Neonatal Surgical Emergencies - UCD Emergency Medicine

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The risk of unsuspected surgicalemergencies during the neonatal periodhas decreased over the past several yearsbecause of widespread use ofultrasonographyfor fetal screening.However, surgical emergencies unique tothe neonatal period still continue toplague the unsuspecting emergencyphysician. Most surgically correctabledisorders in the neonate will present withvomiting, gastrointestinal bleeding, orrespiratory distress. This article willprovide the emergency phvsician withthe typical presentation, diagnostic workup, and treatment options for surgicallycorrectable problems in the neonate.ClinPed Emerg2002, ElsevierMed 3:3-13.CopyrightScience(USA). All rightsNeonatalSurgicalEmergencireserved.By PamelaJ. Okada,MD and Barry Hicks,MDDALLAS,TEXASTHE SCOPE OF PEDIATRIC SURGERY is broad and encompasses a wide variety of diseases. Many surgical diseaseprocesses are age related. There are several common surgical emergencies that physicians caring for neonates willencounter in the emergency department.The most commonneonatal surgical emergencies of the gastrointestinaltract areoutlined in Table 1. This article will review common neonatalsurgical emergencies that present with vomiting, bleeding, orrespiratory distress.NeonatalSurpicalDisordersAssociatedwith VomitingSurgical disorders associated with vomiting include intestinalobstruction,malrotationand midgut vo1vulus, Hirschsprung’sdisease (HD), meconium ileus (MI), and abdominal wall defects.Other common emergencies, such as incarcerated inguinal hernia, hypertrophicpyloric stenosis, and trauma, have been discussed elsewhere in this issue.IntestinalFrom the Department of Pediatrics,Division of Emergency Medicine,University of Texas, SouthwesternMedical Center at Dallas, Dallas, TX; andthe Department of Surgery, Division ofPediatric Surgery, University of Texas,Southwestern Medical Center at Dallas,Dallas, TX.Address reprint requests to Pamela J.Okada, MD, Department of Pediatrics,University of Texas, SouthwesternMedicalCenter,5323HarryHinesBoulevard, Dallas, TX 75390.Copyright 2002, Elsevier Science(USA). All rights reserved.1522-8401/02/0301-0002835.00/Odoi: nal atresias involving the duodenum, jejunum, ileum,and colon together are the most common causes of intestinalobstruction in the newly born, affecting between 1 in 2,000 and1 in 5,000 live births.1 There is equal representation of the sexes.Duodenal obstruction is postulated to occur as a result of incomplete recanalization of the duodenal lumen during the tenth weekof gestation. Jejunoileal atresia is believed to be the result of latemesenteric vascular accidents in utero.Bilious vomiting is the most common presenting symptom in anewborn with intestinal obstruction. Although abdominal distension is typical of distal atresias, the abdomen may be flat or evenscaphoid in duodenal lesions. Abdominaldistentionis mostprominent in ileal atresia, whereas polyhydramniosand jaundiceNEONATALSURGICALEMERGENCIES/OKADAANDHICKS3

4NEONATAL SURGICAL EMERGENCIES/ OKADA AND HICKSTABLEI. CommonNeonatalSurgicalEmergenciesof the GastrointestinalTractIntestinal obstructionDuodenum,jejunum, ileum, colonAtresia, web, stenosisMalrotationand midgut nalwall ingenterocolitisDuplications,Meckel’s diverticulum,Incarceratedinguinal herniaHypertrophicmesenteric cystspyloric stenosisTrauma (considernonaccidentalon the type of intestinal atresia, different surgicalstrategies are indicated. In general, bowel reconstruction is achieved by an end-to-end (or end-toside) anastomosis.2Survival rates exceed 90%. Late complicationsfrom repair of duodenal atresia occur in approximately 12% to 15% of patients and include stricreflux, gastritis, peptic ulcer disease, gastroesophagealreflux, and choledochalcysts.and MidgutVolv lusThe incidence of malrotationis 1 in 500 livebirths.3 Twenty-five percent to 40% of patients withsymptomaticmalrotationpresent within the firstweek of life, 50% present