Pediatric Small-Bowel Obstruction

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Background

Many different pathologic processes can cause pediatric small-bowel obstructions. These processes can be divided into acute intestinal obstructions and chronic, partial intestinal obstructions. These conditions can be further subdivided into those that present in the immediate postnatal period and those that occur later in childhood (see the images below). (See Etiology, Presentation, and Workup.)


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Small-bowel obstruction visible on plain radiograph caused by intussusception in a 5-month-old patient.


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Surgical photograph of a transition zone in an infant with small bowel obstruction.

Intestinal obstruction occurs in about 1 in 1,500 live births. Intestinal obstruction should be suspected in any child with persistent vomiting, distention, and abdominal pain, because delayed diagnosis and treatment can lead to devastating consequences. Infants and young children with intestinal obstruction present with pain, irritability, vomiting, and abdominal distention. Small-bowel obstructions progress to decreased or no bowel movements. Undiagnosed or improperly managed obstructions can progress to vascular compromise, which causes bowel ischemia, necrosis, perforation, sepsis, and death. (See Prognosis, Presentation, and Workup.)

Congenital obstructive lesions of the intestines can be viewed as intrinsic (atresia, stenosis, meconium ileus, aganglionic megacolon) or extrinsic (malrotation, constricting bands, intra-abdominal hernias, duplications). An attempt should be made to locate the lesion preoperatively to guide the surgical approach. (See Workup and Treatment.)

When the obstruction is complete, there should be little difficulty in clinical recognition, but when it is incomplete or intermittent, the diagnosis may pose considerable difficulty. Polyhydramnios frequently accompanies high intestinal obstruction. When polyhydramnios has been noted, the infant's stomach should be aspirated immediately after birth. Aspiration of 15-20 mL or more of gastric fluid, especially if it is bile stained, is suggestive of a high intestinal obstruction.[1] (See P resentation and Workup.)

Patient education

For patient education information, see the Digestive Disorders Center, as well as Abdominal Pain in Children, Hernia, Vomiting and Nausea, Constipation in Children, and Colic.

Pathophysiology

The normal bowel contains gas and chyle, which is the sum of food and salivary, gastric, biliary, pancreatic, and intestinal secretions. Chyle continues to accumulate even without oral intake. Intrinsic or extrinsic blockage of the small bowel leads to accumulating secretions that dilate the intestine proximal to the obstruction.

Increased peristaltic contractions and intraluminal pressure may cause frequent loose stools and flatus early in the disease course. Vomiting is also an important sign of obstructed children, and its characteristics can suggest the level of the obstruction. Intestinal absorption and lymphatic drainage decrease if intraluminal pressure exceeds capillary and venous pressure in the bowel wall.

The bowel becomes ischemic when capillary blood flow stops, allowing bacteria to pass into the peritoneum; from that point, it passes into the bloodstream, leading to septicemia by a process known as bacterial translocation. Peritoneal fluid is constantly secreted by the visceral peritoneum and absorbed by the parietal peritoneum, mostly in the diaphragmatic abdominal surface, where the diaphragmatic pores can be distended as much as 3 times their normal size to allow the passage of bacteria.

The colonized fluid is then transported via the lymphatic channels into the thoracic duct, which drains in the jugulosubclavian angle of Pirogoff, allowing bacteria to enter the circulation and causing septicemia. Bacteria injected into the peritoneum can be cultivated from peripheral blood only 6 minutes after the injection, confirming the extremely rapid flow from the peritoneum into the systemic circulation.

Perforation can develop as the ischemia leads to bowel necrosis. First, lymphatic obstruction occurs because of the lesser pressure in these vessels. This is followed by venous obstruction, which accelerates the edema process because blood enters the affected bowel segment but does not have a drainage route. Finally, the continuous increase in the bowel wall pressure blocks the arterial vessels, leading to ischemic necrosis and perforation. Massive third spacing of fluids rapidly leads to shock, contributing to morbidity and mortality. This sequence may occur more rapidly in a closed-loop obstruction with no proximal escape for bowel contents.

Etiology

Intussusceptions

See the image below.


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Surgical photograph of an 8-month-old patient with ileocolic intussusception.

Intussusception is the most common cause of intestinal obstruction in infants and children aged 3 months to 6 years and is the second most common cause of acute abdomen in this age group. It occurs when a proximal segment of the intestine (called the intussusceptum) telescopes or invaginates into the lumen of another, immediately adjacent distal segment (called the intussuscipiens). Most intussusceptions are idiopathic. A lead point is identified in only 2-8% of cases. See the image below.


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Small-bowel obstruction visible on plain radiograph caused by intussusception in a 5-month-old patient.

Although the cause of intussusception is unknown in 90-95% of children, a viral etiology is suspected because of intussusception’s seasonal predisposition for spring and autumn, as well as a higher incidence of adenoid hypertrophy in children who suffer intussusceptions.

Gastroenteritis, rotavirus infection, or allergic stimuli are believed to cause intestinal lymphoid tissue to swell and become a lead point to pull the mass into the adjacent proximal intestine. In patients younger than 1 month and older than 3 years, pathologic lesions serve as the lead points that produce the condition.[2]

An analysis by Okimoto et al of 71 stool samples from pediatric patients with intussusception indicated that adenovirus is also a risk factor for the development of intussusception, with the risk being particularly high in children over age 2 years.[3]

Intussusception is a well-described complication of patients with Meckel diverticulum,[4] Waugh syndrome, cocaine abuse, laxative use, and even antibiotic use, presumably due to motility derangements caused by some of these agents. Intussusception has also been described in patients with parasites, particularly Ascaris lumbricoides.[5] In Henoch-Schönlein purpura, mucosal hematomas are thought to act as lead points.[6] Acute appendicitis in patients with Burkitt lymphoma has also been reported as an etiology.[7]

Peutz-Jeghers syndrome (PJS) is a rare cause of intussusception in older children; in this condition, hamartomatous polyps, usually located in the small bowel, act as the lead point. van Lier et al studied 110 patients with PJS, 69% of them presented at least one episode of intussusception, 95% of those were located in the small bowel, and 92.5% required surgical correction. Most polyps acting as lead points were bigger than 10 mm; thus, they recommend enteroscopic surveillance, with resection of larger polyps (10-15 mm) to prevent intussusception in patients with PJS.[8] Similarly, familial polyposis coli and juvenile polyposis can also cause intussusceptions, and a vermiform appendix may occasionally cause the disease. Familial cases of intussusception have been described. Suspect intestinal lymphomas in all children older than 6 years with intussusception.

Extensive retroperitoneal dissections are known to predispose children to postoperative intussusceptions, probably because of intestinal dysmotility in these patients. It usually involves the small bowel alone and occurs within 2 weeks of a previous laparotomy.[9] Blunt abdominal trauma has also been known to cause intussusception.

Intussusceptions are believed to begin with an intestinal spasm around a lead point; the bowel relaxes just distally to this spasm, which allows the longitudinal muscle fibers to draw the contracted portion of bowel into the relaxed portion.

In some patients, recognizable lead points are found, such as Meckel diverticulum, appendicitis, intestinal polyps, duplications, lymphosarcomas, and, rarely, foreign bodies. See the image below.


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Surgical image of a laparotomy on a 7-month-old girl with ileocolic intussusception. An edematous and erythematous cecal appendix was found to be acti....

Compression of the mesentery at the point of invagination occurs from the start, leading to immediate venous compression, venous stasis, and edema. Goblet cells pour copious amounts of mucus into the intestinal lumen. The engorged hyperemic intestinal mucosa seeps blood, which mixes with the mucus to form the currant jelly stool that occurs in 60% of patients. Tissue pressure eventually exceeds arterial pressure, and necrosis ensues within 24 hours.

The peak age of presentation is between the ages of 5 and 10 months. Intussusception is more common in males. Less than 1% of intussusceptions are found in neonates; however, cases have been reported in newborns and premature babies. Early diagnosis and prompt treatment prevent catastrophic complications. In 95% of cases, the intussusception is in the ileocecal area. Ileoileal and colocolic intussusceptions are rare.

Occasionally, an ileoileal intussusception of the terminal ileum may progress through the ileocecal valve, a condition known as ileoileocolic intussusception. Ileoileal intussusceptions are seen as a postoperative complication after extensive retroperitoneal dissections, as in surgery for neuroblastoma or Wilms tumors.

Management includes radiographic reductions with air enema and, if necessary, open reduction with bowel resection. Reports have concluded that laparoscopy is a reasonable alternative to pediatric intussusception, even in the event of requiring a bowel resection.[10]

Incarcerated hernias

The overall incidence of inguinal hernias in childhood ranges from 0.8-4.4%. The incidence is up to 10 times higher in boys than in girls. The incidence is much higher in premature infants; inguinal hernias develop in 13% of infants born before 32 weeks' gestation and in 30% of infants weighing less than 1000 g. (See the images below.)


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Small-bowel obstruction caused by an incarcerated inguinal hernia in a 2-month-old infant with bilateral inguinal hernias as well as an umbilical hern....


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Incarcerated left inguinal hernia.

During the third month of gestation, the abdominal peritoneum protrudes at the internal inguinal ring and extends to the scrotum to form a diverticulum known as the processus vaginalis. In females, this diverticulum is called the canal of Nuck and extends through the internal inguinal ring to the labia majora.

At birth, the processus vaginalis is open and in communication with the peritoneal cavity in about 80% of babies. Closure takes place progressively during the first 2 years of life, with an estimated 20-30% incidence of patency at age 2 years and then little further decline. This patent processus vaginalis becomes a hernia only when it contains abdominal viscera.

