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Necrotizing Enterocolitis         (NEC)    Case presentaion            By   Dr. ASHRAF HAMED  prof. Pediatric Surgery   Al...
Case presentationMALE saudi baby ,5days old  ,preterm(35weeks gestational age)with  history of PROM for >48 hour,referred ...
O/E 19-4-24 at 3pm The baby looks severly ill,dehydrated,toxic facies &    poor perfusion B W:2.4Kgm Unstable vital signs:...
Plain x- ray:showed pneumoperitoneumBlood chemistry:WBC….1.300/cmm;platelets…17000/cmm;HG….9.8gm%,.PT&PTT>2MINABG……….sever...
CONT.   The baby admitted in NICU and    immediately started aggressive    resuscitations with IV fluids and    antibioti...
Case presentationWe inserted penrose sheet drain at right lower  quadrant under local anaesthesia which  brought air and f...
20/4 at 10:00 a.m.Pt submitted for laparotomy and we  found:Sever faecal peritonitis and amulgmation of   intestine with p...
Also there were 2 yellowish dirty,   non viable patches, but not yet   perforated 1st one 15 cm from   DJF and the 2nd 15 ...
at 7:30 pm urine output was 5 ml, with    appearance of sclermatous skin changes &    muscle stiffness .21/4 at 9:00 a.m.T...
case diagnosed as acute renal failure so,   managed by:--Lasix I.V. 5 mg / kg state-   D/C amikine-   Adjust dose of vanco...
2 4/4Development of purpura fulminans   ,ulceration, oral,ETT bleeding with   platelets 10,ooo but pt passed blackish   st...
The finding of 2nd laparotomy (29-4-24)The previous two yellowish dirty non viablepatches in the jejuneum were perforated ...
Gastrograffin follow   through done and   showed no leakage   of the dye with   healing of the   proximal   perforating.Th...
The pt became deeply jaundiced with   elevated liver enzymes, ⇑ total and   direct bilirubin and his body weight   decreas...
CASE PRESENTATION
CASE PRESENTION2/6/24So,we decided to close the jejunostomy.colostomy became functioning after 2 days   postoperatively . ...
colostomy
After closure of colostomy
Nectotizing EnterocolitisIntroductionit is the most common newbornsurgical emergency, with a mortalityrate that far excee...
Nectotizing Enterocolitis   It usually occurs on the tenth day of life,   but it may develop on the first day, several   w...
Nectotizing Enterocolitis N.E.C. is widely accepted as a complication of prematurity in which there is intestinal hypoxia...
EpidemiologyI – Incidence  Overall incidence of NEC is 2-5% of all NICU  admissions.  The incidence of NEC is approximat...
Epidemiology   Incidence varies between hospitals    and also within the same institution in    different periods reflect...
Epidemiology  Mean age of onset is 3-4 days for term  infants and 3-4 weeks for infant born at  less than 28 week’s gesta...
NECROTIZING    ENTEROCOLITIS   Pathophysiology:    UNKNOWN    CAUSE…….
CIRCULATORY INSTABILITYPRIMARY INFECTIOUS AGENTS                                           Hypoxic-ischemic eventBacteria,...
EpidemiologyII Risk FactorsDespite several decades of research theetiology and pathogenesis remainedelusive.There is wid...
Epidemiology .Prematurity The most dominant risk factor for NEC  is the degree of Immaturity.   – 90% of cases are prematu...
Epidemiology  2 –Enteral Feedings        > 90% of infants with NEC have been fed        provides a source for H2 product...
EpidemiologyB – Umbilical Catheterization-Embolization of catheters may result inembolization of mesenteric arteries.-Infu...
EpidemiologyD-– Extreme Low birth weightIt was proved that the incidence of NEC is    higher in those babies with birth   ...
EpidemiologyF. Infection-   Although no specific single organism    was implicated in the diseaseG. Hypotension & ShockH. ...
Epidemiology4. Maternal Risk Factors1) Pre-eclampsia2) Placental insufficiency3) Prolonged PROM4) Drugs as Heroin         ...
Pathogenesis Most investigators suggested that NEC  resulted from intestinal mucosal injury  from low - Flow states, or h...
PathogenesisIndirect injuries are the result of mucosalcell hypoxia from low flow states: .Shock .Hyperviscosity .Vascu...
Pathogenesis*   Once the mucosa has been injured,bacteria in the lumen can breach the gut barrierAnd initiate an inflammat...
