Loading…

Flash Player 9 (or above) is needed to view presentations.
We have detected that you do not have it on your computer. To install it, go here.

Like this presentation? Why not share!

Necrotizing Enterocolitis

on

  • 1,603 views

 

Statistics

Views

Total Views
1,603
Views on SlideShare
1,603
Embed Views
0

Actions

Likes
1
Downloads
53
Comments
0

0 Embeds 0

No embeds

Accessibility

Categories

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

    Necrotizing Enterocolitis Necrotizing Enterocolitis Presentation Transcript

    • Problem Based Paediatrics
      The Septic Preterm baby
      (Sepsis & NEC)
      Dr Amjad IMAM
    • The Nurse on the Special Care Unit calls you to review MK, an infant born at 28 weeks, now 10 days old,who was being weaned off ventilation.
      He now become unwell, desaturating on handling and with temp instability
      What are your differentials?
      What do you needs to find out in your history?
    • What are your differentials?
      Septicaemia
      Meningitis
      Pneumonia
      Necrotising enterocolitis(NEC)
      Intraventicular Haemorrhage(IVH)
      Apnea of prematurity
      Respiratory distress syndrome(RDS)
      Patent ductus arteriosus(PDA)
    • What do you need to find out in your Hx?
      How & when MK condition changed? Sudden or overtime.
      Has his ventilatory requirement altered?
      What feeding regime is he on and is he tolerating feed?
      Ask about content of nappies!,is there any blood or malaena?
      Any abdominal distention?any neurological symptoms(Seizure?)
      Obstetric Hx? Reason of prematurity(multiple gestation,infection,antepartum haemorrhage)
      Growth retardation? Type of delivery?
      Did mother received steroids before birth?
    • MK was born by SVD at 28 weeks gestation after premature labour.
      Twenty four hour beforeonset of contraction there was a spontaneous rupture of membrane at which time mum was given an I/M injection of steroid. MK was transferred to special baby unit and initially was doing well.
      However he developed difficulty in breathing and was started on CPAP nia nasal cannulae. This did not help and he was sedated intubated and ventilated. He was given surfactant for presumed RDS and antibiotic for possible infection. Blood culture were sterile. For the last 3 days his ventilation has been improving and the neonatologist were planning a trial of extubation.
      Today he has had frequent episodes of desaturationto70%&accompanying bradycardia to 60/min. Today he has stopped tolerating his N/G feeds of formula milk and started vomiting. His temp has been upto 38 C and down to 35 C.
      What features will you look for on examination ?
    • What feature will you look for on examination?
      Colour; jaundice , cyanosis, mottling or rash?
      Examine chest: recession? I/c,,s/c, Crackle or Crepitation?
      Pulse, BP,perfusion: sign of shock?
      Assess his hydration?
      Assess CVS: PDA?bounding pulse,machinery murmer?
      Feel abdomen: skin tense and shiny?distention? Gaurding?
      Auscultation for bowl sound, transillumination(Perforation NEC?)
      CNS: bulging fontanelle? Sing of raised ICP?
    • MK is clearly unwell. His breathing is rapid and as you watch his oxygen sat. falls to 75%. His abdomen is grossly distended and is tympanic to percussion but does not transilluminate. His nurse tells you that his last nappy contained very dark stools.
      His temp is 37.8C , Pulse 195, BP 40/20,
      RR 45, Capillary refill time 4 sec & Oxygen Sat 85%
      What is your immediate management?
      What antibiotic therapy will you start?
      What investigations will you perform?
    • What is your immediate management?
      Nill by mouth, TPN
      Naso gastric tube, decompression of stomach
      Antibiotics
      Support circulation. Rx shock
      Ventilatory support
      Surgical intervention?
      What antibiotic therapy will you start?
      Broad spectrum with anti anaerobe= Pen+Gent+Metro
      What investigation will you perform?
      FBC , U&E , Clotting , ABG, Blood culture,
      Stool occult blood & culture
      Abdominal X-ray
    • Some of the MK’sinvestigations are back:
      Haemoglobin 9.5 g/dl
      WCC 1.2 10*9/L
      Platelets 19 10*9/L
      The abdominal X-Ray showed distended loops of bowel with thickening of the bowel wall, with intramural air and air in the portal tract.
      How to you interpret these result?
    • MK’s condition suddenly deteriorate. He becomes more tachycardiac and his ventilation deteriorates and his blood pressure fall . Measurement of his abdominal circumference confirm that the distension has increased . His abdomen now transilluminate.
      What has happened?
    • What has happened?
      MK had NEC with bowl perforation.
      He requires emergency resuscitation(fluid bolus+ionotropic support+FFP) followed by paediatric surgery referral?
