Pediatric Surgery 2 (Respiratory and Gastrointestinal Conditions).pdf

Danilo M. Valle Cruz, M.D. | 01.12.16 | SURGERY

PEDIATRIC SURGERY II: Respiratory and Gastrointestinal Conditions o

BLACK TEXTS = Texts from the presentation / lecture; ITALICIZED TEXTS = Transcripts from the recording / Lecturers inputs; GREEN TEXTS = Texts / Info from the old file/previous transes; BLUE TEXTS = Input from the reference book RED TEXTS = Emphasized content

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The Book-Reference for this lecture is NOT Schwartz’ Principles of Surgery but Fundamentals of Pediatric Surgery by Peter Mattei, 2011 Part V – VIII.

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LECTURE OUTLINE I. RESPIRATORY CONDITIONS 1. Congenital Diaphragmatic Hernia (CDH) 2. Diaphramatic Eventeration 3. Congenital Pulmonary Airway Malformation (CPAM) 4. Congenital Lobar Emphysema (CLE) 5. Pulmonary Sequestration II. GASTROINTESTINAL CONDITIONS 1. Esophageal Atresia (EA) and Tracheoesophageal Fistula (TEF) 2. Gastrointestinal Reflex (GER) 3. Gastrointestinal Atresia/Stenosis a. Pyloric Atresia b. Pyloric Stenosis 4. Neonatal Intestinal Obstruction 5. Duodenal Malformations a. Duodenal Atresia b. Duodenal Stenosis c. Duodenal Web 6. Jejuno-Ileal Atresia 7. Colonic Atresia and Stenosis a. Colon Atresia b. Colon Stenosis 8. Malrotation and Midgut Volvulus (MGV) 9. Meconium Ileus 10. Necrotizing Enterocolitis

RESPIRATORY CONDITIONS 1. CONGENITAL DIAPHRAGMATIC HERNIA (CDH)  EPIDEMIOLOGY o 1:4000-5000 live births o 1:2000 stillbirths included o Syndromic Variants  Have been linked to chromosomal defects such as Trisomy 18, 19, 21-23; 15q 24-26 deletions, Turner’s syndrome o Associated anomalies: 40%, associated with >50 syndromes  PATHOPHYSIOLOGY o During the formation of the diaphragm, the pleural and the coelomic cavities remain in continuity by means of the pleuroperitoneal canal.

The posterolateral communication is the last to be closed by the developing diaphragm. Failure of w/c leaves a posterolateral defect allowing the viscera to fill the chest cavity. Pleuroperitoneal membranes separate the pleural and abdominal cavities by the 8th week of gestation. There are two main types based on the location of the defect: Bochdalek Hernia and Morgagni Hernia

A. BOCHDALEK HERNIA – Posterolateral defect – Occurs in 80-90%, L>R – With a (+) sac in Bilateral  May be indistinguishable from a hernia sac in congenital diaphragmatic hernia  Uncommonly can result to pulmonary hypoplasia  Persistent fetal circulation (PFC) and pulmonary hypertension are not usually seen o Acquired  Due to paralysis of the phrenic nerve  Mediastinal tumors  Congenital heart surgery as in BlalockTaussig surgery for patients with Tetralogy of Fallot  Birth trauma as in Erb’s palsy during difficult delivery  Why birth trauma? REVIEW your anatomy of the nerve supply of the diaphragm. The phrenic nerve originates mainly from the 4th cervical nerve, but also receives contributions from the 4th and 3rd cervical nerves (C3-C5). Brachial plexus injuries can cause paralysis to various regions in the arm, forearm, and hand depending on the severed nerves. CLINICAL MANIFESTATIONS o May be asymptomatic o Typically presents acutely as respiratory distress and tachypnea in the newborn o Feeding intolerance from discoordinated sucking and breathing o Recurrent respiratory infection and wheezing o Exercise intolerance in older children DIAGNOSIS o Chest X-Ray – to note the rib levels of the diaphragm o Motion Studies as in Ultrasound or Fluoroscopy – confirmatory TREATMENT o Small Eventration – may be observed

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Large Eventration – plication; sometimes we excise the central portion of the diaphragm for biopsy to differentiate it from CDH  Transthoracic or Transabdominal  Open Approach or Minimally Invasive Techniques