within the first month,75% present before 1 year of age, and there is a 2:lmale predominancein cases presenting in the neonatal period. Malrotation of the midgut occurs whentrauma)are more frequently associated with jejunal atresia.Approximatelyone third of newly born infants withduodenal atresia have associated Down’s syndrome.Other subtle signs of intestinal obstruction include respiratory difficulty,excessive salivation,presence of an abdominal mass, jaundice (within 24hours of birth), and lethargy.2Abdominal plain films show a characteristic double bubble sign, showing air bubbles in the stomachand a dilated proximal duodenum in duodenal atresia (Fig 1). In jejunoileal atresia, abdominal filmsshow air fluid levels proximal to the lesion. Themore distal the obstruction, the greater the numberof air fluid levels and distended loops of bowel. Acontrast enema will show a small unused “microcolon” in most infants with jejunoileal atresia.A nasogastric or orogastric tube should be passedto decompress the stomach and duodenum. Intravenous fluids are given to maintain adequate urineoutput and normoglycemia.Surgery is not urgent.The infant must be evaluated thoroughly for associated malformations,especially cardiac anomalies.Duodenal atresia has been associated with abnormal developmentof the pancreas (annular pancreas) and Down’s syndrome (30% to 50%). There isalso an association with malrotation,congenitalheart disease, and esophageal atresia.For duodenal malformations,most surgeons willperform a diamond-shapedduodenoduodenostomyusing a standard side-to-side or proximal transverse-to-distal longitudinal anastomosis. DependingFigure I. Double bubble sign in duodenal atresia.

NEONATAL SURGICAL EMERGENCIES! OKADA AND HICKSFigure 2. Malrotationwith midgut voIvuIus.the normal rotational process and fixation of theintestine fail to occur during the seventh to twelfthweek of gestation.Malrotation typically presents in the first monthof life with bilious vomiting and sudden onset ofabdominal pain (crying). In older infants and children, symptoms may be vague and may includechronic, intermittentvomiting and cramping abdominal pain, failure to thrive, constipation, bloodydiarrhea, and hematemesis. Physical examinationmay exhibit a normal abdominal examinationin50% of patients. One third of patients present withabdominal distension without tenderness. Boweldistension, abdominal pain, and evidence of peritonitis occurs as intestinal ischemia progresses tonecrosis. As ischemia progresses to infarction, fever, peritonitis, abdominal distension, profound dehydration and vascular collapse worsen.In the newborn, volvulus can rapidly result insignificant bowel compromise with abdominal distention, bloody stools, and eventually hypovolemicshock and peritonitis.An upper gastrointestinal(UGI) contrast study is the most reliable method todiagnose malrotation. The malrotated duodenum isoften “coiled” to the right of the midline giving acorkscrew appearance (Fig 2). A cutoff appearanceof the contrast (“beak”) suggests obstruction fromvolvulus5Evaluation, resuscitation, and preoperative preparation proceed simultaneouslyin patients withsuspected malrotation with volvulus. In the emergency department, volume resuscitation, gastric decompression, and broad-spectrumantibiotics areadministered. The operative procedure for the correction of malrotation,called the Ladd procedure,includes derotation of the volvu1us, division of mesenteric bands, separation of the duodenojejunalmesentery from the cecocolic mesentery, and appendectomy.An appendectomyis performed because the colon is positioned on the left side of theabdomen during a Ladd procedure. Subsequent development of appendicitis could be confusing. Agastrostomy is rarely indicated.With viable intestine,postoperativecare isstraightforward,and prognosis is excellent. The lifetime risk of adhesive small bowel obstruction is 1%to 1O%.3 Volvulus should not recur. With extensiveischemic bowel and intestinal necrosis, the bowel isuntwisted