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Objectives Identify presenting symptoms of various neonatal surgical conditions. Describe initial management of the neonate with abdominal wall defects. Identify three factors that contribute to the development of Necrotizing Enterocolitis. Josanne M. Paxton RN,MS,CNNP Banner University Medical Center Tucson Sometimes we encounter the unexpected in the delivery room NRP S.T.A.B.L.E. Airway Breathing Circulation Thermoregulation Glucose Homeostasis What is your next step? STAT call…. You are called STAT to the evaluation room. Mom is a 33 y.o. G6 P5 with no prenatal care. Infant is 4 minutes old when you arrive. She is in the warmer and the L&D staff are stimulating her vigorously. However she is limp and dusky with poor respiratory effort. WAIT…Upon further exam you notice this a. Put the baby on mom’s abdomen for some skin to skin b. Continue to stimulate c. Give BB oxygen 21% d. Initiate positive pressure ventilation A scaphoid abdomen – What are your thinking now??? 1 Diaphragmatic Hernia Prenatal Diagnosis May be notable for polyhydramnios Allows for maternal counseling and expectant management in an ECMO/surgical center Presentation of DH Initial Management Intubate (use of B&M ventilation contraindicated) Immediate passage of a large bore gastric tube Correct acidosis Prevent thermal and metabolic stress Prepare and observe closely for pneumothorax Failed closure of the pleuro-peritoneal canal with migration of the intestines into the thoracic cavity Results in pulmonary hypoplasia Left sided involvement (80%)> right ~1:4000 live births Can be associated with chromosomal and structural abnormalities (Turner’s, Trisomy 18, CHD) Respiratory distress in the first 24 hours (if in 1st 6 hours higher morbidity/mortality) Audible heart tones on right Decreased breath sounds on affected side and possibly presence of bowel sounds Scaphoid abdomen Cyanosis Shock Development of PPHN Diagnosis Made by CXR when loops of bowel are visible in the chest Shift of mediasteinum 2 Respiratory Management Additional Considerations Best results with “delayed” surgery – from a few days to even to a few weeks to ensure acceptable oxygenation and stable pulmonary pressures Gentle ventilation with low pressure and increased FiO2 or HFV Inhaled nitric oxide and surfactant replacement therapy ECMO support if needed Manage hypotension with judicious use of boluses and early initiation of inotropes Cardiac ECHO to evaluate for presence of CHD Total parenteral nutrition Sedation and pain management Surgery when cardio-respiratory status is stable Long term considerations Next Case You are caring for a 12 hour old infant. She delivered to a 25 y.o. G 2 now P2 female with good PNC. Mom has requested some rest and while feeding you notice copious secretions and a bout of severe coughing. The abdomen is soft, non-distended and the infant has passed meconium. Overall survival greater than 80% Chronic lung disease with need for long term oxygen therapy Gastroesophageal reflux is common Neurodevelopmental deficits and hearing loss What are you thinking?? Esophageal Atresia Tracheal Esophageal Fistula Failure of the tracheoesophageal septum to divide into separate digestive and respiratory segments 1:3000-5000 live births History of polyhydramnios 10% have VATER association – vertebral defects, anal anomalies, TE fistula, esophageal atresia, radial limb or renal anomalies Types of TEF/EA >80% of lesions <1% of lesions 3 Presentation Diagnosis TEF/EA Excessive salivation/drooling/vomiting Inability to pass gastric tube Respiratory distress secondary to aspiration Abdominal distress secondary to air trapping Passage of a nasogastric tube which meets resistance Confirmation by x-ray which reveals the NG tube in the upper esophagus Gasless stomach suggests isolated esophageal atresia H type fistula may not be diagnosed until later after recurrent aspiration episodes Stabilization of EA/TEF Maintain prone position with head elevated to prevent reflux and aspiration of gastric secretions Placement of a replogle in the upper esophagus with connection to low intermittent suction Keep replogle patent with q 2 hours irrigation Keep infant quiet to minimize introduction of air into the GI tract Broad spectrum antibiotics Avoid B&M ventilation Choanal Atresia Bone (90%) or membrane protrudes into nasal passage causing a stenosis or atresia Occurs in 2-4 infants