3. CONGENITAL PULMONARY AIRWAY MALFORMATION (CPAM)  Previously known as congenital cystic adenomatoid malformation (CCAM) and congenital lung cyst  PATHOPHYSIOLOGY o Cystic proliferation of the terminal bronchiolar structures with an associated suppression of alveolar growth o Cysts are lined by cuboidal or columnar epithelium o May occur in any lobe or simultaneously in both lobes o Site: common at the left lower lobe o Type I may be confused with congenital diaphragmatic hernia (CDH), congenital lobar emphysema, pneumatocoeles, and pulmonary sequestration  CLASSIFICATION o Stocker (Pathologic) Classification – most important classification is type I (because this type has a favorable prognosis)  I – single, large, or multiple, >2cms  II – smaller, more numerous, 5mm (echolucent)  Microcystic - R) followed by the right middle lobe, may also occur in the lower lobes o Associated abnormalities include cardiac anomalies:  Cardiac defects occur in as much as 14%  Enlarged left atrium or major vessel compressing the ipsilateral bronchus  CLINICAL MANIFESTATIONS o Mild respiratory distress to full-fledged respiratory failure o Hyperexpanded hemithorax is pathognomonic  DIAGNOSIS o Chest X-Ray – usually sufficient  Hyperlucency with adjacent lobar compression and atelectasis o CT Scan – for stable patients, confirmatory o Bronchoscopy – contraindicated because the lung is already hyperexpanded; doing bronchoscopy will further hyperexpand the lung and cause rupture resulting to pneumothorax  DIFFERENTIAL DIAGNOSES o Foreign Body o Mucus Plug  TREATMENT o Complete Lobectomy o Open or Thorascopic Approach o Timing is symptom-dependent

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PROGNOSIS o Excellent

5. PULMONARY SEQUESTRATION  PATHOPHYSIOLOGY o Cystic mass of nonfunctioning lung parenchyma which does not communicate with the tracheobronchial tract by normally related bronchi o May be due to failure of the pulmonary artery to develop fast enough to supply the whole of the growing lung, leading to formation/persistence of a systemic arterial supply from the aorta  TYPES o Intralobar  90%  Left lower lobe > Right lobes o Extralobar  10%  Variable but usually basilar and above the left hemidiaphragm  Commonly found in cases of congenital diaphragmatic hernia  Therefore during the repair of CDH, you may opt to resect this lesion  CLINICAL MANIFESTATIONS o Intralobar – recurrent pulmonary infections o Extralobar – rare  DIAGNOSIS o Chest X-Ray o CT Scan or MRI – confirmatory o Aortography/Angiography o Color Doppler Ultrasound – presence of an anomalous blood supply from the aorta  This would detect blood flow to the lesion  TREATMENT o Intralobar  Segmentectomy or Lobectomy  Open or Thoracoscopic Approach o Extralobar  May be observed  PROGNOSIS o Excellent REVIEW: 1. Common Differentials for CDH: CCAM, CLE, PS 2. Management for Respiratory Conditions: a. CDH: Medica b. CCAM: Surgical (Lobectomy) c. PS: Surgical if Intralobar (Lobectomy) d. CLE: Surgical (Lobectomy)

GASTROINTESTINAL CONDITIONS 1. ESOPHAGEAL ATRESIA (EA) AND TRACHEOESOPHAGEAL FISTULA (TEF)  EPIDEMIOLOGY o 1:4000 live births  PATHOPHYSIOLOGY o Uncertain o Esophagus and trachea normally divide into separate tubes by 34-36 days of gestation o Interruption in the separation process is the traditional explanation to the development of TEF, but does not explain why EA forms  ASSOCIATED ANOMALIES o Isolated EA – no definitive genetic mutation o Syndromic EA – mutations have been identified (e.g. N-myc, Sox2, CHD7) o VACTERL Association  Vertebral Abnormalities : 15%  Anointestinal Abnormalities : 8%  Cardiac Abnormalities : 38%  Tracheoesophagel Abnormalities  Renal Abnormalities : 15%  Limb Abnormalities : 19%  Hydrocephalus  Other Abnormalities : 16% o Associated Anomalies  Cardiac : 23%  Musculoskeletal : 18%  Anointestinal : 16%  Anorectal Malformation : 9%  Duodenal Atresia : 5%  Malrotation : 4%  Genitourinary : 15%  Head and Neck : 10%  Mediastinal : 8%  Chromosomal : 6%  Pulmonary : 2%  GROSS-VOGT CLASSIFICATION Type A EA/Pure EA 8-10% Type B EA + Proximal TEF 1% Type C EA + Distal TEF (commonest) 85% Type D EA + Proximal and Distal TEF 2% Type E H-Type/ Isolated TEF 8%  CLINICAL MANIFESTATIONS o Regurgitation or drooling (excessive salivation) o Choking or coughing o Abdominal distention (Types CDE) o Scaphoid abdomen in pure TEF (Type A)