and reduced into the abdominal cavity.Twelve to 24 hours later, a “second look” proceduremay be performed to assess bowel viability. Thisallows the surgeon to resect the necrotic bowel andto create an enterostomy at the distal end of thenormal bowel. Bowel reconstructionis performedin a later operation. These patients may developshort gut syndrome and may become dependent ontotal parenteral nutrition (TPN).The most serious complication of malrotation ismidgut volvulus with necrosis of the entire midgut.Mortality in infants with malrotationranges from2.5% to 24% and is influenced by the presence ofnecrotic bowel at laparotomy, the presence of associated anomalies, and younger patient age.4Bilious vomiting in an otherwise healthy infantmust be considered a surgical emergency andshould be considered to be malrotation with midgutvolvulus until proven otherwise. An emergency UGImust be performed as the patient is being evaluated, not on an elective basis.Hirschsprung’sDiseaseHD is a common cause of intestinal obstructionin newborns. It results from absence of ganglioncells in the myenteric plexus of the intestine. Incidence varies from 1 in 4,000 to 1 in 7,000 live birthswith a male to female ratio of 4:l.s It is usually anisolated disorder; however, Down’s syndrome is associated with 4% to 12% of the cases.HD results from the migratory arrest of vagallyderived neuroblasts, which normally reach the rectum by the twelfth week of gestation. Any length ofthe intestine may be involved; however, 80% to 90%

6NEONATAL SURGICAL EMERGENCIES/ OKADA AND HICKSof HD involves only the rectosigmoid colon.5 Thereare no “skip lesions” in the intestine, as HD is afailure of normal neuroblasts to complete their migration from the proximal GI tract to the anus. Amutation in the (RET)-proto-oncogeneappears tobe a major factor in the development of the disease.6 Also, molecules in the endothelin signalingpathway and the SOXlO transcriptionalactivatorhave been implicated.6The typical presentation of a neonate with HDincludes failure to pass meconium in the first 24hours of life, constipation and abdominal distention, bilious emesis, and refusal to feed. In somecases, failure to thrive may be the only initial sign.Barium enema (80% accuracy) shows a transitional zone (funnel-shapeddilatation of bowel) atthe junction for the aganglionic and ganglionic intestine (Fig 3). Rectal suction biopsy (95% accuracy) shows absence of ganglion cells in themyenteric plexus, increased staining of cholinesterase, and the presence of hypertrophiednervebundles. There are 2 surgical approaches: performance of a colostomy in the newborn period with adefinitive pull-through operation at a later date anda primary pull through operation without a colostomy. Currently, there are 3 pull-throughprocedures being used: Swenson procedure, Duhamelprocedure, and Soave’s operation.A very serious complicationof HD is Hirschsprung’s-associatedenterocolitis(HAEC).’ It canoccur before diagnosis and treatment of HD or afterthe definitive pull-throughprocedure and may belethal if not aggressively treated. The mean incidence of HAEC is 25% (range, 17% to SO%)? Therehas been a clear decline in the incidence of HAECover the past 40 years, most likely because of improved and prompt diagnosis of HD. Classic manifestations include abdominal distention, fever, andfoul-smellingstool. Other symptoms include explosive diarrhea, vomiting, fever, lethargy, rectalbleeding, and shock. Physical examination revealsmarked abdominal distension, which is hyperresonant to percussion. Rectal examination results inexplosive discharge of gas and stool.Abdominal radiographs may show the presenceof a distended loop of bowel along the left flank withan abrupt terminationin the pelvis. This is knownas the intestinal “cut-off” sign. Because of the riskof perforation,a contrast enema is not recommended in clinical HAEC.The infant is at risk for HAEC before the diagnosis of HD has been made and after the definitivepull-throughsurgery. Risk factors