PathologyNEC may beI. FOCAL(Isolated) diseaseWhen a single area of bowel is   necrotic or perforatedII.MULTIFOCAL      Mul...
Multi – segmental disease
PathologyInvolvement of both the  large and small  intestine occurs in  44% of cases.III. Pan – Involvement  (NEC totalis)...
Macroscopic Features Grossly distended loops of the intestine  with spotty intramural haemorrhagl and  areas of necrosis ...
Microscopic Features The essential feature are haemorrhage and   necrosis (coagulation necrosis). Mucosal oedema followe...
ComplicationsShort Term1 – Perforation.2 – Septicaema.3 – Metabolic and electrolyte   distubance.4 – Prolonged need for ar...
II – Long Term1. Strictures   - It is the most common long term GIT complication    of NEC, occuring in (10-35%) of all s...
3.FULMINANT SEPSIS4.TPN related complications:Cholestasis;Thrombosis;Infection5. Complications related to stoma:Retraction...
6. Wound complications        Infection, Dehiscence      or Enterocutaneous fistula7. RecurrenceOccurred in 10% (Rennie an...
CLINICAL PRESENTATIONGastrointestinal:           Systemic•   Feeding intolerance     •   Lethargy•   Abdominal distention ...
CLINICAL PRESENTATIONSudden Onset:              Insidious Onset: Full term or preterm      Usually preterm  infants Acu...
BELL STAGING CRITERIASTAGE           CLINICAL               X-RAY TREATMENTI. Suspect      Mild abdominal         Mild ile...
Modified Bell StagesStage       Stage      Systemic     Intestinal           Radiolog                        Signs        ...
Modified Bell StagesStage       Stage          Systemic          Intestinal        Radiologic                            S...
Modified Bell StagesStage        Stage         Systemic Signs            Intestinal     Radiologi                         ...
IMAGING       The cornerstone of the diagnosis of       NEC is plain anteroposterior and       left lateral decubitus radi...
Pneumatosis intestinalis
Pneumatosis intestinalis
Pneumatosis intestinalis
Pneumatosis Intestinalis   hydrogen gas within the bowel wall       A by-product of bacterial metabolism     a. linear st...
3. Portal venous gas•    It appears as linear     branching arborizing pattern     of air over the liver shadow.•    It ma...
5. Intraperitoneal fluid•   It is assoicated with high mortality rate.•   Amenable to paracentesis6. Persistent dilated lo...
Contrast Study It may be used in patients with equivocal  radiologic signs Barrium should never be used Newer water – s...
Ultra- SonographyIt has been used to identifya. Necrotic bowelb. Intraperitoneal fluidc. Portal venous gas•   It is the mo...
MANAGEMENTNon-operativeThe mainstay of treatment for NEC is non-operative   therapy.1.   NPO & gastric suction ⇒ 10 – 14 d...
4. Intravenous fluids: 150 – 250 ml / kg5. TPN6. Blood and Blood products: as needed forcorrection of anaemia and coagulop...
Indications for operation1. Pneumoperitoneum•   This is the only absolute indication for    surgery.•   Relative indicatio...
3. Fixed dilated intestinal loop.4. Ascites•   43% of patient’s ascites will have    bowel necrosis.•   The demonstration ...
Paracentesis5. Positive Paracentesis– Indicated for infants with  extensive pneumatosis  intestinalis or who have failed t...
Operative Managementbed-side Peritoneal drainage* It is insertion of a penrose drain     through a right lower quadrant   ...
Laparoscopy�Clarckand Mackinaly reported the use of laparoscopy    in the treatment of a VLBW infant (900 g) with    perfo...
II. Principles of ResectionA. When a single area of bowel is necrotic or   perforated only limited resection is   necessar...
Segmental NECContrast study  Segmenal necrosis                                    Multiple segments necrotic    of one seg...
III. Multi – segmental disease( > 50%   viable)A. Excision of each diseased segment and   creates multiple stomas.B. “Patc...
C. “Clip and drop-back” Technique•   Obviously necrotic bowel is removed.•   The cut ends are closed with titanium clips.•...
Pan – Involvement = Nec Totalis                                                 Operation                                 ...
IV. Pan – Involvement = Nec TotalisThe Treatment options1. Simple closure of the abdomen2. Resection of all necrotic bowel...
Prevention   �Breast milk   �Antenatal Steroid therapy   �Oral immunoglobulins   �Oral antibiotics   �Probiotics(Lact...