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Presence of pneumonia (aspiration pneumonia or chemical peritonitis – Type CD) o Associated anomalies – 55% (VACTERL-H) DIAGNOSIS o Prenatal Ultrasound  Polyhydramnios (>90%) – more than 2L  Failure to visualize a fetal stomach  Upper esophageal distention during swallowing “pouch” sign o Thoracic MRI  100% sensitive, not cost-effective  Its use is still being evaluated o Postnatal Diagnosis  Inability to pass an NGT (French 10) into the stomach, usually stops at 12 cm level from the nostrils or 9-10 cm from the alveolar ridge  Misdiagnosis: coiling, traumatic perforation, descent via proximal and distal fistulous tract  Plain Abdominal X-Ray: may visualize the dilated upper pouch  Chest X-Ray: NGT coiling (French 5) o VACTERL Work-Up  2D Echocardiography  Lateralize the arch of the aorta  Right-sided arch in 5%  Left (approach is posterolateral thoracostomy)  Cardiovascular assessment – identifies the most important predictors of survival  Spinal X-Ray/Ultrasound  Skeletal X-Ray (“Babygram”)  KUB Ultrasound  Bronchoscopy if stable TREATMENT o Medical – attention to the respiratory status  Treat pneumonia with broad spectrum antibiotics  Treat acid reflux with acid blockers or PPIs  Suctioning may be performed intermittently o Surgical  Primary Repair – rarely a surgical emergency  Delayed or Staged Repair  Long Gap EA: >3.5cms or 3 ½ vertebral bodies  Extremely/Ultra-Long Gap EA: >5cms  Open vs Thoracoscopic Approach o Feeding Gastrostomy o Ligation of the TEF – in very unstable cases

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To prevent reflux and to oxygenate the involved lung o Livaditis Circular Myotomy – 1.5 cms apart, can lengthen by about 1 cm o Esophageal Replacement – long gap; may use the colon, stomach, jejunum, ileum o Isolated TEF Type E – ligated via the right low cervical approach  COMPLICATIONS o Anastomotic Leak (10-15%) o Stricture (10-20%) o Gastroesophageal Reflux o Recurrence  MODIFIED WATERSON CRITERIA (SPITZ) o Prognosis is based on weight and associated anomalies Group Birth Characteristics Survival I >1,500 g 97% II 1mL/kg/hr o The compensation for severe metabolic alkalosis is respiratory acidosis which is produced by hypoventilation. o Patient with severe metabolic alkalosis therefore will not breathe well post-operatively. o Fredet-Ramstedt Pyloromyotomy via Laparotomy or Laparoscopy o Feeding: between 6-18 hrs. post-operatively o Emesis encountered in 65-90% COMPLICATIONS o Perforation o Bleeding o Wound infection o Recurrence MEDICAL MANAGEMENT o Reserved for patients with poor operative risks o Requires prolonged post-pyloric feeding via feeding tube (6-12 months)