per 10,000 births Associates anomalies including CHARGE (coloboma, heart disease, atresia chonana, retarded growth & developemnt, genital hypoplasia and ear anomalies), Treacher collins, TEF 4 Presentation of Choanal Atresia Cyanosis and retractions when infant is sleeping which resolve with crying Respiratory distress and desaturations Difficulty with feeding Diagnosis is made when unable to pass a naogastric tube through the nares Manage with oral airway and gavage feeding until repair Omphalocele Abdominal Wall Defects Gastroschisis Intestinal herniation Omphalocele Herniation of the through a defect in the abdominal wall usually to the right of the umbilical cord abdominal viscera into the umbilical cord & usually contained within the peritoneal sac. Gastroschisis Cause unknown 1:5,00 live births High incidence of associated anomalies (30-50% cardiac, 10-40% chromosomal) Gastroschisis Stomach, large and small intestine are commonly herniated, may also involve bladder and uterus 1:4-10,000 births Uncovered bowel is exposed to amniotic fluid leading to problems (paralytic ileus, ischemia) Low incidence of associated defects suggests mechanical problem Overall survival 90% with higher mortaltiy if complex Initial Stabilization Important to keep bowel well perfused by avoiding kinking Keep stomach and bowel decompressed with passage of nasogastric tube Cover with warm saline soaks and sterile plastic wrap or isolation bag Keep NPO Broad spectrum antibiotics +/- intubation Prevent hypothermia 5 Fluid resuscitation may be necessary especially in gastroschisis secondary to 3rd spacing into tissue and peritoneal space with subsequent hypovolemia and shock Long Term Complications Prolonged postoperative dysmotilty is common and interferes with enteral feeds If a complex defect at risk for more complications: Short bowel syndrome Bowel obstruction NEC Infection What is your next question? A. B. C. D. Was the emesis projectile? What color was the emesis? Did emesis come out of the nose? What is the volume of the emesis? Manage with a silo until repair Emesis in a Newborn This is a 37 2/7 week gestation male infant who delivered to a 21yo G1 now P1 mom by c-sect for FTP. Normal pregnancy and APGARS were 8 and 9. He has voided normally and stooled once. He is now 72 hours old and has been having some difficulty with breast feeding. During a lactation consult infant has a moderate emesis and abdomen seems slightly distended. Remember A well neonate with bilious vomiting is a surgical emergency and should be treated as a mid gut volvulus until proven otherwise 6 Intestinal Obstructions Bilious emesis is suggestive of an intestinal obstruction Obstructions presenting with bilious emesis Intestinal malrotation and mid gut volvulus Intestinal atresias (distal duodenum, jejunal and ileal) Meconium plug and ileus Hirschsprung’s Malrotation with or without Volvulus – surgical emergency Malrotation – failure of the intestines to properly rotate and affix to the posterior wall of the abdomen during fetal development. Often associated with other abdominal wall defects Volvulus – twisting of the bowel Can develop ischemia and necrosis within one hour of clinical symptoms Clinical Presentation 1/3 of all cases occur within the first week of life Bilious vomiting persistent or intermittent Dehydration and electrolyte depletion can occur rapidly Diarrhea and bloody stools May present as a chronic problem or progress to rapid deterioration and shock What are your next steps NG/OG placed to low continuous suction IV hydration – may need bolus Blood gas to assess acid base status CBC, chemistry panel, blood culture Broad spectrum antibiotics Prevent thermal and metabolic stress Assist ventilation as necessary Radiologic evaluation unless critical Surgical consult Malrotation and Volvulus Diagnosis and Management X-ray with scanty or airless abdomen is an ominous sign UGI is diagnostic if the infant is stable enough for study Surgical repair must be done as soon as possible to untwist the bowl and allow for reperfusion. 