Incarcerated hernias occur when the contents of a hernia sac cannot be reduced back into the abdominal cavity. Incarcerated or nonreducible hernias may contain small bowel, cecal appendix (Amyand hernia), omentum, or, rarely, Meckel diverticulum (Littre hernia). In girls, the ovary and/or fallopian tube are usually incarcerated. When a part of the bladder wall or the colonic wall is contained in the hernia sac, it is called a sliding hernia.

Umbilical hernias are the result of an incompletely closed umbilical ring. Most spontaneously resolve by age 2 years (80%).

The risk of incarceration in premature infants is increased, being as high as 31% in some series.[11] Incarcerated hernias can be inguinal, femoral, or umbilical. Inguinal and femoral incarcerated hernias are most common in both sexes.

Femoral hernias, which tend to incarcerate, are extremely rare in children and are the only hernias that occur in girls more often than in boys. Femoral hernias often present as recurrent hernias after inguinal hernia repair, most likely because the surgeon was misled by the findings of a processus vaginalis at the initial surgery and missed the actual hernia defect. These are uncommon in infants.[12]

Incarceration represents the most common complication associated with inguinal hernias. In several large series, incarceration was reported in 6-18% of patients. The incidence could be as high as 30% for infants younger than age 2 months. Most inguinal hernias in children are indirect hernias. Most direct hernias in the pediatric population occur following repair of an indirect hernia.

Umbilical hernias are very common in children, rarely incarcerate, and often close spontaneously by age 5 years.

Unless there is clear peritonitis or bowel compromise, incarcerated inguinal hernias can usually be reduced manually using a taxis technique. Up to 80% of incarcerated hernias can be reduced this way.[13]

In girls, an incarcerated ovary may be present in the hernial sac, in which case, vascular compromise risk is high (33%).[14]

Internal hernias are extremely rare and cause bowel obstruction in children. Hernias in the mesentery, mesocolon, mesosigmoid, and Winslow foramen[15] and defects in the falciform ligament have been described.[16]

Malrotation of bowel with midgut volvulus

The reported incidence of malrotation is 1 in every 500 infants. It can be isolated or associated with other malformations, including congenital diaphragmatic hernia, abdominal wall defects, intestinal atresias, and Beckwith-Wiedemann syndrome.[17]

Intestinal malrotation refers to errors of midgut rotation around the superior mesenteric artery axis and the subsequent fixation of the midgut in the peritoneal cavity. Nonrotation, incomplete rotation, reversed rotation, and alterations of fixation (including the internal hernias [mesocolic, paraduodenal] and the mobile cecum) are among the many embryonic variants of the anomaly. (See the images below.)


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Upper GI contrast study showing a malrotation with lack of normal C-shaped duodenum and the small bowel "hanging" on the right side of the abdomen.


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Contrast enema with an abnormally located cecum in a patient with malrotation.

The primitive gut, which forms during the fourth week of embryonal life, is divided into the foregut, midgut, and hindgut. The largest of these, the midgut, is the only portion that undergoes rotation by herniating extraembryonically into the umbilical cord and rotating 270° in a counterclockwise direction around the superior mesenteric artery on its journey back to the abdominal cavity by 11 weeks' gestation. This produces the normal C-shaped configuration of the duodenum and results in the cecum coming to rest in the right lower quadrant of the abdomen.

For unknown reasons, midgut rotation can arrest at any point, most commonly rotating 180° and leaving the cecocolic loop in the right upper quadrant. Dense peritoneal bands (ie, Ladd bands) cross from the malpositioned right colon across the duodenum to the right lateral abdominal wall. This configuration leaves a narrow mesenteric root and creates a predisposition to clockwise torsion of the midgut, while the Ladd bands themselves can obstruct the duodenum.

Theories of malrotation are based on anatomic and pathologic findings, but the actual rotation movements have not been seen in human embryos. Evidence suggests that, at least in rats, the midgut never rotates around the superior mesenteric artery and that the final normal position and fixation of the midgut are probably due to differential growth of specific intestinal segments rather than to rotational movements.

Malrotation is always present in patients with abdominal wall defects (gastroschisis, omphalocele) and in patients with congenital diaphragmatic hernia. It is often associated with other congenital and acquired lesions of the gastrointestinal (GI) tract, such as Hirschsprung disease, intussusception, and atresia of the jejunum, duodenum, and esophagus.

In children, the most common form of malrotation occurs when the process of rotation is incomplete and the ligament of Treitz or the cecum is abnormally located or fixed. The mesenteric attachment of the midgut to the posterior abdominal wall is narrow and predisposes the midgut to twist around an axis formed by the superior mesenteric artery (midgut volvulus). Complete volvulus of the bowel for more than 1-2 hours can totally obstruct blood supply to the bowel, leading to complete necrosis of the involved segment. (See the image below.)


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Surgical photograph of necrotic bowel in a patient with midgut volvulus.

Postoperative adhesions

Adhesive small-bowel obstruction is a surgical complication, with postoperative adhesions being responsible for about 3-8% of the intestinal obstructions in infants and children.

Laparotomy for inflammatory conditions renders the patient particularly prone for adhesive small-bowel obstruction. Adhesions occur in areas of ischemia or serosal damage. Rough tissue handling, foreign material, residual blood in the peritoneal cavity, and mass ligatures in the omentum increase its likelihood.[18]

A single adhesion causes most obstructions, regardless of the nature of the previous illness or type of abdominal surgery. The postsurgical onset of obstructive symptoms can take from 2 days to 10 years to occur, although most adhesions (>50%) occur within the first 3-6 postoperative months; few occur after 2 years.

The incidence of adhesive small-bowel obstructions seems to be lower after laparoscopic procedures than after laparotomy.[19]

Annular pancreas

Annular pancreas is a rare congenital anomaly seen in 1-3 of every 20,000 autopsies performed. Annular pancreas occurs when the ventral pancreatic bud fails to rotate behind the duodenum, leaving pancreatic tissue fully encircling the second portion of the duodenum. This results in a nondistensible ring of pancreatic parenchyma and a functional stenosis.

In children born with the condition, the second portion of the duodenum is either partially or completely surrounded by pancreatic tissue. Most cases of annular pancreas are diagnosed early in life when patients present with symptoms of duodenal obstruction.[20]

Annular pancreas involves a lesion that consists of a thin, flat ring of histologically normal pancreatic tissue that surrounds the descending duodenum in an anomalous position. Annular pancreas results from abnormal rotation of the ventral pancreatic bud, and usually functions normally, barring development of pancreatitis or an obstruction of the duct of Wirsung.

An annular pancreas can be asymptomatic or can cause external compression on the second portion of the duodenum, which creates a partial or complete obstruction. Annular pancreas is almost invariably associated with an intrinsic cause of duodenal obstruction (duodenal atresia).

Mesocolic hernia

Mesocolic hernia is a rotation abnormality.[21] Nonfixed colonic and duodenal mesenteries lead to formation of potential hernia pouches, which transiently and recurrently entrap the bowel and cause partial obstructions. The exact incidence of mesocolic hernia is not known, because most cases are asymptomatic. (See the image below.)


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Mesocolic hernia.

The median age at presentation in one series was 13 years, with an age range of 6-19 years. The most common presenting symptom was diffuse abdominal pain lasting 1 day.[22]

The internal hernias may be right sided or left sided and can sometimes incarcerate and strangulate. Mesocolic hernias can also occur when a mesenteric defect is not properly closed during retroperitoneal surgery.

Necrotizing enterocolitis

Necrotizing enterocolitis (NEC) is the most common neonatal gastrointestinal emergency, predominantly affecting low-birth-weight, premature infants. The risk of developing NEC is inversely proportional to gestational age and weight at birth. The more premature the infant, the later this condition occurs after birth.[23] Fetal growth restriction and compromise may be additional specific risk factors.[24]

NEC can produce strictures that subsequently cause intestinal obstruction. The most common sites for these strictures are the terminal ileum and the colon. Strictures usually occur within 1-6 months following an acute NEC episode. In patients with NEC, whether a systemic inflammatory response triggered by a perinatal physiologic stress results in intestinal ischemia, bacterial overgrowth, breakdown of the mucosal barrier, and bacterial translocation is unclear.

Strictures from NEC occur most often in premature infants. These strictures account for 15% of deaths in infants older than 1 week whose birth weights were less than 1500 g. However, although prematurity and the associated immaturity of the gut mucosa account for 90% of cases, 10% of NEC occurs in term infants.[25]

Intestinal strictures occur in patients with NEC regardless of management. Retrospective and prospective studies have reported an incidence of strictures of between 10% and 35% for medically and surgically managed patients.

While the exact cause of NEC remains unknown, multiple factors probably lead to ischemic or hypoxemic insult of the intestinal mucosa, followed by bacterial invasion of the denuded mucosa with gram-negative septicemia and intestinal necrosis. Complement activation product C5a (anaphylatoxin) has been reported to be a contributing factor leading to mesenteric ischemia/reperfusion injury, which is a predisposing factor in the pathogenesis of NEC.[26]

NEC can be regarded as an immunoinflammatory response by the immature and inexperienced gut to environmental antigens such as enteral nutrition and the presence of commensal bacteria. The primary infectious process likely results in enteroinvasion, release of inflammatory mediators, toxin production, ileus, gas production, bowel distention, increased intraluminal pressure, and vascular compromise, which causes loss of mucosal integrity, and bacterial translocation, which results in a systemic inflammatory response.

The most prominent risk factor is prematurity with aggressive hypertonic enteral feedings; however, NEC is seen in 15% of patients that have never been fed. Full-term newborns with polycythemia or congenital heart disease have higher risk for NEC,[27] as do infants who had umbilical arterial or venous catheters in situ. Other risk factors include hypertonic feeding solutions that damage the mucosal epithelium of the intestine and episodes of apnea with ischemia of the GI tract.