Take Home Messages   Go slow!!!!!   Breast is best!!!
NEC  اشرف حامدi
NEC  اشرف حامدi
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NEC اشرف حامدi

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NEC اشرف حامدi

  1. 1. Necrotizing Enterocolitis (NEC) Case presentaion By Dr. ASHRAF HAMED prof. Pediatric Surgery Al Azhar university
  2. 2. Case presentationMALE saudi baby ,5days old ,preterm(35weeks gestational age)with history of PROM for >48 hour,referred from El zulfi general hospital as a case of sepsis with ?NEC.There was history of bleeding per rectum since second day of life and oliguria ,as the baby passed only 5 ml urine in last 24 hour.
  3. 3. O/E 19-4-24 at 3pm The baby looks severly ill,dehydrated,toxic facies & poor perfusion B W:2.4Kgm Unstable vital signs: low BP,pulse:170/min,temp:38.5 The abdomen was severly distended with erythema of abdominal wall. Generalized tenderness. Absent bowel sound (died silent)
  4. 4. Plain x- ray:showed pneumoperitoneumBlood chemistry:WBC….1.300/cmm;platelets…17000/cmm;HG….9.8gm%,.PT&PTT>2MINABG……….severe acidosis.
  5. 5. CONT. The baby admitted in NICU and immediately started aggressive resuscitations with IV fluids and antibiotics(claforan,flagyl infusion and vancomycin),NGT decomression of the stomach
  6. 6. Case presentationWe inserted penrose sheet drain at right lower quadrant under local anaesthesia which brought air and faecal matter to give chance for improvement of general condition,meanwhile packed rbcs, platelets and FFP were given with continous IV fluids resuscitation.
  7. 7. 20/4 at 10:00 a.m.Pt submitted for laparotomy and we found:Sever faecal peritonitis and amulgmation of intestine with pyogenic membrane covering it.we discovered oedema and hyperaemia of the descending colon and big necrotic segment in the sigmoid colon up to level of peritoneal reflection over the rectum.
  8. 8. Also there were 2 yellowish dirty, non viable patches, but not yet perforated 1st one 15 cm from DJF and the 2nd 15 cm distal to the 1st one which were Imbricated with interrupted lambert sutures with 5/0 viryl .Lt hemicolectomy done with hartman’s procedure closure of distal stump and the proximal end as a terminal colostomy .
  9. 9. at 7:30 pm urine output was 5 ml, with appearance of sclermatous skin changes & muscle stiffness .21/4 at 9:00 a.m.The whole body got oedematous and baby gained 300 gm post- operatively due to renal shut down as only 5 ml urine passed.- Signs of fulminant sepsis in the form of persistant hypotension, poor perfusion and scleroderma that carrying out bad prognosis. C.B.G. also showed mixed acidosis on high ventilation sitting.
  10. 10. case diagnosed as acute renal failure so, managed by:--Lasix I.V. 5 mg / kg state- D/C amikine- Adjust dose of vancomycin and cefotaxim serum urea 16.7 mmol/l serum.Creatinine 147 mmol.T .protein 23&albumin 12albumin 20% 1 gm 1kg over 1 hour given stat then lasix as before9:00 pm pt passed 31 cc clear urine after that ttt with progressive improvement of renal function and urine output.
  11. 11. 2 4/4Development of purpura fulminans ,ulceration, oral,ETT bleeding with platelets 10,ooo but pt passed blackish stool from stoma.28/4Sub- cutaneous wound collection without burst abdomen.faccal matter coming from the wound with sluggish instestinal sounds but x-ray abdomen ----- no pneumoperitoneum so, 2nd laparatomy done
  12. 12. The finding of 2nd laparotomy (29-4-24)The previous two yellowish dirty non viablepatches in the jejuneum were perforated so,refreshment of the edges and repair with 5/0vicryl single layer interrupted for theproximal one and for the distal one we took itsproximal end as a jejunostomy and the distalend closed. (jejunostomy at Rt iliac fossa)
  13. 13. Gastrograffin follow through done and showed no leakage of the dye with healing of the proximal perforating.Then we started oral feeding through N.G.T. and every now and then correction of anaemia and thrombocytopenia.