      He was taken to theatre and partial bowel resection is performed. He was kept on antibiotics+TPN and monitored closely.
      He was gradually reintroduced enteral feeds.
    • Neonatal Sepsis
    • Definition & Incidence
      Clinical syndrome of systemic illness accompanied by bacteremia occurring in the first month of life
      Incidence
      1-8/1000 live births
      13-27/1000 live births for infants < 1500g
      Mortality rate is 13-25%
      Higher rates in premature infants and those with early fulminant disease
    • Early Onset
      First 5-7 days of life
      Usually multisystem fulminant illness with prominent respiratory symptoms (probably due to aspiration of infected amniotic fluid)
      High mortality rate
      5-20%
      Typically acquired during intrapartum period from maternal genital tract
      Associated with maternal chorioamnionitis
    • Late Onset
      May occur as early as 5 days but is most common after the first week of life
      Less association with obstetric complications
      Usually have an identifiable focus
      Most often meningitis or sepsis
      Acquired from maternal genital tract or human contact
    • Nosocomial sepsis
      Occurs in high-risk newborns
      Pathogenesis is related to
      the underlying illness of the infant
      the flora in the NICU environment
      invasive monitoring
      Breaks in the barrier function of the skin and intestine allow for opportunistic infection
    • Causative organisms
      Primary sepsis
      Group B streptococcus
      Gram-negative enterics (esp. E. coli)
      Listeria monocytogenes, Staphylococcus, other streptococci (entercocci), anaerobes, H. flu
      Nosocomial sepsis
      Varies by nursery
      Staphylococcus epidermidis, Pseudomonas, Klebsiella, Serratia, Proteus, and yeast are most common
    • Differential Diagnosis
      Clinical signs and symptoms are nonspecific
      Differential diagnosis
      - NEC
      RDS
      Metabolic disease
      Hematologic disease
      CNS disease
      Cardiac disease
      Other infectious processes (i.e. TORCH)
    • Clinical presentation
      Temperature irregularity (high or low)
      Change in behavior
      Lethargy, irritability, changes in tone
      Skin changes
      Poor perfusion, mottling, cyanosis, pallor, petechiae, rashes, jaundice
      Feeding problems
      Intolerance, vomiting, diarrhea, abdominal distension
      Cardiopulmonary
      Tachypnea, grunting, flaring, retractions, apnea, tachycardia, hypotension
      Metabolic
      Hypo or hyperglycemia, metabolic acidosis
    • Diagnosis
      Cultures
      Blood
      Confirms sepsis
      94% grow by 48 hours of age
      Urine
      Don’t need in infants <24 hours old because UTIs are exceedingly rare in this age group
      CSF
      Controversial
      May be useful in clinically ill newborns or those with positive blood cultures
    • Investigation
      White blood cell count and differential
      Neutropenia can be an ominous sign
      I:T ratio > 0.2 is of good predictive value
      Serial values can establish a trend
      Platelet count
      Late sign and very nonspecific
      Acute phase reactants
      CRP rises early, monitor serial values
      ESR rises late
      Other tests: bilirubin, glucose, sodium
    • Radiology
      CXR
      Obtain in infants with respiratory symptoms
      Difficult to distinguish GBS or Listeria pneumonia from uncomplicated RDS
      Renal ultrasound and/or MCUG in infants with accompanying UTI
    • Management
      Antibiotics
      Primary sepsis: ampicillin and gentamicin
      Nosocomial sepsis: vancomycin and gentamicin or cefotaxime
      Change based on culture sensitivities
      Don’t forget to check levels
    • Supportive therapy
      Respiratory
      Oxygen and ventilation as necessary
      Cardiovascular
      Support blood pressure with volume expanders and/or pressors
      Hematologic
      Treat DIC with FFP and/or cryo
      CNS
      Treat seizures with phenobarbital
      Watch for signs of SIADH (decreased UOP, hyponatremia) and treat with fluid restriction
      Metabolic
      Treat hypoglycemia/hyperglycemia and metabolic acidosis
    • GBS Prophylaxis
      GBS is the most common cause of early-onset sepsis
      0.8-5.5/1000 live births
      Fatality rate of 5-15%
      10-30% of women are colonized in the vaginal and rectal areas
      Most mothers are screened at 35-37 weeks gestation
    • Necrotizing Enterocolitis
    • Necrotizing Enterocolitis
      One of the most serious GI diseases of neonates, especially preterm infants.
      Intestinal necrosis that can involve all layers of the bowel.
      Most commonly involves the ileum and colon but can occur anywhere.
    • Epidemiology
      Variable incidence
      Cases often cluster
      90-95% of cases are in preterm infants (<34 wks GA)