7 Duodenal Obstruction Double Bubble sign on plain radiograph May be diagnosed on prenatal ultrasound with polyhydramnious (5060% of cases) and a dialted fluid filled stomach Bilious emesis 1/3 have associated Trisomy 21 May have complex cardiac anomalies and should have an evaluation before surgery Reflects distention with air in the stomach and duodenum If complete atresia air will not be seen in the rest of the abdomen Meconium Ileus Presentation Intestinal obstruction which results from the presence of thickened meconium at the ileocecal valve Distention of the ileum and atrophy of the colon Associated with Hirshpungs, prematurity, hypomagnesemia and hypotonia Nearly all have Cystic Fibrosis (10-15% of patients with CF present with meconium ileus) Diagnosis Additional Management Soap bubble appearance on x-ray Distended loops of bowel with air fluid levels Free air in the peritoneal cavity Gastrographin enema (used in diagnosis, and may break up meconium and relieve obstruction Abdomial distention Bilious vomiting Failure to pass meconium within 24-48° Not all meconium ileus is the same Simple – ileal obstruction with proximal dilatation, bowel wall thickening and calcifications Complicated - Intrauterine perforation may occur resulting in calcifications, adhesions and at worse, ascites and peritonitis Warm saline enemas Surgery with resection of the compromised bowel and primary anastomosis Long term Nutrition At risk for TPN cholestasis Pulmonary management 8 Hirschsprung’s disease Congenital aganglionic megacolon Risk Factors Can be genetic with abnormal locus on chromosome 10 in some families Anoxic episodes prior to birth Those with Down’s Syndrome have a higher risk Associated with cleft lip or palate Imperferate anus Absence of ganglion cells that cause ineffective conduction of peristalsis Slowing of the fecal material propulsion Functional obstruction Potential pertonitis and shock Incidence approximately 1:5,000 live births Symptoms Delayed passage of meconium from 24-48 hours Alternating constipation and diarrhea Abdominal distention Vomiting Feeding may be tolerated several days before symptoms occur Enterocolitis Failure to thrive Diagnosis Dilated loops of bowel on x-ray Contrast enema MAY reveal dilated bowel followed by atrophied bowel Retained contrast in colon on x-ray following day Explosive stool following rectal exam Dx confirmed absence of the ganglion cells rectal bx Treatment and Outcome Saline rectal irrigation every 6 hours Perineal pull through Colostomy may be indicated if there is enterocolitis or the bowel is enlarged Most patients will have normal bowel habits however 5-10% may have longterm problems with constipations or incontinence 9 Necrotizing Enterocolitis NEC NEC - A Case Review Most commonly acquired surgical emergency in preterm VLBW infants Incidence is inversely proportional to birth weight – 4 -11. 5% Mortality ranges from 10 – 50% Little progress has been made towards the prevention Labor History Newborn Delivery Information Admitted for severe preeclampsia at 32 weeks Treated with hydralazine and labetalol Given Magnesium and Betamethasone Received multiple doses of antibiotics Progressed to a NSVD Risk Factors for NEC Multifactorial 32 yo G1 P0→now 1 Good PNC History of hyperlipidemia Medications - PNV, folic acid GBS positive All other prenatal labs WNL Delivery of an African American male infant at 32 6/7 weeks Presented with good heart rate tone and cry Onset of mild grunting Received CPAP at 40% APGARS 8 and 8 Birth weight 1860gms AGA Additional Risk Factors Prematurity – most prevalent in VLBW 85% occur in infants <1500gms or <32 weeks GI immaturity including impaired intestinal motility and decreased nutritional absorption PIH and intrauterine growth restriction Maternal chorioamnionitis Maternal smoking Feeding Immature immunological response (IgA) may facilitate bacterial translocation Abnormal intestinal colonization Increased pro-inflammatory response resulting in intestinal damage and epithelial cell death (apoptosis) Maternal History Unstandardized approach Formula feeding Breast Milk fortifier Prolonged antibiotic therapy > 5 days Blood transfusion 10 Early Neonatal Course Patient was admitted to NICU, placed on CPAP, IV fluids and antibiotics Weaned to room air and off CPAP by 8 hours of life First week: Hyperbili with phototherapy x 5days Week 2 On DOL 8 infant appears to be tolerating feeds - 34 ml every 3 hours, no aspirates or emesis, voiding and stooling normally However nurse reports that infant is hypotonic and pale Has also noted several brief apnea and bradycardia episodes with lowest sat 80% Feeds started on DOL 1 EBM or DBM only and advanced 1ml every 6 hours (11/kg/day) Antibiotics dc’d after negative culture at 48 ◦ Is there anything you are concerned about ? On Further Exam Presentation of NEC non-specific Infant is lethargic with minimal response Abdomen does not appear distended Marked sensitivity to exam with abdominal guarding and crying. And with the diaper change there is a bloody stool Any additional concerns? Apnea and bradycardia Unstable temperature Irritability or lethargy Emesis Bloody stools 60-75% of tube fed infants will have guaiac positive stools Gastric aspirates Abdominal distention Variable evidence that gastric residuals predict NEC L Parker What is abnormal (volume color) ? Should they be re-fed or discarded? Does it verify feeding tube placement? 