  14. 14. The pt became deeply jaundiced with elevated liver enzymes, ⇑ total and direct bilirubin and his body weight decrease to 1.9 kg as stoma extrude the milk undigested after feeding through N.G.T., so, at 1st we changed to N.G.T. drip method.There is little increase of body weight to 2 kg.So, we started T.P.N. through Rt subclavian veiv(cut doun) when all other substitutes failed. Also, with little improvement.
  15. 15. CASE PRESENTATION
  16. 16. CASE PRESENTION2/6/24So,we decided to close the jejunostomy.colostomy became functioning after 2 days postoperatively . also, we stopped T.P.N. because of increasing liver enzymes.Then patient tolerated gradually NGT feeding and passed post operative smoothly till discharged at 26/6/24 and 2 months later the patient came for closure of colostomy
  17. 17. colostomy
  18. 18. After closure of colostomy
  19. 19. Nectotizing EnterocolitisIntroductionit is the most common newbornsurgical emergency, with a mortalityrate that far exceeds that of any othergastrointestinal condition requiringoperation.It is a syndrome of acute intestinalnecrosis.NEC is a disease of paradoxes. Ittypically affect the preterm infant but
  20. 20. Nectotizing Enterocolitis It usually occurs on the tenth day of life, but it may develop on the first day, several weeks, or even months after birth. The disease frequently appears sporadically but can present in epidemic – like clusters. Most patients who develop the disease were fed enterally, but babies who have never been fed also are susceptible.
  21. 21. Nectotizing Enterocolitis N.E.C. is widely accepted as a complication of prematurity in which there is intestinal hypoxia, usually due to a low perfusion state which results in mucosal injury and allows translocation of bacteria into the intestinal wall and portal venous system. Two-Thirds of patients respond to medical management, only about one- third require surgical intervention.
  22. 22. EpidemiologyI – Incidence Overall incidence of NEC is 2-5% of all NICU admissions. The incidence of NEC is approximately 1-3 cases/1000 live births in the u.s. or about 25,000 new cases of NEC worldwide / year. The incidence is much higher in premature (90-93%)and extreme low birth weight infants.
  23. 23. Epidemiology Incidence varies between hospitals and also within the same institution in different periods reflecting periodic epidemics It occurs more commonly among infants fed formula( 9o to 95% enterely fed)compared to those who have been fed with breast milk.
  24. 24. Epidemiology Mean age of onset is 3-4 days for term infants and 3-4 weeks for infant born at less than 28 week’s gestation. Mortality rate varies(30-40%) with a higher rate in advanced NEC (stage III or with perforation) and in infants with birth weight 1000gm or less( >80%).
  25. 25. NECROTIZING ENTEROCOLITIS Pathophysiology: UNKNOWN CAUSE…….
  26. 26. CIRCULATORY INSTABILITYPRIMARY INFECTIOUS AGENTS Hypoxic-ischemic eventBacteria, Bacterial toxin, Virus, Fungus Polycythemia MUCOSAL INJURYINFLAMMATORYMEDIATORS ENTERAL FEEDINGSInflammatory cells (macrophage) Hypertonic formula or medicationPlatelet activating factor (PAF) Malabsorption, gaseous distentionTumor necrosis factor (TNF) H2 gas production, EndotoxinLeukotriene C4, Interleukin 1; 6 production
  27. 27. EpidemiologyII Risk FactorsDespite several decades of research theetiology and pathogenesis remainedelusive.There is wide controversy about thistopic .
  28. 28. Epidemiology .Prematurity The most dominant risk factor for NEC is the degree of Immaturity. – 90% of cases are premature infants – immature gastrointestinal system  mucosal barrier  poor motility – immature immune response – impaired circulatory dynamics
  29. 29. Epidemiology 2 –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 >20kcal/kg/day 3 – Infant related conditions A. Perinatal asphyxia & hypoxic ischaemia It has more significant role in term and near term infants.
  30. 30. EpidemiologyB – Umbilical Catheterization-Embolization of catheters may result inembolization of mesenteric arteries.-Infusion of medications such as calciummay cause vasospasm and frankintestinal necrosis.C - Congenital heart disease EspeciallyPDA and cyanotic heart disease.