      ~10% infants < 1500 grams birth weight (2 – 22%)
      1-2% Japan, 7% Austria, 14% Argentina, 28% Hong Kong (VLBW)
    • Epidemiology
      Age at onset is inversely related to gestational age
      Typically occurs in preterm infants at >7 days (2nd to 3rd week of life)
      25% of cases occur at > 1 month of age
    • Risk Factors
      Prematurity (umbilical lines, low apgar scores, PDA, )
      Enteral feeding
      Vasoconstrictive drugs (cocaine, indomethacin, pressors)
      Bacterial colonization
      Polycythemia
      Exchange transfusion
      Multiple gestations?
      Congenital heart disease, arrhythmias
    • Enteral feeding
      NEC occurs almost exclusively after enteral feedings
      Feeding rate??
      Slow careful increases may decrease NEC incidence
      No difference between slow feeding advances of 15cc/kg/day (13%) and faster advances of 35cc/kg/day (9%)
      Breast Milk .vs. Formula??
      The incidence of NEC is lower in infants fed breast milk versus formula
      Breast milk increases the diversity of bacterial species colonizing the GI tract of preterm infants
    • Bacterial colonization
      ELBW infants (<1000g) have a decreased number of bacterial species colonizing the GI tract
      Antibiotics decrease the number of bacterial species in the GI tract
      Preterm infants have a decreased colonization with Bifidobacteria/Lactobacillus which may be protective against NEC
    • Etiology???
      Hypoxemia, acidosis, low cardiac output
      Splanchnic ischemia
      hypertonic feedings mucosal edema/ulceration
      Abnormal gut immunity bacterial colonization
      Invasive infection of bowel wall
      Portal system and lymphatics
      Pneumatosis, portal gas endotoxin release
      Transmural bowel necrosis Sepsis, DIC, Shock
      perforation
    • Clinical Signs(GI system)
      Feeding Intolerance
      Gastric residuals
      Emesis
      Bilious residuals/emesis
      Abdominal distention
      Bloody stools
      Carbohydrate intolerance
      Abdominal pain
      Irritability
      Ileus
    • Clinical Signs (systemic)
      Temperature instability
      Hypo or hyperglycemia
      Lethargy
      Apnea
      Bradycardia
      Poor perfusion
      Shock
    • Clinical Hallmark
      Guiac positive stools
      Abdominal Distention
      Gastric residuals
      (pneumatosis intestinalis)
    • Diagnostic Findings
      Hypotension
      Neutropenia or neutrophilia
      Thrombocytopenia
      Acidosis
      Coagulopathy
    • Radiographic Findings
      Dilated loops
      (width of lumbar vertebral bodies as objective criteria)
      Ileus (sentinel loop)
      Thickened bowel walls
      Pneumatosis intestinalis
      Portal venous gas
      Ascites
      Intraperitoneal free air
    • Dilated Loops
    • Dilated Loops
    • Gasless Abdomen
    • Pneumatosis
    • Pneumatosis (? Free Air)
    • Portal Gas
    • Pneumatosis, Portal Gas
    • Free Air
    • Free Air
    • Classification (Bell Stages)
      Stage I - Suspected NEC
      Mildly ill (temperature, apnea, lethargy)
      Mild GI signs (residuals, abdominal distention, heme positive stools)
      Minimal x-ray findings (normal, dilation, ileus)
      Stage II – Definite NEC
      More clinical findings (mild acidosis, mild thrombocytopenia)
      More GI signs (absent bowel sounds, abdominal tenderness)
      More x-ray findings (pneumatosis, portal gas)
      Stage III – Advanced NEC
      Severe clinical illness (hypotension)
      Increased GI signs (marked abd distention, tenderness, signs of peritonitis)
      Ominous x-ray findings (ascites, free air)
    • Treatment
      NPO
      GI decompression
      Sepsis workup (blood culture, LP, …)
      Antibiotics (amp/gent .vs. amp/gent/clinda)
      Respiratory (intubation, mechanical ventilation)
      Cardiovascular (volume, pressors)
      Hematologic (platelets, clotting factors)
      Metabolic (acidosis)
      FEN (hyperalimentation)
      Serial studies (3 way abdominal x-rays, CBC, coags, ABG’s, lytes,)
    • Surgical Management
      30 to 50% of NEC cases will require surgical intervention
      Bedside drainage (usefull in critically ill infants)
      Laparotomy
      Resection (may not do anything for pan-intestinal nec)
      Ostomy .vs. primary reanastomosis
    • Complications of NEC
      Complications occur in about half of infants surviving NEC
      Strictures (25-35%)
      Adhesions
      Abscesses
      Fistulas
      Malabsorption
      Short Bowel Syndrome
      TPN and central line complications
    • Outcomes
      Mortality 10-30%
      ELBW infants have an increased mortality
      Increased morbidity in survivors
      Developmental delay when compared to age-matched controls
      Increased morbidity secondary to NEC is independent of birth weight, intraventricular hemorrhage or periventricular hemorrhage.