Mortality rates from NEC are high, ranging from 15-30%, with higher risk of mortality for patients treated surgically.[28] There is strong evidence that half of the survivors have neurodevelopmental outcomes lower than their peers without NEC.[29]

Gastric volvulus[30]

Gastric volvulus is quite rare. Fewer than 100 cases have been described in the literature since it was first reported in children by Dujon in 1902. It refers to a stomach rotation resulting in complete obstruction of its lumen. It may be acute or chronic. Acute gastric volvulus represents a surgical emergency, requiring prompt recognition and treatment in order to achieve survival.

Two different types of gastric volvulus are recognized. In the mesenteroaxial type, the stomach rotates on its transverse axis, perpendicular to a line between the cardias and the pylorus. Organoaxial gastric volvulus occurs in its cardiopyloric axis.

Association to other anatomical defects is the rule; however, idiopathic cases have been described.

Clinical findings include sudden epigastric pain, nausea and vomiting, and the inability to pass a nasogastric tube (Brouchardt triad). Upper abdominal distension is common.

Radiographically, it is characterized by severe gastric distension with air-fluid levels. Left diaphragmatic elevation and gastric pneumatosis are possible. Some patients show only an isolated simple gastric bubble. See the image below.


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Plain abdominal film of a 6-year-old male patient with MRCP (mental retardation and cerebral palsy), with organo-axial gastric volvulus. Note the gros....

If left untreated, gastric ischemia ensures, leading to necrosis, perforation, peritonitis, and death.

During surgery, the stomach must be devolvulated (untwisted) and fixed to the diaphragm. Necrosis requires gastric resection, with anastomosis or diversion, depending on the peritoneal findings. Associated anatomical defects should be repaired simultaneously.

Causes of chronic, partial intestinal obstructions

Most chronic, partial intestinal obstructions are due to anatomic abnormalities such as intestinal duplications, hernias, and intestinal stenosis. Rarely, children may experience obstruction due to trichobezoar; this usually occurs in young females with trichotillomania (an irresistible desire to pull out one's own hair) or trichophagia (in which an individual eats hair or wool). When the trichobezoar has a long tail that extends beyond the stomach into the small intestine, it is called Rapunzel syndrome.

Cecal volvulus

Cecal volvulus is a rare disorder of nonfixation (ie, a mobile cecum), rather than a complete malrotation. Cecal volvulus most commonly occurs as axial twisting of the cecum, ascending colon, and terminal ileum. It has also been described in patients who have undergone a Malone antegrade continence enema (MACE) procedure, in which the cecal appendix is used as a tubular conduit between the abdominal wall and the cecum, creating a stoma through which the patient can get an antegrade enema to achieve "social continence."[31]

Duplication cysts

See the image below.


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Surgical photograph of a 3-year-old male patient with an obstructive, noncommunicating ileal duplication.

Duplications of the alimentary tract make up a group of rare malformations that vary greatly in appearance, size, location, and symptoms. Intestinal duplications can be either cystic or tubular in shape. They have been reported to occur anywhere along the GI tract, from the tongue to the anus, although most are located in the terminal ileum near the ileocecal valve. Duplications are seen in 1 of every 4500 autopsies; 85% of cases are detected by age 2 years.[32]

The embryogenesis of rectal duplications has been attributed to the pinching off of diverticula that are present in the 8-week-old to 9-week-old embryo. The reported association of spinal abnormalities makes the split notochord mechanism another probable origin of rectal duplications.

The 3 characteristics of alimentary tract duplications, as proposed by Ladd and Gross, include (1) contiguity with and strong adherence to some part of the alimentary tract, (2) a smooth muscle coat (usually in 2 layers), and (3) a mucosal lining that consists of 1 or more types of cells normally observed in the alimentary tract.[33]

Most duplications are truly enteric cysts; few of them actually represent attempts to double the alimentary tract. The intestinal epithelium may or may not correspond to the epithelium of the adjacent intestinal structure. Gastric mucosa is the most common ectopic tissue found.

Intestinal obstruction, bleeding, infection, and carcinomatous degeneration have been observed with these anomalies, and early correct diagnosis is vital. Most symptoms are caused by the mass effect, and the duplication causes either a partial or complete small-bowel obstruction.

Causes of immediate postnatal small-bowel obstructions

Most of these obstructions are the result of jejunoileal atresia (see the images below), meconium ileus, or extrinsic or intrinsic duodenal obstructions. Jejunoileal atresia (ie, complete obstruction) and stenosis (ie, incomplete obstruction) are extremely important causes of neonatal intestinal obstruction. Atresia, which accounts for 95% of cases, is a congenital obstruction secondary to complete occlusion of the intestinal lumen. In about 25% of these patients, atresia is associated with major GI anomalies (eg, malrotation, meconium ileus, volvulus, omphaloceles, gastroschisis).


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Upper GI contrast study demonstrating a jejunal atresia with a proximal dilated atretic bowel and lack of passage of contrast into the distal small bo....


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Surgical photograph of the patient in the previous image depicting the proximal dilated atretic jejunum.


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Surgical image of a laparotomy on a 2-day-old female patient with congenital small bowel obstruction. A type I jejunal atresia without mesenteric gap ....


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Contrast-enhanced upper gastrointestinal film showing a duodenal atresia on a 2-day-old newborn.

Stenosis is the cause of the remaining 5% of cases. It is a partial congenital obstruction caused by incomplete intraluminal occlusion. Both entities appear to be caused by incomplete vacuolization of the embryonic intestine during the cord phase of intestinal development. Patients with intestinal atresia are epidemiologically characterized by low gestational age and low birth weight.

Meconium ileus

Meconium ileus occurs almost exclusively in patients with cystic fibrosis (CF) and is usually the earliest clinical manifestation: 10-15% of patients with CF have meconium ileus, and 90% of patients with meconium ileus have CF.

Meconium ileus is caused by hyperviscous secretions produced by the small intestine’s mucous glands. Meconium ileus is the most severe clinical expression of exocrine pancreatic insufficiency; the lack of normal pancreatic exocrine secretions is the most important factor in the formation of the thick meconium. These secretions cause a thick and tarlike in utero meconium that has a low water content. This abnormally sticky meconium adheres firmly to the small intestinal mucosa and produces intraluminal obstructions. The involved bowel segment may dilate and may even perforate or develop a volvulus.

Meconium plug syndrome or meconium obstruction does not appear to be associated with CF or Hirschsprung disease in extremely low birth weight infants.

Duodenal obstructions

Duodenal obstructions in newborns may be partial or complete and they may be secondary to extrinsic or intrinsic abnormalities. Duodenal atresia and stenosis are believed to be caused by failure of recanalization or vacuolization of the duodenum after the embryologic cord stage, when the lumen is completely obliterated. Duodenal atresia completely obliterates the duodenal lumen; duodenal stenosis only partially or incompletely obstructs the duodenal lumen.

Duodenal atresia and stenosis are relatively rare causes of obstruction, with a frequency of 1 in 2,500-10,000 live births.[34, 35] Although duodenal atresia is at least 4 times more common than duodenal stenosis, stenosis occurs more often in the duodenum than in other portions of the GI tract and may remain undetected until adulthood.

Duodenal atresia has a high rate of associated anomalies (50%): trisomy 21 (31%), malrotation (20%), congenital heart disease (30%), esophageal atresia (10%), genitourinary anomalies (11%), and anular pancreas (20%). Polyhydramnios occurs in approximately 40% of patients, and this clinical finding suggests a more proximal intestinal obstruction in the fetus.

The 3 basic morphologic features of duodenal atresias are as follows:

Jejunoileal atresia

See the image below.


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Surgical image of a laparotomy on a 2-day-old female patient with congenital small bowel obstruction. A type I jejunal atresia without mesenteric gap ....

Jejunoileal atresia is believed to result from intrauterine mesenteric vascular accidents that cause devascularization. Lack of normal vacuolization is thought to be the cause of all type I atresias, which may occur anywhere. Vascular accidents with different degrees of infarction are then thought to be the cause of other types of atresias, which may include not only intestinal, but also mesenteric, defects.

The extent of atresia and the appearance of the atretic intestinal segment vary according to the timing and degree of the disruption of the mesenteric blood supply.

Small-bowel atresia variably reduces the size of the colon. The volume of intestinal secretions and amniotic fluid that passes through the colon in fetal life determines its size in the newborn. Atresia blocks this fluid flow through the colon, thus limiting colon growth; however, passage of meconium does not rule out intestinal atresia, because the vascular insult that leads to the atresia may occur after the recanalization phase of the intestinal development.

Jejunoileal atresias are twice as common as duodenal atresias and are also more common than colonic atresias. Males and females are equally affected. Usually jejunoileal atresias are single atresias (multiple atresias occur in 6-20%). In order of location and frequency, jejunoileal atresias occur as follows:

In the case of jejunoileal atresias, the obstruction is mechanical; it is caused by the presence of bile, lanugo, and meconium distal to the atresia. In contrast to duodenal atresia, this occlusion happens after intestinal development has been completed.

Following this occlusion, an ischemic injury develops, caused by 1 of the following:

Epidemiology

Occurrence in the United States

Malrotation of the bowel with midgut volvulus occurs at a rate of 1 case per 500 infants. Jejunoileal atresia and stenosis have a combined reported incidence of 1 case per 1500-5000 live births. These conditions are common among patients with maternal polyhydramnios; 38% have jejunal atresia, and 15% have ileal atresia. Overall, the atresia is almost equally divided between the jejunum (51%) and ileum (49%).

Jejunoileal atresia is twice as common as duodenal atresia and is more common than colonic atresia. Duodenal atresia and stenosis, collectively, are relatively rare causes of obstruction that occur at a rate of just 1 case per 2,500-10,000 live births.[34, 35] The incidence of alimentary tract duplications is 1 case per 4500 population.

