/gross blood in stool
Abdominal mass
Erythema of abdominal wall
Lethargy
Apnea/respiratory distress
Temperature instability
Hypotension
Acidosis
Glucose instability
DIC
Positive blood cultures
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
distention
Occult blood in stools
RADIOLOGICAL FINDINGS
Pneumatosis Intestinalis
extension of
pneumatosis intestinalis
into the portal venous
circulation
product of bacterial
metabolism
a. linear streaking
pattern
linear branching
lucencies overlying
the liver and extending
to the periphery
associated with severe
disease and high
mortality
more diagnostic
b. bubbly pattern
appears like retained
meconium
less specific
Pneumoperitoneum
free air in the peritoneal
cavity secondary to
perforation
falciform ligament may be
outlined
football sign
surgical emergency
LABORATORY FINDINGS
CBC
neutropenia/elevated
WBC
thrombocytopenia
Acidosis
metabolic
Hyperkalemia
increased secondary to
release from necrotic
tissue
DIC
Positive cultures
blood
CSF
urine
stool
PROGNOSIS
Tergantung pada tingkat keparahan penyakit
Terkait dengan komplikasi akhir
Striktur
Sindrom usus pendek
Malabsorpsi
Fistula
Abses
MOST COMMON
CASE
o BY DB, 30 hari, laki-laki, MRS tgl 7-11-2013. by
dilahirkan spontan, presentasi kepala, ketuban warna
kuning, langsung menangis. Uk : 32 minggu, BBl : 1700
gram, PB : 45 cm
o Klien di rawat di ruang bayi RSU K selama 5 hari lalu
di pulangkan.
o Bayi kuning saat umur 13 hari kemudian di bawa ke
bidan dan langsung di pulangkan dengan obat puyer
o Tgl 7-11-2011 klien di bawa ke RS X langsung ke IGD
dengan keluhan mencret sejak 3 hari SMRS >3x/hari
sedikit-sedikit darah (-) lendir (-) warna kuning
o Perut membesar sejak 1hari SMRS, pada pemeriksaan
fisik didapatkan hipertimpani, perut cembung,
o Kembung pada bayi sejak 1minggu SMRS
o Saat pengkajian : KU mencret dan perut membesar
CASE
Kesadaran :somnolen
GCS
:456
TD____/____mmhg
RR = 20x/mnt
N; 112x/menit
BB= 2,7 kg
Suhu 37,5C
TB= - cm
PENUNJANG
1.foto otot polos perut : terdapat gambaran
akumulasi gas di
usus.
2.Laboratorium
Tanggal 8 Nopember 2011
Lekosit
: 8500 / ul (N = 3500-10000)
Hb
: 8,0 gr/dl (N = 11,0-16,5)
Hematokrit : 22,6 % (N = 35-50)
Trombosit : 232000 /ul (N = 150000-390000)
GDS
: 361 mg/dl (N = >200)
Ureum
: 11,7 mg/dl (N = 10-50)
Albumin
: 3,33 gr/dl (N = 3,5-5,5)
TREATMENT
Nasogastric decompression
low intermittent suction
Antibiotics
Amp/Gent; Vanc/Cefotaxime
Clindamycin
suspected or proven
perforation
Surgical Consult
suspected or proven NEC
indications for surgery:
portal venous gas;
pneumoperitoneum
clinical deterioration
despite medical
management
positive paracentesis
fixed intestinal loop on
serial x-rays
erythema of abdominal wall
TUGAS
Berdasarkan ilustrasi kasus di atas
buatlah ASKEP dan temukan masalah
keperawatan yang dapat muncul
Lakukan analisis terhadap kasus tersebut
TERIMAKASIH