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4. NEONATAL INTESTINAL OBSTRUCTION  CLINICAL MANIFESTATIONS o Cardinal Signs:  History of polyhydramnios (>2000 ml)  Bilious vomiting in the newborn means obstruction unless proven otherwise  Can be seen also in patients w/ sepsis & adynamic ileus  Physical examination: +/abdominal distention depends on the level of GIT involved  Failure to pass meconium w/in the 1st 24-48 hours of life  LOCATION o Proximal  Bilious vomiting  Minimal abdominal distention  Plain Abdominal X-Ray: paucity of gas, no distention; rule out malrotation and midgut volvulus (MGV) o Distal  Bilious vomiting  Abdominal distention  Plain Abdominal X-Ray: calcification (meconium peritonitis secondary to perforation of the small intestine), pneumatosis/PPN (necrotizing enterocolitis)  DIAGNOSIS o Plain Abdominal X-Ray  Complete obstruction with/no distal air in the pre-sacral area  Incomplete obstruction with some gas more distally in the bowel o Contrast Enema Study – water-soluble and not barium enema as barium enema can result to peritonitis  (+) Microcolon  Jejunoileal Atresia  Meconium Ileus (Small Intestine)  (-) Microcolon  Hirschsprung’s Disease  Small Left Colon Syndrome (seen in children of mothers who are diabetic)  Meconium Plug (Large Intestine) 5. DUODENAL MALFORMATIONS  Intrinsic Obstruction o Duodenal Atresia – complete o Duodenal Stenosis/Web/Duplications – partial

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Extrinsic/Partial Obstruction o Annular Pancreas o Malrotation with Ladd’s Bands o Preduodenal Portal Vein Other Associated Biliary Abnormalities o Biliary Atresia (BA) o Gallbladder Agenesis o Common Bile Duct (CBD) Stenosis o Choledochal Cysts (CDC) ASSOCIATED ABNORMALITIES (50%)  Trisomy (21-30%)  Isolated Cardiac Defect (30%)  Other GIT Anomalies (25%) o Prematurity (45%) o Growth Retardation (33%) – may be due to deprivation of swallowed amniotic fluid CLASSIFICATION o Stenosis – mostly involve the 3rd or 4th part of the duodenum o Atresia LEVEL OF OBSTRUCTION o Preampullary: 10-15% (non-bilious vomiting) o Postampullary: 85% (bilious vomiting)

a. DUODENAL ATRESIA  GREY-SKANDALAKIS CLASSIFICATION o Type 1: intact diaphragm or membrane that is formed by mucosa and submucosa; muscularis is intact (“windsock” deformity; inserting an NG tube will cause intussusception) o Type 2: two blind ends are connected by a short fibrous cord with intact mesentery o Type 3: blind ends are separated and with mesenteric defect  DIAGNOSIS o 30-59% (to 81%) have history of maternal polyhydramnios in the third trimester o Down Syndrome is present in approximately 1/3 of all cases o Prenatal Ultrasound  dilated fluid-filled stomach and duodenum  usually detected between 7th and 8th month age of gestation or even as early as 5th month age of gestation  “double bubble sign” – 44% of cases if with (+) history of maternal polyhydramnios o Decompression by Vomiting or Orogastric Tube (OGT) Aspiration  Instill 40-60 mL of air to reproduce the “double bubble”

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Plain Abdominal X-Ray  Usually sufficient to confirm the diagnosis if there is antenatal suspicion of duodenal obstruction and the clinical presentation is consistent with proximal bowel obstruction  “Double bubble sign”; air-filled stomach and 1st portion of the duodenum with no distal air  If with distal air, the air from the stomach inserts into the bifurcation CLINICAL MANIFESTATIONS o Bilious vomiting in the first few hours of life due to incompetence of the pylorus o Non-bilious thereafter o On physical examination, +/- abdominal distention, abdomen is usually scaphoid o OGT aspirate: >20 mL suggests obstruction, 90% survival o Most death are related to severe cardiac defects

b. DUODENAL STENOSIS  DIAGNOSIS o Plain Abdominal X-Ray: “double bubble sign” is usually not present o Upper Gastrointestinal Series  TREATMENT o Duodeno-duodenostomy c. DUODENAL WEB  DIAGNOSIS o Plain Abdominal X-Ray: incidental finding  TREATMENT o Vertical Duodenotomy o Partial Excision of Web  Avoid injury to the inserting pancreatico-biliary duct  Oversewing the mucosa  Horizontal closure 6. JEJUNO-ILEAL ATRESIA  EPIDEMIOLOGY o Incidence: 1:2,000-5,000 live births (M=F)  PATHOPHYSIOLOGY o Believed to be due to antenatal fetal mesenteric vascular accident:  In Utero Volvulus  Malrotation  Gastroschisis  Intussusception  Internal hernia  CLINICAL MANIFESTATIONS o Bilious vomiting o Progressive abdominal distention  LOUW CLASSIFICATION Type I Mucosal atresioa with intact muscularis Type II Atretic ends connected by a fibrous band Type III A Atretic ends are separated by a V-shaped mesenteric defect Type III B “Apple peel” or “Christmas tree” deformity Type IV Multiple, “string of sausage” or string of beads appearance  DIAGNOSIS o Plain Abdominal X-Ray  Level  Calcification (12%)  Note: the more distal the obstruction, the more distended the abdomen, the greater the number of obstructed loops o Barium Enema  Rotation and its caliber