Sex-related demographics

The male-to-female ratio for incarcerated hernias is 8:1. Hernias occur on the right in about 60% of males, on the left in 25%, and bilaterally in 15%. Females have bilateral inguinal hernias more often than do males. Malrotation of the bowel with midgut volvulus can affect either sex. Neither duplication cysts nor jejunoileal atresia and stenosis exhibit a sexual predilection.

Age-related demographics

Intussusception can occur at any time in life, but the idiopathic form is primarily a childhood disease, developing especially during infancy. Peak occurrence is in infants aged 5-10 months; average age is about 7-8 months.

Most patients with inguinal hernias present during the first year of life. Approximately one third are younger than 6 months at the time of surgery.

Most patients with symptomatic malrotation of the bowel with midgut volvulus present in early infancy. Approximately 50% of patients present in the first month of life, and 80% present in the first year of life. Midgut volvulus has reportedly occurred in utero. Fewer patients (ie, 6-20%) present at ages older than 1 year; these patients tend to have a longer course of vague symptoms (eg, intermittent, bilious vomiting; chronic abdominal pain).

Most patients with duplication cysts present in early childhood or infancy, although some may not develop symptoms until much later. Many duplication cysts are diagnosed within the first week of life, 60% are identified during the first 6 months of life, and 85% are identified by age 1 year.

For annular pancreas, the age of onset of obstructive symptoms widely varies; sometimes, these do not develop until adulthood. Many pediatric patients present in the newborn period with complete duodenal obstruction, often after the first feeding.

NEC occurs in 90% of premature infants weighing less than 1500 g; however, 10% of NEC occurrences are in the term infant.

Jejunoileal atresia causes obstruction in the immediate postnatal period. Patients with duodenal stenosis may remain asymptomatic until late childhood or may progress to complete obstruction; symptom onset depends upon the degree of stenosis. Patients with duodenal atresia or annular pancreas present in the first 24 hours of life.

Meconium ileus and meconium plug syndrome present in the first few days of life. A rare entity similar to meconium ileus that presents later in life is called meconium ileus equivalent or distal intestinal obstruction syndrome.

Prognosis

Mortality and morbidity in pediatric small-bowel obstruction depend on the type of lesion that causes the intestinal blockage, whether it is a closed-loop or strangulated obstruction, and the time elapsed before diagnosis and definitive, adequate treatment. Mortality is low with early diagnosis and treatment. If left untreated, strangulated obstructions are always lethal. Mortality rates may reach 65% if more than 75% of the small bowel is necrotic at the time of laparotomy. Strictures and adhesions are late complications of treated obstructions. Too much bowel damage can cause malnutrition due to short-bowel syndrome.[36]

Long-term survival in patients with duodenal atresia or stenosis is approximately 86%. Most of the morbidity and mortality is related to cardiac anomalies. This includes patients with annular pancreas.

Although intussusception-associated infant deaths in the United States have declined substantially since the late 20th century, some of these deaths may have been preventable because they were apparently related to delayed or reduced access to health care.

The survival rate at 1 year is approximately 92% in patients with uncomplicated meconium ileus and 89% in patients with complicated disease.

Necrotizing enterocolitis (NEC) is a leading cause of death among patients in neonatal intensive care units, carrying a mortality rate of 15-30%.[37] Mortality is higher in surgically treated infants, reaching up to 50%. Extent of disease does impact mortality. Infants with pan-intestinal involvement show a 33% survival rate, compared with 69.5% survival for multifocal disease. Isolated NEC has an 88% survival rate.[28]

Survivors show a fair amount of long-term complications, including short bowel syndrome, abnormal growth, and neurodevelopmental delay. The incidence of intestinal failure among infants undergoing surgical treatment for NEC is high. Its risk is increase in patients with low birth weight, antibiotic use, ventilator use, and greater extent of bowel resection.[38]

Intestinal resections have been reported in about 1.4-1.8% of patients with incarcerated inguinal hernias. The incidence of testicular infarction and atrophy ranges from 4-12%; young infants seem to be at higher risk.

History

Obtain a complete medical history, specifically including information on prior malignancies, radiation therapies, and abdominal or pelvic surgeries. A history of repetitive abdominal pain with vomiting indicates a chronic, partial small-bowel obstruction.

Obtain as much history as possible from the child. Younger children are likely to recall recent events, whereas adults remember more remote events. Physicians should seek an accurate chronology of the disorder. Asking when the child was last completely healthy may provide a more accurate assessment of the child's pathophysiology.

Bilious vomiting in the neonate should be considered secondary to a mechanical obstruction until proven otherwise, and every newborn with this symptom warrants emergent surgical evaluation.

Abdominal pain in patients is common. Caregivers may describe an infant or small child with abdominal pain as irritable or inconsolable. Pain from a small-bowel obstruction is usually colicky. It is described as cramplike and episodic, persisting for a few minutes at a time. A child with obstructive pain may be unable to remain immobile on the examining table. Constant pain occurs later in the disease course, when strangulation, perforation, or both have occurred.

Vomiting is a classic symptom of mechanical obstruction. Emesis caused by a proximal obstruction is usually of gastric content or is bilious if the obstruction is distal to the ampulla of Vater. In distal ileal obstructions, vomit is feculent.

Other issues to focus on include the following:

Intussusception

Intussusception usually causes a sudden onset of severe colicky abdominal pain that often causes a child to draw up both legs. Children appear healthy between paroxysms of pain. As the intussusception progresses, the child becomes progressively more irritable and lethargic until shock develops. Vomiting occurs in the early phase of the illness and is bilious in 30% of cases. Early in the course of the disease, stools are normal, but they rapidly become bloody and mucoid within the first 12 hours.

The classic triad described for intussusception, which consists of colicky abdominal pain; a sausage-shaped, palpable abdominal mass; and currant-jelly stools, is actually found in only 20% of cases. Postoperative intussusception occurs within 2-3 weeks after an extensive retroperitoneal dissection (Wilms tumor, pancreatic surgery, or neuroblastoma). It is usually an ileoileal intussusception, and affected patients lack the palpable mass and rectal bleeding. Patients usually present with crampy abdominal pain, anorexia, bilious vomiting, abdominal distension, and irritability.

Hernia

An incarcerated hernia is usually associated with signs and symptoms of intestinal obstruction (eg, bilious vomiting, abdominal distention, constipation, obstipation). A tender, edematous, slightly discolored to pale mass in the inguinal area may extend down into the scrotum. A swollen, erythematous mass that becomes erythematous to violaceous and is exquisitely tender usually indicates a strangulated hernia. Fever and toxicity suggest frank necrosis of the incarcerated organ and impending or completed perforation.

Patients with mesocolic hernias typically have repeated episodes of colicky abdominal pain and vomiting. These symptoms spontaneously subside when the hernia spontaneously reduces. Patients with incarcerated hernias have continuous pain, abdominal distention, fever, nausea, and vomiting.

Acute midgut volvulus

The hallmark of acute midgut volvulus is the sudden onset of bilious vomiting, which may be projectile vomiting and, on occasion, have a coffee-ground appearance or contain frank blood. History may reveal feeding problems, with transient episodes of bilious vomiting or failure to thrive. Abdominal distention or a palpable mass may not be evident, because the obstruction occurs very proximally in the GI tract. Older children typically describe colicky abdominal pain. Stools are usually absent, but those that do occur yield positive results on guaiac tests. Bright red blood passed through the rectum implies intestinal ischemia.

Adhesion

Postoperative adhesive small-bowel obstructions usually cause a sudden cramplike abdominal pain, followed by anorexia, nausea, and bilious vomiting. Bowel movements typically cease shortly after symptom onset. Clinical manifestations vary according to whether the obstruction is proximal or distal and the stage of the obstruction.

Duplication

Presentation of duplication cysts primarily depends on the type of mucosal lining and on cyst location. At least 16% of small-bowel duplications contain gastric mucosa and may manifest with peptic ulceration and GI hemorrhage. Spheric cystic duplications may enlarge sufficiently to cause obstruction. Always consider duplication cysts in the differential diagnosis of a vomiting infant or child with a palpable, solid abdominal mass and abdominal distention. These cysts may also act as the lead point for an intussusception or form the apex of a volvulus.

Abdominal gastric and duodenal duplications may be confused with pyloric stenosis, because of their similar presentation. Older patients may present with chronic, intermittent vomiting caused by recurring partial obstruction or with an unexplained GI hemorrhage.

Because 20% of patients with rectal duplications have fistulae, drainage of mucous or pus through the anus or a perianal fistula is not uncommon.

Intestinal atresia and stenosis

Intestinal atresia or stenosis can occur anywhere along the GI tract, and the anatomical location of the obstruction determines the clinical presentation. Most newborns present with bilious emesis, a distended upper abdomen, and a scaphoid hypogastrium. Signs of dehydration are not uncommon. Jaundice is present in 32% of these children. A history of polyhydramnios on prenatal ultrasonography (28%), prematurity (35%), or low birth weight (25-50%) can be helpful hints in the diagnosis.

The cardinal symptom of duodenal atresia is vomiting. Because 85% of atresias are postampullary, most patients present with bile-stained vomit in the first 24 hours of life. Most patients exhibit little or no upper abdominal distention because of the high level of the obstruction. Dehydration, weight loss, and obstipation subsequently develop if treatment is delayed.

Newborns with jejunoileal atresia or stenosis present with bilious vomiting and jaundice; these infants may not pass meconium in the first day of life. Bilious vomiting is more common with jejunal atresia. Abdominal distention occurs more often in patients with ileal atresia.

