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Necrotising enterocolitis
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Why you need to know about NEC
Scary Very sick, very quickly First signs: Increased aspirates Abdominal distension
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Framework Most common GI emergency in the NICU 1-5% of admissions
GIT and systemic Combination of factors (some known, some unknown): Immature gut Vascular insult Metabolic insult
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Who?
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Risk factors Prematurity: Why prems? Younger more prone
10% of infants <1500g Why prems? Immaturity of motility (less mobile, more disorganised) Greater permeability of gut (less barrier)
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Risk factors (cont’d) Relative hypoxia: Acute insult (e.g. asphyxia)
Cardiopulmonary disease (that includes all the RDS babies!) Polycythaemia (watershed areas)
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Risk factors (cont’d) Enteral feeds: Rare in unfed infants
Breast-feeding lowers risk Formula and stored EBM have less immunoprotective factors ?Mechanism: substrate for bug breeding (partial malabsorption of carbohydrate, fats; add relative dysmotility...)
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Risk factors (cont’d) Feeding patterns – controversial:
?Rate of increase: no relationship (Cochrane database review) ?Timing of initiation of feeds: no relationship (Cochrane database review) Minimal enteral or trophic feeds do not increase incidence of NEC
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Why? Nobel Prize answer No clear unifying theory One possibility:
Loss of mucosal integrity (ischaemic/toxic): infarction Bacterial proliferation (?aided by feeds) Invasion Transmural necrosis, perforation, peritonitis
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When? Classically 2-3 weeks after enteral feeds introduced (prems)
First week of life (terms) (Anytime: be on guard especially e.g. the NICU graduate feeding and growing in SCN)
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Nursing observation sheet
Increased volumes of gastric aspirate Bilious aspirate (2/3 cases) Bloody stools Temperature fluctuations A&Bs “Vitals” – evolving systemic shock
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Abdominal distension – most frequent early sign (70%)
Firm, tender (baby doesn’t like palpation), perfusion
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Changes in stool (bloody)
Worry when... Abdominal distension Feed intolerance Changes in stool (bloody) (especially when timing/set-up for NEC)
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Immediate action Consider: Treat baby before chasing tests!
“Resuscitation”: things you can do before and while you’re chasing confirmation of diagnosis; “Investigations”: seeking further weight to add to clinical suspicion of diagnosis Treat baby before chasing tests!
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Treating baby (“pre-investigation”)
Involve senior medical staff Manage as acute abdomen: Hold/stop feeds Ensure NGT down Treat shock (initial fluid bolus/es if required) IV access (after ordering AXR) for resuscitation and bloods
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Investigations AXR: supine and lateral decubitus Bloods: FBE U&Es
Blood culture (including anaerobic) Blood gas (CRP as baseline)
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AXR findings Early: non-specific intestinal dilatation, oedema
Free intra-peritoneal gas Portal venous gas (25%?) Pneumatosis (70-80%) Persistent, fixed sentinel bowel loop
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Tangent 1 – Intraperitoneal gas
Supine AXR: “Double wall sign” (Rigler’s sign) Visualization of falciform ligament (Silver’s sign) “Football sign” – abnormal lucency over liver, or central part of abdoemn Morrison’s pouch (hepatorenal abscess) – visible free edge of liver
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Intraperitoneal gas (cont’d)
Lateral decubitus: Patient right-side up May need to wait (up to 15mins) to allow air to rise! Lateral shoot-through
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Rigler’s sign (child post-VP shunt insertion)
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NEC complicated by pneumoperitoneum
Rigler’s sign (white arrows); falciform ligament (black arrow); free air over liver; intramural gas in bowel in left lower quadrant
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NEC complicated by perforation
“Football sign” (small black arrows); falciform ligament (large arrow)
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NEC complicated by pneumoperitoneum
Air in Morrison’s pouch – the liver edge is outlined
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Pneumoperitoneum Subtle lucency outlined by arrows in image on left; pneumoperitoneum confirmed on lateral decubitus
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Tangent 2 - Ultrasound Portal vein U/S is more sensitive than AXR in detecting portal venous gas Detection of pneumatosis
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Ultrasound of pneumatosis
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Bloods
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Bloods findings FBE: U&Es: Gas: acidosis (metabolic or combined)
WCC: too high or too low Platelets: too low (50%) – poorer prognosis (Hb/h’crit: rule out polycythaemia as exacerbating factor) U&Es: Na+: too high or too low K+: usually too high Gas: acidosis (metabolic or combined) (Blood group: especially if possible transfer)
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Management Check previous management happening:
Nil orally (order TPN!) NGT down (check position on AXR) IV access Fluid resuscitation/circulatory support (may need inotropes)
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Management (cont’d) Antibiotics: Treat derangement of:
Usually triple (including anaerobic cover) e.g. ampicillin, gentamicin, metronidazole Bacteraemia in up to 30% Treat derangement of: Electrolytes (Na+, K+) Blood gas derangement (ventilation, fluid +/- NaHCO3) Strict fluid balance (and watch urine output)
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Decision-making Appropriate site for management: here, or transfer to RCH (access to surgeons) Liaison with RCH surgery and RCH Neonatal Unit (+/- NETS) AXR for surgeons to view If for transfer: resuscitation, medical optimization of baby’s status
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Medical management Nil orally for 7-10 days (TPN)
Antibiotics for 10 days ?Peritoneal drainage (especially in VLBW)
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Medical management (cont’d)
Respiratory support (abdominal splinting) Inotropic support prn Fluid, electrolyte management Regular surveillance of abdomen for complications (e.g. perforation)
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Surgical management Laparotomy Especially if perforation
Resection, stoma formation May leave borderline bowel, opt for “second-look” laparotomy
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Prognosis Serious illness: 20-40% mortality (NEC with perforation)
Laparotomy = major surgery Degree of resection can have long-term consequences (e.g. short-gut syndrome)
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Take home points (for regs!)
Beware nursing concern re big bellies and aspirates Especially either on an upward trend Bilious aspirate is never a good thing Feel the belly every day ?Most important part of daily examination Any suspicion: Involve senior (hard diagnosis, serious illness) Initial management measures (won’t harm baby)
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Acknowledgements Images from: Royal Women’s Hospital, Melbourne.
Williams H. Perforation: how to spot free intraperitoneal air on abdominal radiograph. Arch Dis Child Educ Pract Ed 2006; 91: ep54-ep57.
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