  31. 31. EpidemiologyD-– Extreme Low birth weightIt was proved that the incidence of NEC is higher in those babies with birth weight 1500 gm or less.E -DrugsI) Theophylline→ toxic oxygen radiclesII) Oral Vitamin E→interfere with killing of bacteriaIII) Indomethacin→vasoconstriction→↓mesenteric blood flow
  32. 32. EpidemiologyF. Infection- Although no specific single organism was implicated in the diseaseG. Hypotension & ShockH. PolycythemiaI Exchange TransfusionJ ThrombocytosisK AnaemiaL RDS
  33. 33. Epidemiology4. Maternal Risk Factors1) Pre-eclampsia2) Placental insufficiency3) Prolonged PROM4) Drugs as Heroin 34
  34. 34. Pathogenesis Most investigators suggested that NEC resulted from intestinal mucosal injury from low - Flow states, or hypoxia, with secondary bacterial invasion. These factors may initiate the disease process by injuring the protective barriers of the intestine (The mucosa). The injury can be direct or indirect. Direct injuries are caused by bacteria or by exposure to hypertonic solution.
  35. 35. PathogenesisIndirect injuries are the result of mucosalcell hypoxia from low flow states: .Shock .Hyperviscosity .Vascular obstruction Or generalized hypoxia ⇒ birth asphyoxia →lung or heart disease
  36. 36. Pathogenesis* Once the mucosa has been injured,bacteria in the lumen can breach the gut barrierAnd initiate an inflammatory cascade, causingfurther damage and eventual intestinalnecrosis. The presence of substrate provided byFeedings, bowel stasis and reduction indefences of the local gut Mucosa ⇒ Allfacilitate bacterial proliferation.
  37. 37. PathologyNEC may beI. FOCAL(Isolated) diseaseWhen a single area of bowel is necrotic or perforatedII.MULTIFOCAL Multi – segmental disease (> 50% viable.).The most common site of NEC is the terminal ileum, the second most common site in the left colon..The disease can occur anywhere from the stomach to the rectum.
  38. 38. Multi – segmental disease
  39. 39. PathologyInvolvement of both the large and small intestine occurs in 44% of cases.III. Pan – Involvement (NEC totalis) Account for 19% of the cases Characterized by necrosis of at least 75% of the gut.
  40. 40. Macroscopic Features Grossly distended loops of the intestine with spotty intramural haemorrhagl and areas of necrosis with serosal gas collection. The diseased bowel wall may be thinned with fibrinous exudate covering the serosal surface. Mucosal ulceration with associated epithelial sloughing may be extensive.
  41. 41. Microscopic Features The essential feature are haemorrhage and necrosis (coagulation necrosis). Mucosal oedema followed with formation of a pseudo-membrane of fibrinous exudates and necrotic cellular debris. The necrosis may progressively involve all layers of the bowel to the serosa.
  42. 42. ComplicationsShort Term1 – Perforation.2 – Septicaema.3 – Metabolic and electrolyte distubance.4 – Prolonged need for artificial ventilation with its hazards.
  43. 43. II – Long Term1. Strictures - It is the most common long term GIT complication of NEC, occuring in (10-35%) of all survivors.2 – Short bowel syndrome The most important determinant of future GIT function is the absence or presence of ileocecal valve, regardless of the length of gut resected. The syndrome refers to malabsorption and under nutrition after extensive bowel resection.
  44. 44. 3.FULMINANT SEPSIS4.TPN related complications:Cholestasis;Thrombosis;Infection5. Complications related to stoma:Retraction,Prolapse&Parastomal hernia6. adverse neurodevelopmental outcomesDelays in “locomotor,” “hearing and speech,” “intellectual performance” and “personal and social” skills.[
  45. 45. 6. Wound complications Infection, Dehiscence or Enterocutaneous fistula7. RecurrenceOccurred in 10% (Rennie and Roberton 2002)8. Others:Chronic anaemia & malabsorptionEye complicationAbscess & Fistula formation
  46. 46. CLINICAL PRESENTATIONGastrointestinal: Systemic• Feeding intolerance • Lethargy• Abdominal distention • Apnea/respiratory• Abdominal tenderness distress• Emesis • Temperature instability• Occult/gross blood in • Hypotension stool • Acidosis• Abdominal mass • DIC• Erythema of abdominal • Positive blood cultures wall