Annular pancreas

In annular pancreas, the duodenum is often compressed at a point distal to the ampulla of Vater, making bilious vomiting a hallmark symptom. Abdominal distention is typically minimal, because of the proximal location of the obstruction. Patients may not pass meconium, or bowel movements may cease abruptly. A more insidious form of chronic, partial duodenal obstruction may also occur.

Necrotizing enterocolitis

The clinical features of NEC are nonspecific and often include lethargy, temperature instability, and abdominal distention. Other common symptoms include bilious vomiting, gross or occult rectal bleeding, abdominal tenderness, redness of the abdominal wall, and the presence of reducing substances in the stool. Discoloration of the abdominal wall is indicative of bowel perforation. Apparently, clinical parameters are not good predictors of NEC outcome.

Cecal volvulus

The presenting symptoms of cecal volvulus include pain, distention, constipation or obstipation, and vomiting.

Meconium ileus

In patients with meconium ileus, symptoms depend on the level of the obstruction (which is usually the terminal ileum) and may include vomiting (usually bile-stained), failure to pass meconium in the first 48 hours of life, and possible abdominal distention. Patients may also present with generalized peritonitis (meconium peritonitis), a meconium pseudocyst, or obstruction due to an intestinal atresia.

Physical Examination

Patients do not develop fever unless the blood supply to the obstructed bowel becomes compromised, which may allow bacterial translocation and subsequent sepsis.

In children who present late in the course of their illness, poor capillary refill, hypotension, and even shock may occur as a result of increasing third spacing of fluid into the bowel lumen.

Abdominal tenderness may be minimal and diffuse or localized and severe. The abdomen may be tympanic to percussion. Patients who develop peritonitis obviously have severe pain and rebound tenderness.

Bowel sounds can be characterized as follows:

During abdominal examinations, look for hernias in the groin, femoral triangle, and obturator foramina. (Careful physical examination is most useful in the diagnosis of an incarcerated hernia.) Perform a pelvic examination to exclude a genitourinary pathology as the cause of the obstruction.

In intussusception, physical examination of the abdomen occasionally reveals a tender, sausage-shaped mass that is variable in size and firmness, with spasms of pain. Because most intussusceptions are ileocolic, patients may present with Dance sign (empty right lower quadrant). See the image below.


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Clinical photograph of a 5-month-old male patient with characteristic currant-jelly stools due to intussusception.

In patients with a postoperative adhesive small-bowel obstruction, physical examination may reveal abdominal distention and hyperactive high-pitched bowel sounds. Patients usually have a diffuse and poorly localized tenderness that improves with proximal decompression by a suction tube.

Patients with NEC have a wide variation in clinical presentation, from feeding intolerance to shock; however, specific clinical signs that should raise high suspicion include abdominal distention, bluish discoloration of the abdominal wall, and blood in the stool. Refer to the Bell’s staging criteria, which are still widely used to classify the staging of NEC; the criteria provide a clinical and radiographic assessment of the disease.[39] See the image below.


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Clinical image of a micro-premature baby boy with discoloration on the right lower quadrant of the abdomen, due to intestinal perforation secondary to....

During rectal examination, keep the following in mind:

Approach Considerations

Signs and symptoms of bowel obstruction, especially in newborns, may be subtle; physicians should maintain a high index of suspicion. Moreover, rapid decisions about the need for surgical intervention can mean the difference between full recovery and massive bowel loss.

Bilious vomiting in a newborn should immediately lead physicians to suspect a bowel obstruction and to initiate an immediate workup and a surgical consultation. Admit any child with suspected small-bowel obstruction for observation, even if the diagnosis of obstruction is unclear.

The following laboratory tests may be useful in patients with small-bowel obstruction:

Results can include the following:

Imaging Studies

Obtain flat decubitus and upright radiographs of the abdomen. Study radiographs for signs of dilated small-bowel loops and air-fluid levels produced by the layering of air and intestinal content. Absent colonic or rectal gas also indicates a complete bowel obstruction.

The pattern of bowel gas on plain radiography can help to differentiate between proximal and distal bowel obstructions. Drawing an imaginary line from the right upper quadrant to the left lower one is helpful in establishing the level of the obstruction. The jejunum corresponds to the left upper three fifths of the small bowel, whereas the right lower two fifths of it represents the ileum.

When intestinal perforation is suspected and the child cannot be placed in an upright position, a left lateral decubitus film with horizontal beam is helpful in diagnosing free intraperitoneal air because it facilitates identification of free air around the hepatic density.

Contrast studies such as upper GI series and contrast enemas can help to determine obstruction location. Contrast studies also reveal whether the obstruction is intrinsic or extrinsic to the bowel. Remember to always use hydrosoluble contrast to avoid severe barium peritonitis in patients with a perforation.

Abdominal computed tomography (CT) scanning should not be obtained when the diagnosis is evident on radiography because this would only delay treatment and subject the child to unnecessary radiation. CT scanning helps to identify causes of chronic partial obstructions, as well as abscesses, tumors, and other causes of acute abdominal pain.

Ultrasonographic examinations reveal many intestinal abnormalities, including tumors, mesenteric cysts, and intussusceptions.

Intussusception

In approximately 60% of intussusception cases, plain abdominal radiography reveals the head of the intussusceptum projecting into the air-filled colon. Abdominal radiography may also reveal scattered air-fluid levels that suggest an ileus or partial obstruction. A left lateral decubitus film aids in the initial diagnosis of intussusception by revealing air or stool in the cecum and ascending colon.[41, 42] See the image below.


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A barium enema on a 1-year-old male patient depicts an ileocolic intussusception.

Contrast radiography using a barium enema can be therapeutic, as well as diagnostic. A classic sign is a coil spring appearance caused by the tracking of barium around the lumen of the edematous intestine. Air and water enemas have been used to reduce intussusception. Pneumatic reduction under fluoroscopic guidance and hydrostatic reduction under ultrasonographic monitoring are the preferred techniques. The aim should be a success rate of at least 90% in idiopathic intussusception. (See the image below.)


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Barium enema revealing a coil spring appearance caused by the tracking of barium around the lumen of the edematous intestine in intussusception.

Ultrasonography is useful in some cases and may have high sensitivity in as many as 75% of patients. The characteristic finding is a target or bull's eye configuration, consisting of 2 rings of low echogenicity that are separated by an intermediate hyperechoic ring visible on a cross-sectional image of intussuscepted bowel. See the image below.


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Image of intussusception by ultrasound on a 9-month-old male patient.

Intussusception has been recently identified by capsule endoscopy.[43]

Incarcerated hernia

In complete bowel obstruction, air-fluid levels are visible on plain radiography. The bowel may be visible within the inguinal canal and scrotum. Ultrasonography may reveal the incarcerated viscera in the inguinal canal or the umbilical ring and can be useful in difficult cases. (See the image below.)


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Small-bowel obstruction caused by an incarcerated inguinal hernia in a 2-month-old infant with bilateral inguinal hernias as well as an umbilical hern....

A careful physical examination is more helpful than imaging studies for the diagnosis of incarcerated inguinal or umbilical hernias. Incarcerated hernias are diagnosed clinically, and no imaging studies are required. Determining the level of the obstruction is not that important because the treatment does depend on this finding.

Malrotation of the bowel with midgut volvulus

Plain abdominal radiography sometimes reveals a double-bubble sign that depicts air-fluid levels in the stomach and in the distended duodenum (see the image below). The abdomen often appears gasless on abdominal plain radiography. Distended loops of small bowel are only occasionally visible, because the point of obstruction is proximal, in the third portion of the duodenum.


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Radiograph depicting the double-bubble sign characteristic of duodenal atresia.

Definitive diagnosis of midgut volvulus requires contrast studies. Barium enema findings may provide indirect evidence by revealing an ectopically placed right colon and cecum, but a high or mobile cecum is common in many asymptomatic infants. In fact, 10-15% of patients with malrotation have barium enema findings that appear normal.

An upper GI series is a quicker and more direct approach, with high sensitivity and accuracy, making it the criterion standard study for malrotation with or without volvulus. The duodenum usually has a "C" shape, and the duodenojejunal junction is localized to the left of the midline.[44]

In malrotation, the duodenum lacks its normal shape and does not cross the midline. Duodenal obstructions due to volvulus, Ladd bands, or angulation are evident. The classic patterns of volvulus are the "bird beak," in cases involving complete duodenal obstruction, or the "corkscrew,” in cases involving incomplete obstruction.

Postoperative adhesive small-bowel obstruction

Supine and upright abdominal radiography reveals dilated, gas-filled loops of small intestine, with multiple air-fluid levels scattered throughout the abdomen above the obstruction site. Air in the colon usually indicates a partial obstruction, although determining whether a gas-filled loop is the colon or small bowel is difficult in infants. Demonstrating gas in the rectum is the only way to be certain of gas in the colon.

Oral administration of water-soluble contrast media (Gastrografin) with subsequent abdominal radiography is useful in deciding whether to perform early surgery in cases in which the obstruction cannot be determined to be partial or complete.[45, 46] If the contrast is found in the large bowel 6-8 hours after administration, the obstruction is presumed to be partial, and the patient can be conservatively managed without an immediate operation. The technique has been successfully used in children.[47]

Duplication cysts

Plain radiography usually reveals a soft-tissue mass within the abdomen that displaces the adjacent bowel and causes the obstruction. An upper GI contrast series may reveal stenosis or extrinsic compression by a mass. Technetium scanning can be used to image duplications that contain ectopic gastric mucosa.

For most abdominal duplications, ultrasonography is more expedient and provides greater detail than does conventional contrast radiography. Ultrasonography reveals either a sonolucent mass with good wave transmission because of its clear fluid content, or an echogenic mass secondary to hemorrhage that has inspissated material within the duplication. Intra-abdominal enteric duplication cysts are increasingly likely to be prenatally detected.[48]

Annular pancreas

Although an annular pancreas is often not diagnosed until surgery, plain abdominal radiography may reveal the double-bubble sign characteristic of duodenal obstruction. An upper GI series reveals a diminished duodenal lumen.