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Small intestine versus large intestine If the diagnosis is uncertain or distal obstruction is suspected  (+) Microcolon  Jejunoileal Atresia  Meconium Ileus  (-) Microcolon  Hirschsprung’s Disease  Small Left Colon Syndrome  Meconium Plug TREATMENT o Laparotomy  Once the diagnosis of complete intestinal obstruction is considered (i.e. staggered airfluid levels, clinical picture) o Surgery depends on the type of atresia  Resection + Anastomosis (End to Back)  Ileostomy + Distal Mucus Fistula (DMF) – if ischemic or necrotic

7. COLONIC ATRESIA AND STENOSIS  EPIDEMIOLOGY o Incidence: 1:15,000 to 20,000 live births  PATHOPHYSIOLOGY o In utero vascular compromise of the mesentery to the large bowel o Most affected areas are the transverse and the sigmoid colon which have floppy mesentery that are prone to volvulus a. COLON ATRESIA  CLINICAL MANIFESTATIONS o Failure to pass meconium within the 1st 24 hours of life o Abdominal distention o Bilious vomiting  DIAGNOSIS o Plain Abdominal X-Ray  Dilated intestines with air-fluid levels  “Soap bubble” appearance (air + meconium) o Contrast Enema  Blind distal end of a microcolon  TREATMENT o Right colon and transverse colon: primary resection with end-to-end anastomosis or colostomy o Sigmoid: colostomy with subsequent closure after 3-6 months  PROGNOSIS o 90-100% survival

8. MALROTATION AND MIDGUT VOLVULUS (MGV)  EMBRYOLOGY o 6th week – midgut herniates into the umbilical cord o 10th week – begins its return to the abdominal cavity o Midgut undergoes 270o counterclockwise rotation around the superior mesenteric artery which results in the ligament of Treitz being in the LUQ and the cecum in the RLQ  PATHOPHYSIOLOGY o MGV can occur at any age but commonly in the first few weeks of life o May lead to infarction of the entire midgut (necrosis can occur in 1-2 hours) o May result to short gut syndrome o Occurs in 70% of infants with malrotation  CLINICAL MANIFESTATIONS o Feeding intolerance o Bilious emesis (77-100%) – 1st sign of MGV o Abdominal pain/ irritability o Hematochezia/ hematemesis o Circulatory collapse o Early Stage: minimal signs o Advanced: erythema and edema of the anterior abdominal wall, shock o Chronic Obstructive Symptoms  Intermittent abdominal pain  Vomiting (occasionally bilious)  Failure to thrive  May be misdiagnosed as GERD  DIAGNOSIS o Plain Abdominal X-Ray  Non-specific, neither R/I or R/O malrotation  Paucity of gas throughout the intestine with few scattered AFL  “Double bubble” sign (20%)  “Duodenal Triangle” – triangular gas shadow in the RUQ (upright view) o Upper Gastrointestinal Series  Gold standard, most reliable diagnostic tool  Incomplete rotation with duodenojejunal junction, displaced to the right  Failure of the ligament of Treitz or duodenojejunal flexure to cross to the left of the midline  Suggestive of MGV  Cork-screw appearance with right-sided bowel loops  Cut Off Sign  Beak Sign

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Barium Enema: displaced or high lying cecum, unreliable o Ultrasound and CT Scan: suboptimal TREATMENT o Exploratory Laparotomy o Detorsion in a Counter-Clockwise Direction o Ladd’s Procedure ± Appendectomy  The procedure involves surgical division of Ladd's bands, widening of the small intestine's mesentery, performing an appendectomy and correctional placement of the cecum and colon. Advanced Ischemia o Reduce the volvulus without Ladd’s Procedure then “2nd look” operation after 24-36 hours o Conservative resection Recurrent Volvulus o Uncommon o Can still occure after Ladd’s Procedure MORTALITY o 4+-8%