include delay indiagnosis of HD, increased length of the aganglionicsegment, and Down’s syndrome. Once HAEC develops, the infant is at increased risk for future development of enterocolitis.Treatment includes bowel rest, rectal washouts,and intravenous fluids and antibiotics. Mild casescan be treated with oral metronidazole.An emergency diverting stoma may be required in patientswho fail to improve with medical management. Thisstoma must be performed in normally innervatedbowel, as confirmed by frozen section evaluation.Mortality rates of HAEC range up to 33% and tend tobe higher in children with other abnormalities,such as Down’s syndrome.MeconiumFigure3. Bariumenema;transitionzonein HD.IleusMI occurs in 15% of newborns with cystic fibrosisand in 1 per 5,000 to 10,000 live births.1 It ischaracterized by impaction of thick meconium inthe distal ileum leading to a functional bowel obstruction. Most (90% to 95%) of these infants havecystic fibrosis and thus have deficits of pancreaticenzymes in the intestine.l Complicated MI resultswhen a volvulus or perforation of the bowel occursleading to meconium peritonitis. This may occurprenatally.MI is usually identified immediately after birth.After a few hours of life, marked abdominal distension and bilious vomiting occurs. Physical exami-

NEONATAL SURGICAL EMERGENCIESI OKADA AND HICKSnation shows thickened bowel loops that are oftenvisible and palpable through the abdominal wall.Rectal examination is difficult because of the smallcaliber of the rectum.Plain abdominal films show distended loops ofintestine with thickened bowel walls. Meconiummixed with swallowed air will give a characteristic“ground-glass” appearance without air fluid levels.Calcification, free air, and very large air fluid levelssuggest bowel perforation,which requires urgentsurgery. A contrast enema demarcates a microcolon (Fig 4). Reflux of contrast into the ileum showsthe plugs, which are located in the distal smallintestine. The small bowel is of narrower caliberdistal to the meconium plug and is dilated proximalto the plug.UncomplicatedMI may initially be treated witha water-solublecontrast enema and intravenousfluids. The hypertonicityof the radiopaque agentdraws fluid into the bowel and facilitates passage7and expulsion of meconium. When repeated contrast enemas are unsuccessful, laparotomy is indicated to evacuate the obstructingmeconiummanually or by enterotomy irrigation.AbdominalWall DefectsAbdominal wall defects, such as omphaloceleand gastroschisis, are challenging surgical emergencies at the time of birth. Complications after repairare more likely to be encounteredby the emergency physician. Table 2 summarizes these 2 s.8-10NeonatalSurgicalDisordersAssociatedwithGI BleedingInfants with upper gastrointestinal(GI) bleedingmay present with coffee-ground emesis, hematemesis, melena, or hematochezia.Fortunately,upperGI bleeding in infants is usually benign and selflimiting and rarely requires surgical intervention.Lower GI bleeding may be more serious. Infantsmay present with bright red blood from the rectum,melena, or hematochezia. Bleeding can result fromMeckel’s diverticulum, polyps (although rare in infants), lymphonodularhyperplasia, anorectal fissures, or intestinalduplications.Necrotizingenterocolitis must be suspected in premature andstressed full-term infants. Other causes, previouslydiscussed, are malrotation, intussusception(rare inthe newborn) and HD.NecrotisingFigure4. Microcolonin Ml.EnterocolitisNecrotizing enterocolitis(NEC) is primarily adisease of premature, low-birth-weightinfants andusually presents in the immediate newborn period.It is the most common gastrointestinalemergencyseen in the neonatal intensive care unit, occurringin 3% to 5% of all admitted infants.11 For the emergency physician, it is important to remember thatNEC can also develop in full-term infants. Infants athigh risk are those with a history of congenitalheart disease, perinatal asphyxia, hypoglycemia,polycythemia,respiratorydistress, maternal cocaine use, or maternal pre-eclampsia.l*The clinical presentation of a full-term neonatewith NEC is similar to the preterm infant. Subtle