  47. 47. CLINICAL PRESENTATIONSudden Onset: Insidious Onset: Full term or preterm  Usually preterm infants Acute catastrophic  Evolves during 1-2 deterioration days Respiratory  Feeding intolerance decompensation Shock/acidosis  Change in stool Marked abdominal pattern distension  Intermittent Positive blood culture abdominal distention  Occult blood in stools
  48. 48. BELL STAGING CRITERIASTAGE CLINICAL X-RAY TREATMENTI. Suspect Mild abdominal Mild ileus Medical distention Work up for NEC Poor feeding Sepsis EmesisII. Definite The above, plus Significant Medical Marked abdominal Ileus NEC distention Pneumatosis GI bleeding Intestinalis PVGIII. Advanced The above, plus Pneumo- Surgical Unstable vital signs Peritoneum NEC Septic Shock
  49. 49. Modified Bell StagesStage Stage Systemic Intestinal Radiolog Signs Signs ical Sign I IA Temperature −⇑Gastric .IntestinalSuspected instability aspirate .mild dilutation NEC Apnea abdominal .Mild ileus Bradycardic distension Lethergy .Emesis .Faecal occult Blood I IB Same as IA Bright red blood per Same as IASuspected rectum NEC
  50. 50. Modified Bell StagesStage Stage Systemic Intestinal Radiologic Signs Signs al Sign II II A Same as IA Same as IB + •Intestinal Definite (mildly ill) .absent bowel dilatation NEC sound •Ileus .Abd. Tenderness •Pneumatosis intestinalis II II B Same as II A plus: Same as II A plus Same as II A Definite (moderat *Metabolic Acidosis *Defenite Abd. plus NEC ely Ill) *Mild Distension +portal vein Thrombocytopenia +Abd. Celluitis gas + Lower Abd. + Ascites Quadrant mass *Absent bowel sound
  51. 51. Modified Bell StagesStage Stage Systemic Signs Intestinal Radiologi Signs cal Sign III III A Same as II B plus Same as II B Same as II BAdvanced (Severely Ill) * Hypotension plus plus NEC * Bradycardia *Generalized * Definite * Severe Apnea Peritonitis Ascites * Combined respiratory *Marked &metabolic acidosis Abd.Tenderness * DIC *Abd. * Neutropenia and Distension * Anuria *abd Wall Erythema III III B Same as III A plus Same as III A Same as III AAdvanced (Severely ill sudden perforation plus plus & bowel Increased pneumoperito perforation) Distension neum
  52. 52. IMAGING The cornerstone of the diagnosis of NEC is plain anteroposterior and left lateral decubitus radiography.1. Bowel distensionIt is the earliest and most common radiologic finding in patients with NEC (55% to 100% of cases)2. Pneumatosis intestinalis• It is intramural gas (mainly hydrogen)• The frequency ranges from19% to 98%.
  53. 53. Pneumatosis intestinalis
  54. 54. Pneumatosis intestinalis
  55. 55. Pneumatosis intestinalis
  56. 56. Pneumatosis Intestinalis hydrogen gas within the bowel wall  A by-product of bacterial metabolism a. linear streaking pattern  represents subserosal air  more diagnostic b. bubbly (cystic form)pattern o More common o . represent submucosal air o appears like retained meconium o less specific
  57. 57. 3. Portal venous gas• It appears as linear branching arborizing pattern of air over the liver shadow.• It may be fleeting and accounting for 9% to 20%. Portal vein gas is associated with poor prognosis.4. Pneumoperitoneum• It is best noted in left lateral decubitus• Pneumoperitoneum may occur without intestinal perforetion (barotraume).
  58. 58. 5. Intraperitoneal fluid• It is assoicated with high mortality rate.• Amenable to paracentesis6. Persistent dilated loops* When a single loop or sevseral loops of dilated bowel remained unchanged in position and configuration for 24 to 36 hours usually occurs in full-thickness necrosis.
  59. 59. Contrast Study It may be used in patients with equivocal radiologic signs Barrium should never be used Newer water – soluble agents as isotonic metrizamide which produce excellent specification of the gut.
  60. 60. Ultra- SonographyIt has been used to identifya. Necrotic bowelb. Intraperitoneal fluidc. Portal venous gas• It is the most applicable tool in patient with gasless abdomen and to localize intra-abdominal fluid for paracentesis.