9. MECONIUM ILEUS  EPIDEMIOLOGY o Affected patients almost always have cystic fibrosis  PATHOPHYSIOLOGY o Produces obstruction from impaction of meconium in the distal ileum o Inspissation is caused by lack of pancreatic enzymes  CLINICAL MANIFESTATIONS o Bilious vomiting o Progressive abdominal distention o Failure to pass meconium  DIAGNOSIS o Prenatal Ultrasound  Intra-abdominal or scrotal calcifications  Distended bowel loops o Plain Abdominal X-Ray  Dilated bowel loops with no air-fluid levels  “Ground glass appearance” – small bubbles of gas entrapped in the inspissated meconium  “Eggshell pattern” – intraperitoneal calcification suggestive of prenatal intestinal perforation o Contrast Enema under Fluoroscopy  Confirmatory  Microcolon  Pellets of meconium in the terminal ileum

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Failure to reflux into the terminal ileum (suggestive of complicated meconium ileus or an associated atresia) TREATMENT o Uncomplicated  Water-soluble contrast enema  Commonly with the use of gastrograffin  Every 12 hours for several days o Complicated  Perforation  Vascular compromise  Resection of distended terminal ileum  Flushing of meconium pellets with diluted Nacetylcystein or NSS  End to End Anastomosis  Ileostomy  Ileostomy with Distal Mucus Fistula (DMF)  Bishop-Koop Anastomosis  Mikulicz Double Barrel Enterostomy

10. NECROTIZING ENTEROCOLITIS  EPIDEMIOLOGY o Most frequent and lethal gastrointestinal disorder affecting almost exclusively the stressed premature neonate (1-3:1000 live births) o Multifactorial in origin  PATHOPHYSIOLOGY o Mechanism is still underfined o Breakdown of mucosal barrier and colonization with indigenous bacterial flora o The more immature the infant at birth, the greater the risk of acquiring NEC o Usually develops at the 10th day of life (7-21 days of life) when the gastrointestinal tract is colonized by coliforms o Common isolates include: Escherichia coli, Enterobacter spp., Klebsiella spp., coagulasenegative Staphylococcus  RISK FACTORS o Prematurity o Initiation of enteral feeding o Bacterial infection o Intestinal ischemia (Asphyxia) o Umbilical artery cannulation o Patent ductus arteriosus o Cyanotic heart disease o Maternal cocaine abuse o Premature and Enteral Alimentation  The only consistent epidemiology precursors of NEC

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 No enteral feeding in 10% Full Term Infants  Low risk  5-25% of cases develops within the first few days of life STAGES (BELL CLASSFICATION) o I – suspect, show features of NEC o II – definite, established case o III – advanced, with evidence of necrosis or perforation o Modification includes clinical, gastrointestinal, and radiographic findings CLINICAL MANIFESTATIONS o Milk feeding intolerance – 1st sign o Physiologic instability o Abdominal distention (ileus) o Hematochezia o Bilious vomiting o Anterior abdominal wall edema and erythema o Ascites o Jaundice DIAGNOSIS o Hematologic Profile o Imaging Studies  Plain Abdominal X-Ray  Ileus  Pneumatosis intestinalis (pathognomonic, 98%)  Portal venous gas (10%)  Intraperitoneal fluid (10%)  Persistently dilated bowel loops  Pneumoperitoneum – foot ball sign in supine view  Ultrasound: portal venous gas, pneumatosis, ascites  MRI – prohibitively difficult in preterm infants, more feasible in full term but rarely necessary  Contrast Study - relatively contraindicated TREATMENT o Conservative Management – 75% success in uncomplicated cases  NPO for 10-14 days  OGT with intermittent suction  Broad-spectrum antibiotics  Hypotension – crystalloids, blood products, and pressors or inotropes  Mechanical ventilation to maintain oxygenation if needed  Total parenteral nutrition o Surgical Indications

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Pneumoperitoneum Hepatoportal vein gas Significant acidosis (pH