25-66 % error rate Can you accurately measure gastric content volume? Depends on feeding tube size, if holes in gastric fluid, aspiration technique If I have to look at one more aspirate tonight I am going to pull my hair out… 11 Dare we not check residuals?? Small randomized, prospective study Torrazza, Parker et al 2015 61 infants 23-32 wks <1250g Hypothesis – NGR ↑ intake at 2 weeks full feeds more quickly - not statistically significant Group 1 without routine evaluation of GR reached full feeds nearly 6 days earlier Group 2 with routine evaluation of GR Required parenteral nutrition 6 more days Rate of adverse outcomes did not differ between the 2 groups Pre-Feed Abdominal Circumference vs Residuals Small randomized controlled trial by Kaur et al 80 patients 27-34 weeks less than 1500g Feeding Interruptions Gastric residual group – feeding intolerance bilious asp, asp >50% of previous feed or >3ml Abdominal circumference group – if >2cm above baseline feeds were interrupted and residuals were checked Results When the AC measurement was used as criteria for feeding intolerance Earlier achievement of full feeds by 4 days Less feeding interruptions Shorter duration of parenteral nutrition Staging of NEC Bell’s Criteria Stage 1. Suspected NEC: Gastric residuals, abdominal distention, occult or gross blood in stool, x-ray normal to mild distention, temperature instability, apnea, bradycardia Stage 2. Definite NEC Mild to moderate systemic illness, absent bowel sounds, abdominal tenderness, pneumotosis intestinalis or portal venous gas, metabolic acidosis, decreased platelets Back To NEC Staging of NEC Bell’s Criteria Stage 3. Advanced NEC Severely ill with acute decompensation, signs of peritonitis, hypotension, metabolic and respiratory acidosis, DIC, abdominal distention, pneuperitoneum 12 Our Patient initial management 72 hours later NPO Replogle to LIS Initial WBC 11.2, Plts 244 no bandemia Blood gas pH 7.38 CO2 50 HCO3 30 Lactate 1 Hgb 18 Glucose 62 Blood culture sent Ampicillin and Gentamicin started Laboratory changes Diagnosis - radiologic Respiratory acidosis Metabolic acidosis Thrombocytopenia Neutropenia Anemia Blood culture negative Hgb remained stable Platelets were 20,000 Anything concerning? Pneumotosis intestinalis (distal ileum & proximal colon) Pneumoperitoneum (indicates perferation) Gas in the portal vein Fixed dilated loops of bowel 13 Medical Management NPO Frequent abdominal films Labs – Hcts, electrolytes, platelets Maintain acid/base balance Respiratory support as needed Antibiotics Ampicillin Gentamycin MetroNIDAZOLE if worsening or perfs Stabilization Indications for Surgical Intervention Decompress stomach Support cardiovascular status with fluids and low dose Dopamine Assist ventilation as necessary Prevent thermal and metabolic stress Can We Predict NEC Can We Prevent NEC? Currently the only consistent predictors are prematurity and formula feeds Identification of potential risk factors On the Horizon Development of a risk assessment tool GutCheck - Sheila Gephart PhD May be peritoneal drainage or laparotomy Clinical deterioration despite medical treatment (thrombocytopenia, metabolic acidosis, increasing respiratory support, leukopenia, leukocytosis) Fixed dilated loops of bowel on x-ray Intraperitoneal air Tender abdominal mass Single dose of antenatal steroids Early preferential use of breast milk Standardized feeding guidelines Use of ibuprofen for PDA (vs indomethacin) Avoid the use of H2 Blockers (famotidine, ranitidine) 14 Unanswered questions Does supplementation with probiotics reduce the risk of NEC? Does longer use of empirical antibiotics increase the risk of NEC? Does the use of UAC’s affect NEC? If BM is not available should feedings be delayed vs use of formula? Is donor milk as effective at preventing NEC as mother’s milk? 15