  61. 61. MANAGEMENTNon-operativeThe mainstay of treatment for NEC is non-operative therapy.1. NPO & gastric suction ⇒ 10 – 14 days2. Cultures:- Blood culture is essential - CSF, Urine, Other Sites cultured as indicated.3. Antibiotics:- Vancomycin Aminoglycoside Flagyl Infusion for at least Cephalosposine 2 weeks
  62. 62. 4. Intravenous fluids: 150 – 250 ml / kg5. TPN6. Blood and Blood products: as needed forcorrection of anaemia and coagulopathy.7. Close Clinical observation ⇒ consists of:a.Frequent physical examinationb.Abdominal radiography every 8 hoursc.C.B.C. Blood gas analysis, serum electrolyte & serum platelet
  63. 63. Indications for operation1. Pneumoperitoneum• This is the only absolute indication for surgery.• Relative indication:2. clinical deterioration despite adequate therapy: a. Erythema and oedema of abdominal wall b. Abdominal mass c. Signs of peritonitis on physical examination d. Increasing acidosis and e. Persistent and progressive thrombocytopenia.
  64. 64. 3. Fixed dilated intestinal loop.4. Ascites• 43% of patient’s ascites will have bowel necrosis.• The demonstration of ascites mandates paracentesis .
  65. 65. Paracentesis5. Positive Paracentesis– Indicated for infants with extensive pneumatosis intestinalis or who have failed to improve on medical management– This is defined as free flowing aspiration of more than 0.5 ml of brown or yellow brown fluid that contains bacteria on gram stain.6.Portal Venous Gas
  66. 66. Operative Managementbed-side Peritoneal drainage* It is insertion of a penrose drain through a right lower quadrant incision under local anaesthesia for extremely ill infants with bowel perforation.
  67. 67. Laparoscopy�Clarckand Mackinaly reported the use of laparoscopy in the treatment of a VLBW infant (900 g) with perforated NEC.Tan et al.:4 babies (500-1000 g) Needlescopic diagnosis is feasible and appears to be safe, even in critically ill baby less than 1000 g. The technique can provide useful information for surgical decision-making and allows for precise placement of the incision over the site of perforation, thus minimizing the trauma from open surgery in this special group of patients. Clark C, MackinlayGA. Laparoscopy as an adjunct to peritoneal drainage in perforated necrotizing enterocolitis. J Laparoendosc Adv Surg Tech A. 2006 Aug;16(4):411-3.39 Tan HL et al. The role of diagnostic laparoscopy in micropremmieswith suspected necrotizing enterocolitis. Surg Endosc. 2007 Mar;21(3):485-7.
  68. 68. II. Principles of ResectionA. When a single area of bowel is necrotic or perforated only limited resection is necessary.• A proximal ostomy and distal mucus fistula are createdB. Resection with primary anastomosis in these conditions i) a sharply localized (proximal)segment of disease ii) undamaged appearance of the remaining intestine. iii) good general condition.
  69. 69. Segmental NECContrast study Segmenal necrosis Multiple segments necrotic of one segment but >50%viable bowel Resection of Resection of necrotic segment necrotic segments Primary stoma Proximal stoma anastomosis!? Muliple anastomoses of distal Contrast defunctionalized bowel study Stoma closure 4-6 weeks
  70. 70. III. Multi – segmental disease( > 50% viable)A. Excision of each diseased segment and creates multiple stomas.B. “Patch, drain, and wait” procedure; which include- Transverse single layer suture approximation of perforations (patch).- Insertion of two penrose drains (drain)- Long-term TPN (wait)
  71. 71. C. “Clip and drop-back” Technique• Obviously necrotic bowel is removed.• The cut ends are closed with titanium clips.• Re-exploration is done 48 to 72 hours later ⇒ All segments are re-anastomosed without any stoma.
  72. 72. Pan – Involvement = Nec Totalis Operation 1.high stoma in proximal viable bowel 2.irrigate distal bowel Perforated No segments perforations No resection Mucus fistula of distal bowel Limited resectionsMucs fistula Muliple Stent deteriorate stabledistal bowel stomas Muliple segmnts over silastic cather TPN for 6-8 weeks Contrast study Multiple resections of scarred segments ananastomosis. Proximal stoma remains Proximal stoma closure in 6 weeks
  73. 73. IV. Pan – Involvement = Nec TotalisThe Treatment options1. Simple closure of the abdomen2. Resection of all necrotic bowel3. Proximal diversion without bowel resection…..second-look operation after 6- 8weeks.
  74. 74. Prevention �Breast milk �Antenatal Steroid therapy �Oral immunoglobulins �Oral antibiotics �Probiotics(Lactobacillus, Bifidobacterium) �Feeding strategies �Glutamine �Arginine �Polyunsaturated fatty acids (PUFA) �Lactoferin �Pentoxifylline
  75. 75. Take Home Messages Go slow!!!!! Breast is best!!!

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