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Necrotizing Enterocolitis

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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.