Ultrasonography provides a reliable method to help diagnose duodenal obstruction, even prenatally in pregnancies complicated by polyhydramnios in the third trimester. It is also a good study to rule out hypertrophic pyloric stenosis as a differential diagnosis.

Necrotizing enterocolitis

Abdominal radiography initially reveals multiple gas-filled loops of intestine and air-fluid levels. Straightening of the bowel wall and bowel wall thickening with intramural air suggest mural edema (railroad sign). A gasless abdomen, a fixed bowel loop, or a ground-glass appearance, which suggests free intraperitoneal fluid, is sometimes encountered.[49] See the images below.


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Plain abdominal film of a premature baby born at 28 weeks of gestation with necrotizing enterocolitis. Note the "railroad sign" (neumatosis intestinal....


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Plain abdominal film on a premature baby girl with necrotizing enterocolitis. Note the air in the biliary tree and the grossly dilated bowel.

Pneumatosis intestinalis is the radiographic hallmark; its presence indicates gas in the bowel wall. Portal venous gas is an ominous sign, and pneumoperitoneum indicates a bowel perforation. Pneumatosis intestinalis and portal venous gas (pylephlebitis) are easily detected using ultrasonography.

A review from Toronto considers color Doppler ultrasonography to be a more accurate method of diagnosing bowel necrosis than plain abdominal radiography.[50]

Mesocolic hernia

An upper GI study with small bowel follow-through during a hernia episode can support the diagnosis. This study usually reveals the intestines bunched together as if enveloped by a sac. Abdominal CT scanning may reveal a mesocolic hernia during nonherniating periods.

Cecal volvulus

Plain abdominal radiography may reveal a large, air-filled loop of colon that occupies the right lower quadrant, in addition to depicting a typical small-bowel obstruction. The characteristic barium enema finding is a bird-beak–shaped deformity, coupled with nonvisualization of the cecum.

Jejunoileal atresia and stenosis

Radiographic findings often reveal thumb-sized intestinal loops and air-fluid levels. A loop of small bowel proximal to the atresia may become grossly distended and filled with fluid, producing the appearance of a mass.

A contrast enema is usually indicated to confirm the diagnosis. The preferred methodology is a water-soluble enema, which aids in distinguishing between small- and large-bowel distention, determining the presence or absence of a microcolon, and locating the position of the cecum relative to possible abnormalities of intestinal rotation and fixation. (See the image below.)


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Upper GI contrast study demonstrating a jejunal atresia with a proximal dilated atretic bowel and lack of passage of contrast into the distal small bo....

An upper GI series reveals the level of obstruction with a grossly distended proximal bowel. Care must be taken to avoid contrast aspiration.

Duodenal atresia and stenosis

Abdominal radiography usually confirms a duodenal atresia diagnosis. Gas and air-fluid levels are present in the stomach and the dilated duodenal bulb (ie, the double-bubble sign), but no air is present in the distal GI tract. These radiographic findings confirm a diagnosis of duodenal obstruction, making further studies unnecessary. See the image below.


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Plain abdominal film on a 3-day-old newborn depicting the classic double-bubble sign for duodenal atresia.

An upper GI series adds no information and creates the potential hazard of vomiting with barium aspiration. If the patient has vomited or has been decompressed using a nasogastric (NG) tube prior to abdominal radiography, the stomach and duodenum may be collapsed, making the correct diagnosis difficult. In such cases, a small amount of air (ie, 10-15 mL) may be injected into the stomach through the NG tube, and radiography may be repeated. (Upper GI studies are useful in the late diagnosis of duodenal web and stenosis.) See the image below.


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Contrast-enhanced upper gastrointestinal film showing a duodenal atresia on a 2-day-old newborn.

Meconium disease

Abdominal radiographic studies reveal multiple air-fluid levels consistent with small-bowel obstruction. The presence of calcifications throughout the peritoneum suggests a prenatal perforation and meconium peritonitis or meconium pseudocyst.

The inspissated meconium often has a ground-glass appearance on radiography. A "soap-bubble" image in the right lower quadrant is characteristic.

A contrast enema is diagnostic and, in many cases, therapeutic for meconium ileus and meconium plug syndrome. In most cases, the contrast enema reveals a microcolon (nonused colon) and meconium pellets in either the terminal ileum (meconium ileus) or the colon (meconium plug syndrome). Gastrografin is the agent of choice. Its osmotic properties pull water into the lumen, which may unplug the intestine.

Approach Considerations

General principles in the medical treatment of small-bowel obstruction include the following:

Patients who do not respond to nonoperative treatment within 12-24 hours require surgical treatment.

Consultations

Consult with a pediatric or general surgeon, depending on availability.

Diet

Administer nothing by mouth (NPO).

Monitoring

Patients with partial small-bowel obstructions can be nonoperatively treated with adequate fluid resuscitation and nasoenteric suctioning. However, close follow-up observation is mandatory for these patients after discharge.

Instruct parents that they must take their child immediately to an emergency department if the child's symptoms (eg, vomiting, pain) recur.

Intussusception

Stabilize the patient's ABCs and replace large fluid losses. Administer NPO to the child and place an NG tube to decompress the obstruction from above. The use of antibiotics is appropriate for management of bacterial translocation.

Barium, water, or air enema reduction is appropriate after surgical consultation if symptom duration is less than 24 hours and if the patient has no signs of peritonitis. Pneumatic reduction seems to be more effective and safer,[51] and it could be considered an optimal first-line treatment.[52] Enemas successfully reduce 80-95% of all intussusceptions, with better success rates in short-duration intussusceptions. Although the classic teaching is to admit any child with an intussusception that is successfully reduced with an enema for observation, in the thought that most recurrences occur during the first 24 hours, Whitehouse et al recently showed that recurrence rates do not differ between children observed as inpatients and those discharged home after successful hydrostatic reduction, suggesting it might be safe, in controlled circumstances, to discharge patients from the emergency department.[53, 54, 55]

Children whose symptoms persist longer than 24 hours, or have signs of peritonitis, should not be considered candidates for enema reduction. The risk of surgery is higher when the lapse between the onset of symptoms and the first attempt of conservative management is longer. Stabilize these children and immediately transport them to the operating room because untreated intussusception is almost always fatal. The recurrence rate is higher after radiographic than after surgical reduction. Surgery is also indicated for patients whose intussusception cannot be reduced after 2 enema attempts. See the image below.


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Surgical photograph of an 8-month-old patient with ileocolic intussusception.

Patients with postoperative intussusceptions require surgery for correction. In most cases, the intussusception can be reduced manually and strangulation is uncommon.

Adhesive Small-Bowel Obstruction

Only about 6-7% of children with adhesive small-bowel obstruction require immediate laparotomy. Approximately one half of these patients respond to medical treatment, which includes NPO, IV fluids, NG decompression, and antibiotics to suppress bacterial translocation and help prolong the viability of ischemic bowel. However, children younger than 1 year tend to respond poorly to conservative management. No single agent or treatment has proven effective in preventing adhesion formation after a laparotomy.

The use of water-soluble contrast via NG tube may decrease the need for surgery in some patients. Water-soluble contrast media (Gastrografin) cause redistribution of intravascular and extracellular fluid into the intestinal lumen because of their hyperosmolarity. As a result, these media decrease intestinal wall edema and act as a direct stimulant to intestinal peristalsis.[56]

Incarcerated Hernia

Stabilize the patient's ABCs and focus on replacing the large fluid losses. Nonoperative reduction of a nonstrangulated hernia is possible in approximately 95-98% of cases. Facilitate the reduction by sedating the patient and placing the patient in a mild Trendelenburg position. Gentle traction on the hernia and the contents of the sac usually suffices to reduce the volume and rapidly retract the contents of the sac into the abdominal cavity. After nonoperative hernia reduction, elective repair may be accomplished 24-48 hours after the edema subsides.

The only contraindication to nonoperative reduction is a long-standing incarceration with evidence of peritoneal irritation.

Antibiotic therapy is usually unwarranted, but critically ill infants with perforation and peritonitis require coverage for aerobic gram-negative organisms and anaerobic infections.

Necrotizing Enterocolitis

At the same time that the patient is suspected of having NEC, he or she should have NPO; IV fluids; antibiotics with gram-negative coverage, as well as coverage for anaerobes; and an NG tube to decompress the abdomen. An emergent surgical consultation is necessary.

In the extremely low ̶ birth-weight infant, it is difficult to determine if free air in the abdominal cavity is due to a spontaneous perforation or NEC. The decision of placing a peritoneal drainage versus a laparotomy depends mainly on how sick the neonate is. Two randomized controlled trials showed no difference in mortality and long-term need for parenteral nutrition in patients undergoing peritoneal drainage or laparotomy for NEC. However, 50% of infants in the peritoneal drainage groups were spared from further surgical intervention, and time to attain full enteral feeds in infants less than or equal to 1000 g was prolonged in this group.[57]

NEC management involves cessation of enteral feeds; gastric decompression on low, continuous suction with a sump-type tube; fluid management to correct hypovolemia; parenteral nutrition with a centrally located IV catheter once fluid resuscitation is complete; and antibiotic therapy.

Direct antimicrobial therapy is aimed at enteric bacteria (eg, Escherichia coli, Klebsiella species, Enterococcus species, anaerobic colonic flora [Clostridia species]).

Serial abdominal examinations are preferably performed by the same examiner. Obtain radiographs of the abdomen, including cross-table lateral films, every 6-8 hours for the first 48 hours. Obtain blood, urine, sputum, and CSF cultures, if indicated.