8NEONATAL SURGICAL EMERGENCIESI OKADA AND HICKSTABLE2. Comparisonof Gastroschisisand OmphaloceleGastroschisisOmphaloceleEpidemiologyI in 20,000 birthsI in 3,000 to I in 10,000 birthsEmbryologyThe anomaly probably results from a rupturethe base of the umbilical cord in an areaweakened by the involution of the rightumbilical vein.ClinicalCharacterized by an intact umbilical cord withloops of intestine herniated through a smalldefect to the right side of the cord. There is nosac covering the intestinal defect. Bowel ismatted and edematous in appearance.Characterized by intestinal loops covered byamniotic membrane and peritoneum. Giantomphaloceles may contain liver as well as loopsof intestine. Infants have a high incidence ofassociated anomalies-chromosomal,cardiac,genitourinary and/or craniofacial anomalies.LocationRight of intact umbilicusProximal part of umbilical cordDiagnosisAntenatalAntenatalTreatmentPrimary repair versus staged repair with silastic siloSmall: One-stage surgical repairLarge: Gradual reduction with silastic siloOther anomaliesRare; intestinal atresiasNumerous; cardiac, chromosomal, BeckwithWiedemann, prune belly syndromeComplicationsMalrotation, midgut volvulus, hypoperistalsis,intestinal atresiaslstenoses, undescended testiclesMalrotation,atultrasoundsigns may include feeding intolerance, abdominaldistension, jaundice, and a change in stooling pattern. More ominous signs and symptoms includeabdominaltenderness,bilious emesis, grosslybloody stools, lethargy, temperature instability, apneic episodes, or respiratory distress.The pathologic hallmarks of NEC are coagulationnecrosis, inflammation,and hemorrhage in the involved segment of intestine. The origin of NEC ismultifactorial.Risk factors include bacterial colonization, intestinal ischemia, hypoxia, and formulafeeding. All of these stimulate proinflammatorymediators that lead to bowel necrosis. Abdominal radiograph findings include ileus, persistent loops,pneumatosisintestinalis (the hallmark of NEC),portal venous gas, gasless abdomen, and pneumoperitoneum(Fig 5). The treatment for uncomplicated NEC (no stricture or perforation) is medical.Current treatment recommendationsare to placean orogastric tube to low intermittentsuction, administer broad-spectrumantibiotics,and to givenothing by mouth for 10 to 14 days. Nutritionalsupport is provided by TPN. This nonoperativemanagement is successful in 75% of patients.14Surgical interventionis indicated if there is evidence of perforation or intestinal necrosis. Relativeindicationsfor surgery include clinical deteri-Failure of development or migration of the foldsthat form at the umbilical ring results in ananterior wall defect. The umbilical cord insertsinto the amniotic sac.ultrasoundmidgut volvulusoration, refractory acidosis, oliguria, hypotension,thrombocytopenia,ventilatoryfailure, portal venous gas, fixed dilated loop of bowel, or erythema ofthe abdominal wall. Surgical interventionsincludeperitoneal drainage, laparotomy with resection andproximal end ostomy, or laparotomy with resectionand primary anastomosis.14Jj Survival rates rangefrom 50% to 70% depending on level of prematurity,severity of disease, and institution. Long-term complications include intestinal strictures and adhesions (10% to 35%) which may result in bowelobstruction, short bowel syndrome (malabsorptionsyndrome), bacterial overgrowth and life-threatening sepsis, electrolyte and water loss from the ileostomy, or cholestasis secondary to prolonged ions are rare congenital anomalies tha

prominent in ileal atresia, whereas polyhydramnios and jaundice NEONATAL SURGICAL EMERGENCIES / OKADA AND HICKS 3 . 4 NEONATAL SURGICAL EMERGENCIES / OKADA AND HICKS TABLE I. Common Neonatal Surgical Emergencies of the Gastrointestinal Tract Intestinal obstruction Duodenum, jejunum, ileum, colon .

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