Strong evidence shows breastfeeding to be a protective measure against NEC.[58] A large Cochrane review supports the use of probiotics, especially in infants weighing more than 1000 g. This is slowly gaining popularity among neonatologists; however, more research is necessary to change this practice.[37, 59, 60]

Small studies have recently suggested that the use of pentoxifylline in adjunct with antibiotics for preterm babies with NEC and sepsis may decrease mortality without any adverse effects.[61]

Meconium Disease

Treatment of meconium ileus requires evacuating the meconium. Nonsurgical methods relieve the obstructions of more than 50% of patients.

The therapy of choice for uncomplicated meconium ileus is nonoperative hyperosmolar enema (Gastrografin or Omnipaque), with enterotomy and irrigation reserved for enema failures. Dilute Gastrografin with N -acetylcysteine may also be administered using an NG tube from above to help loosen the meconium. Distal intestinal obstruction syndrome may be treated in the same way.

Complicated cases (meconium peritonitis, meconium pseudocyst, perforation, intestinal atresia) require exploration and bowel resection with primary anastomosis or stoma creation.

Meconium plug syndrome is usually relieved with rectal stimulation (suppositories, washouts, or contrast enemas).

Surgical Therapy

Intussusception

Intussusception can be reduced by radiographic means in 80-95% of patients. Surgical reduction is indicated when symptoms have been present for more than 24 hours, in the presence of shock that cannot be corrected, when a lead point has been identified, when necrosis or perforation are present, or if the intussusception is irreducible by radiographic means. (See the image below.) The procedure can be performed safely via laparotomy or laparoscopy. Patients operated on laparoscopically have shorter hospital length of stay and a mildly higher incidence of recurrence, although this is not statistically significant.[62]


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Necrotic bowel after surgical reduction of an intussusception.

Incarcerated hernia

After reducing the hernia, elective repair is possible 24-48 hours after the edema subsides. For patients whose hernias cannot be reduced and for patients with strangulation, immediate surgery is mandatory to prevent the incarceration from progressing to perforation and frank peritonitis.

Malrotation of the bowel with midgut volvulus

Preserving intestinal viability requires rapid diagnosis and surgery for malrotation with midgut volvulus. Initiate NG suction and IV hydration when entertaining the possibility of midgut volvulus. If abdominal plain radiographic findings confirm the diagnosis, defer contrast studies and take the child directly to the operating room.

A Ladd procedure is the preferred treatment. It includes evisceration and inspection of the mesenteric root, derotation of the volvulus (which has always been reported to occur in a clockwise direction), lysis of Ladd bands with kocherization of the duodenum along the right abdominal gutter, opening of the visceral peritoneum that covers the mesentery, and replacing the small bowel into the right side of the abdomen and the large bowel into the left side (in a position of nonrotation). It also includes an appendectomy (usually an inversion appendectomy), because the cecum and appendix are located in an unusual place. The procedure can also be laparoscopically performed.[63]

Any frankly necrotic bowel should be resected and end-to-end anastomosis performed unless the peritoneal cavity is grossly contaminated or the condition of the patient does not allow it; in such cases, stomas should be created.

Postoperative adhesive small-bowel obstruction

A possible diagnosis of adhesive small-bowel obstruction requires prompt surgical consultation because delay can lead to intestinal necrosis. The most difficult part is to decide if and when the child is to undergo surgery. As a general rule, the presence of fever, tachycardia, leukocytosis, rebound tenderness, or complete obstruction warrants surgical exploration. Patients usually present with a single-point obstruction. The authors recommend entering the abdomen through a fresh extension of the original incision, to avoid damage to the bowel adhered to the old scar.

Adhesiolysis is the treatment of choice. Only the adhesion causing the obstruction needs to be resolved, since extensive unnecessary adhesiolysis increases the risk of serosal tears and bowel perforations, as well as an increased inflammatory response that may produce further adhesive obstruction. Careful sharp dissection of adhesions with gentle handling of the intestine is imperative. This can be achieved laparoscopically or with laparotomy. Some patients require bowel resection because of perforation or necrosis.[64]

Duplication cysts

The treatment for duplications is surgical excision, even in an asymptomatic patient who is incidentally diagnosed. The prevalence of gastric mucosa suggests that the duplications should not be left indefinitely. The procedure may depend on the location of the cyst.

In esophageal duplications, the cyst is excised, and a mucosectomy is performed if the muscular layer shared with the esophagus is left behind. The entire muscular wall can be excised with the cyst, taking care not to penetrate the esophageal mucosa.

Duplications of the small intestine usually require resection and anastomosis. In rectal duplications, only the mucosal lining usually needs to be excised, because the duplication and normal rectum share the muscularis layer. If malignant degeneration is suspected, total excision, including excision of the normal rectum, may be necessary. Infected duplications may require initial drainage, followed by a staged resection. Laparoscopically assisted resection of ileocecal duplications is safe and effective. See the image below.


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Surgical photograph of a 3-year-old male patient with an obstructive, noncommunicating ileal duplication.

Annular pancreas

Surgical management is similar to that of duodenal atresia. Diamond-shaped duodenoduodenostomy is the preferred approach (Kimura procedure).

Necrotizing enterocolitis

Indications for surgery include pneumoperitoneum, fixed dilated bowel loop, abdominal wall discoloration, or children whose conditions deteriorate or show no improvement with conservative therapy. Portal venous air suggests extensive intestinal necrosis but does not indicate that celiotomy is necessary. See the image below.


View Image

Plain abdominal film on a premature baby girl with necrotizing enterocolitis. Note the air in the biliary tree and the grossly dilated bowel.

The options for surgical management include resection of necrosed bowel with creation of an ostomy, resection and primary anastomosis, or peritoneal drainage.[28] The surgical team decides if peritoneal drainage or laparotomy will be performed on a patient suspected of having NEC. Many surgeons place a peritoneal drain and wait until the patient is stable to take him or her to the operating suite for exploratory laparotomy. However, a meta-analysis showed a higher mortality rate (55%) in patients who underwent peritoneal drainage.[65] If the perforation is due to full-blown NEC, the bowel may continue to necrose and the patient may suffer later form short-bowel syndrome, which has catastrophic long-term complications.

Mesocolic hernia

Surgically reduce the hernia and repair the potential hernia pouch, either electively (for reducible hernias) or emergently (for incarcerated hernias.) See the image below.


View Image

Surgical photograph of a 1-year-old male patient who previously underwent a right radical nephrectomy for Wilms tumor. He presented to the emergency d....

Cecal volvulus

Surgical reduction of the cecal volvulus and pexy to the lateral peritoneal wall is usually required, in addition to fluid resuscitation, bowel decompression, and ABC monitoring.

Jejunoileal atresia and stenosis

Surgical resection of the atretic segment is followed by end-to-end anastomosis. The proximal, dilated bowel may need to be tapered to fit the smaller, distal intestine. Care should be taken to preserve as much intestinal length as possible in order to prevent short-bowel syndrome, mainly in patients with multiple atresias. These have classically been repaired through transverse supraumbilical incision, although single jejunoileal atresias have been successfully approached through a smaller periumbilical incision (as in the one described for hypertrophic pyloric stenosis).[66]

Duodenal atresia and stenosis

The usual treatment for duodenal atresia is a linear or diamond-shaped duodenoduodenostomy (Kimura procedure). Duodenojejunostomy is another option. A duodenal web is much rarer and can be treated with duodenotomy and excision of the web, with or without duodenoplasty.[67]

Meconium ileus

Surgical management by either primary resection and anastomosis or ileostomy is sometimes required.[68]

Medication Summary

Bowel obstructions often require surgical interventions, but start antibiotic administration in the emergency department first. Antibiotic coverage must include gram-negative aerobic and gram-negative anaerobic organisms. (The following list of antibiotics is not all-inclusive.) In addition, broad-spectrum antibiotics should be administered in pediatric small-bowel obstruction when necrosis or perforation is suspected. In NEC, direct antimicrobial therapy is aimed at enteric bacteria (eg, Escherichia coli, Klebsiella species, Enterococcus species, anaerobic colonic flora [Clostridia species]).

Clindamycin (Cleocin)

Clinical Context:  Clindamycin is a lincosamide that is useful in treating serious skin and soft tissue infections caused by most staphylococcal strains. It is also effective against aerobic and anaerobic streptococci, except enterococci.

Clindamycin inhibits bacterial protein synthesis by inhibiting peptide chain initiation at the bacterial ribosome, where it preferentially binds to the 50S ribosomal subunit, inhibiting bacterial growth.

Metronidazole (Flagyl)

Clinical Context:  Metronidazole is an imidazole, ring-based antibiotic that is active against various anaerobic bacteria and protozoa. It is used in combination with other antimicrobial agents (although it is used alone in Clostridium difficile enterocolitis).

Aztreonam (Azactam)

Clinical Context:  Aztreonam is a monobactam that inhibits cell wall synthesis during bacterial growth. It is active against gram-negative bacilli. Aztreonam is effective against aerobic gram-negative organisms.

Cefoxitin (Mefoxin)

Clinical Context:  Cefoxitin is a second-generation cephalosporin that is used to treat infections caused by susceptible gram-positive cocci and gram-negative rods. It is effective against aerobic and anaerobic gram-negative organisms.

Cefotetan

Clinical Context:  Cefotetan is a second-generation cephalosporin that is used to treat infections caused by susceptible gram-positive cocci and gram-negative rods. It is not approved by the US Food and Drug Administration (FDA) for use in children.

Imipenem and cilastatin (Primaxin)

Clinical Context:  This agent is effective against aerobic and anaerobic gram-negative organisms.

Ticarcillin and clavulanate potassium (Timentin)

Clinical Context:  This agent inhibits the biosynthesis of cell wall mucopeptide and is effective during the active growth stage. It is an antipseudomonal penicillin plus a beta-lactamase inhibitor, that provides coverage against most gram-positive, gram-negative, and anaerobic organisms.

Class Summary

Antibiotic therapy must cover all likely pathogens in the clinical setting.

Author

Jaime Shalkow, MD, Head of Surgical Oncology, Division of Surgery, National Institute of Pediatrics, Mexico; Head-Professor of Pediatric Surgical Oncology, Universidad Nacional Autonoma de Mexico

Disclosure: Nothing to disclose.

Coauthor(s)

Adrian Florens, MD, FAAP, Attending Faculty Staff, Department of Pediatrics, Division of Neonatology, John H Stroger Hospital of Cook County

Disclosure: Nothing to disclose.

Jose Asz, MD, Professor of Embryology, Assistant Professor of Surgery and Pediatrics, Faculty of Medicine, Universidad Nacional Autonoma de Mexico; Consulting Staff, Department of General Surgery, National Institute of Pediatrics, Mexico

Disclosure: Nothing to disclose.

Nicholas A Shorter, MD, Professor of Clinical Surgery and Clinical Pediatrics, State University of New York Downstate University; Division Chief, Department of Surgery, Division of Pediatric Surgery, State University of New York Downstate Medical Center

Disclosure: Nothing to disclose.

Chief Editor

Carmen Cuffari, MD, Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

B UK Li, MD Professor of Pediatrics, Division of Gastroenterology, Hepatology and Nutrition, Director, Pediatric Fellowships and Gastroenterology Fellowship, Medical Director, Functional Gastrointestinal Disorders and Cyclic Vomiting Program, Medical College of Wisconsin; Attending Gastroenterologist, Children's Hospital of Wisconsin

B UK Li, MD is a member of the following medical societies: Alpha Omega Alpha, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Jorge H Vargas, MD Professor of Pediatrics and Clinical Professor of Pediatric Gastroenterology, David Geffen School of Medicine, University of California at Los Angeles; Consulting Physician, Department of Pediatrics, University of California at Los Angeles Health System

Jorge H Vargas, MD is a member of the following medical societies: American Liver Foundation, American Society for Gastrointestinal Endoscopy, American Society for Parenteral and Enteral Nutrition, Latin American Society of Pediatric Gastroenterology, Hepatology & Nutrition, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Small-bowel obstruction visible on plain radiograph caused by intussusception in a 5-month-old patient.

Surgical photograph of a transition zone in an infant with small bowel obstruction.

Surgical photograph of an 8-month-old patient with ileocolic intussusception.

Small-bowel obstruction visible on plain radiograph caused by intussusception in a 5-month-old patient.

Surgical image of a laparotomy on a 7-month-old girl with ileocolic intussusception. An edematous and erythematous cecal appendix was found to be acting as a lead point.

Small-bowel obstruction caused by an incarcerated inguinal hernia in a 2-month-old infant with bilateral inguinal hernias as well as an umbilical hernia.

Incarcerated left inguinal hernia.

Upper GI contrast study showing a malrotation with lack of normal C-shaped duodenum and the small bowel "hanging" on the right side of the abdomen.

Contrast enema with an abnormally located cecum in a patient with malrotation.

Surgical photograph of necrotic bowel in a patient with midgut volvulus.

Mesocolic hernia.

Plain abdominal film of a 6-year-old male patient with MRCP (mental retardation and cerebral palsy), with organo-axial gastric volvulus. Note the grossly dilated and obstructed stomach. A gastrostomy feeding tube can be seen in place. Surgical staplers from a previous laparoscopic funduplication are seen near the diaphragmatic crura.

Surgical photograph of a 3-year-old male patient with an obstructive, noncommunicating ileal duplication.

Upper GI contrast study demonstrating a jejunal atresia with a proximal dilated atretic bowel and lack of passage of contrast into the distal small bowel.

Surgical photograph of the patient in the previous image depicting the proximal dilated atretic jejunum.

Surgical image of a laparotomy on a 2-day-old female patient with congenital small bowel obstruction. A type I jejunal atresia without mesenteric gap and a grossly dilated proximal intestine is seen.

Contrast-enhanced upper gastrointestinal film showing a duodenal atresia on a 2-day-old newborn.

Surgical image of a laparotomy on a 2-day-old female patient with congenital small bowel obstruction. A type I jejunal atresia without mesenteric gap and a grossly dilated proximal intestine is seen.

Clinical photograph of a 5-month-old male patient with characteristic currant-jelly stools due to intussusception.

Clinical image of a micro-premature baby boy with discoloration on the right lower quadrant of the abdomen, due to intestinal perforation secondary to necrotizing enterocolitis. An umbilical catheter is in place.

A barium enema on a 1-year-old male patient depicts an ileocolic intussusception.

Barium enema revealing a coil spring appearance caused by the tracking of barium around the lumen of the edematous intestine in intussusception.

Image of intussusception by ultrasound on a 9-month-old male patient.

Small-bowel obstruction caused by an incarcerated inguinal hernia in a 2-month-old infant with bilateral inguinal hernias as well as an umbilical hernia.

Radiograph depicting the double-bubble sign characteristic of duodenal atresia.

Plain abdominal film of a premature baby born at 28 weeks of gestation with necrotizing enterocolitis. Note the "railroad sign" (neumatosis intestinalis) in the hepatic flexure and soap-bubbles in the descending colon.

Plain abdominal film on a premature baby girl with necrotizing enterocolitis. Note the air in the biliary tree and the grossly dilated bowel.

Upper GI contrast study demonstrating a jejunal atresia with a proximal dilated atretic bowel and lack of passage of contrast into the distal small bowel.

Plain abdominal film on a 3-day-old newborn depicting the classic double-bubble sign for duodenal atresia.

Contrast-enhanced upper gastrointestinal film showing a duodenal atresia on a 2-day-old newborn.

Surgical photograph of an 8-month-old patient with ileocolic intussusception.

Necrotic bowel after surgical reduction of an intussusception.

Surgical photograph of a 3-year-old male patient with an obstructive, noncommunicating ileal duplication.

Plain abdominal film on a premature baby girl with necrotizing enterocolitis. Note the air in the biliary tree and the grossly dilated bowel.

Surgical photograph of a 1-year-old male patient who previously underwent a right radical nephrectomy for Wilms tumor. He presented to the emergency department with signs of a mechanical small bowel obstruction. A transition zone is clearly seen at the point where the small bowel is trapped on an internal hernia through a mesenteric gap.

Small-bowel obstruction visible on plain radiograph caused by intussusception in a 5-month-old patient.

Barium enema revealing a coil spring appearance caused by the tracking of barium around the lumen of the edematous intestine in intussusception.

Small-bowel obstruction caused by an incarcerated inguinal hernia in a 2-month-old infant with bilateral inguinal hernias as well as an umbilical hernia.

Radiograph depicting the double-bubble sign characteristic of duodenal atresia.

Upper GI contrast study demonstrating a jejunal atresia with a proximal dilated atretic bowel and lack of passage of contrast into the distal small bowel.

Surgical photograph of the patient in the previous image depicting the proximal dilated atretic jejunum.

Upper GI contrast study showing a malrotation with lack of normal C-shaped duodenum and the small bowel "hanging" on the right side of the abdomen.

Contrast enema with an abnormally located cecum in a patient with malrotation.

Surgical photograph of necrotic bowel in a patient with midgut volvulus.

Necrotic bowel after surgical reduction of an intussusception.

Surgical photograph of a transition zone in an infant with small bowel obstruction.

Incarcerated left inguinal hernia.

Mesocolic hernia.

Surgical image of a laparotomy on a 7-month-old girl with ileocolic intussusception. An edematous and erythematous cecal appendix was found to be acting as a lead point.

Surgical image of a laparotomy on a 2-day-old female patient with congenital small bowel obstruction. A type I jejunal atresia without mesenteric gap and a grossly dilated proximal intestine is seen.

A barium enema on a 1-year-old male patient depicts an ileocolic intussusception.

Clinical photograph of a 5-month-old male patient with characteristic currant-jelly stools due to intussusception.

Plain abdominal film on a 3-day-old newborn depicting the classic double-bubble sign for duodenal atresia.

Contrast-enhanced upper gastrointestinal film showing a duodenal atresia on a 2-day-old newborn.

Surgical photograph of a 3-year-old male patient with an obstructive, noncommunicating ileal duplication.

Plain abdominal film of a 6-year-old male patient with MRCP (mental retardation and cerebral palsy), with organo-axial gastric volvulus. Note the grossly dilated and obstructed stomach. A gastrostomy feeding tube can be seen in place. Surgical staplers from a previous laparoscopic funduplication are seen near the diaphragmatic crura.

Surgical photograph of an 8-month-old patient with ileocolic intussusception.

Plain abdominal film of a premature baby born at 28 weeks of gestation with necrotizing enterocolitis. Note the "railroad sign" (neumatosis intestinalis) in the hepatic flexure and soap-bubbles in the descending colon.

Clinical image of a micro-premature baby boy with discoloration on the right lower quadrant of the abdomen, due to intestinal perforation secondary to necrotizing enterocolitis. An umbilical catheter is in place.

Plain abdominal film on a premature baby girl with necrotizing enterocolitis. Note the air in the biliary tree and the grossly dilated bowel.

Surgical photograph of a 1-year-old male patient who previously underwent a right radical nephrectomy for Wilms tumor. He presented to the emergency department with signs of a mechanical small bowel obstruction. A transition zone is clearly seen at the point where the small bowel is trapped on an internal hernia through a mesenteric gap.

Image of intussusception by ultrasound on a 9-month-old male patient.