Pediatric Small Bowel Obstruction

Pediatric small bowel obstructions have a variable etiology, with processes that 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 (congenital intestinal obstructions) and those that occur later in childhood. (See Etiology, Presentation, and Workup.)

Congenital obstructive lesions of the intestines can be viewed as intrinsic (atresia, stenosis, meconium ileus, aganglionic bowel in Hirschsprung disease) or extrinsic (malrotation, congenital bands, internal hernias, duplications).

Intestinal obstruction should be suspected in any child with persistent vomiting, abdominal distention, and abdominal pain. Delayed diagnosis and treatment can have devastating consequences. Infants and young children with intestinal obstruction present with feeding intolerance, irritability, vomiting, pain, and abdominal distention. Undiagnosed or improperly managed obstructions can progress to intestinal ischemia, which in turn can progress to necrosis, perforation, and sepsis when left untreated. (See Prognosis, Presentation, and Workup.)

Patient education

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

The normal small 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 small bowel obstruction 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 obstruction in children, and its characteristics can suggest the level of the obstruction.

Intestinal absorption, lymphatic drainage, and perfusion are compromised when intraluminal pressure exceeds capillary and venous pressure in the bowel wall. First, lymphatic obstruction occurs because of the lower pressure in these vessels. This is followed by venous obstruction, which accelerates edema formation because blood can enter the affected bowel segment but does not have a drainage route. Finally, the continued increase in bowel wall pressure eventually blocks arterial flow. Bowel ischemia ensues when capillary blood flow stops, allowing bacterial translocation into the peritoneal cavity, which can then lead to peritonitis and sepsis. Perforation can develop as the ischemia leads to bowel necrosis. Moreover, massive third spacing of fluids can lead to shock, further contributing to morbidity and mortality. This sequence may occur more rapidly in a closed-loop obstruction because there is no proximal escape for pressurized bowel contents.

A wide variety of diagnoses can cause small bowel obstruction in children, such as the following:

• Adhesive small bowel obstruction

• Intestinal volvulus

• Malrotation

• Intussusception

• Hirschsprung disease

• Meckel diverticulum

• Omphalomesenteric duct remnant (Meckel band)

• Mesenteric and omental cysts

• Necrotizing enterocolitis

• Incarcerated hernias

• Small intestinal atresia or stenosis

• Meconium ileus/distal intestinal obstruction syndrome

• Internal hernia

• Enteric duplications

• Inflammatory bowel disease

• Intestinal neoplasm

• Foreign material from previous operations, such as surgical staples after laparoscopic appendectomy (rare)[1]

A sampling of the many etiologies that can cause small bowel obstruction in children are discussed in greater detail below.

Intussusception

Intussusception is the most common cause of intestinal obstruction in infants and children aged 3 months to 6 years. Approximately 60% of children are younger than 1 year, and 80-90% are younger than 2 years.[2] The peak age of presentation is between the ages of 5 and 10 months. Intussusception is more common in males.

Intussusception occurs when a proximal segment of the intestine (the intussusceptum) telescopes or invaginates into the lumen of another immediately adjacent distal segment (the intussuscipiens). 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 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. See the image below.

Primary and secondary intussusception

Most intussusceptions are idiopathic, also known as primary intussusception. A lead point is identified in only 1.5-12% of cases; these cases are classified as secondary intussusception.[3]

Primary intussusception accounts for 90-95% of children with intussusception; commonly, a viral etiology is suspected because of this condition's seasonal predisposition for spring and autumn, as well as a higher incidence of adenoid hypertrophy in children who suffer intussusceptions. Cough and diarrhea are common symptoms preceding intussusception, further suggesting that viral infections may be a cause.[4]

Gastroenteritis, rotavirus infection, or allergic stimuli are believed to cause intestinal lymphoid tissue to swell and become a lead point for intussusception.[5] 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.[6] Additionally, although the risk is quite small, some studies have demonstrated an increased risk of intussusception after the administration of monovalent rotavirus vaccination.[7, 8] Given the well-documented benefits of rotavirus vaccination, its benefits likely outweigh the small risk of intussusception. Nonetheless, currently monovalent (RV1, Rotarix) and pentavalent (RV5 RotaTeq) rotavirus vaccines are contraindicated in children with a history of intussusception.

Various conditions have been implicated as causes of secondary intussusception, including Meckel diverticulum, polyps, small bowel lymphoma, duplication cysts, vascular malformations, inverted appendiceal stumps, parasites, Henoch-Schönlein purpura (HSP, also called immunoglobulin [Ig]A vasculitis), cystic fibrosis, hemolytic-uremic syndrome, celiac disease, and Clostridium difficile colitis.[3] Meckel diverticulum is the most commonly identified pathologic lead point in most case series in children.[2]

Neoplastic masses can also act as lead points for intussusception, including primary tumors such as lymphomas and carcinomas, as well as metastatic disease. In particular, intestinal lymphomas are a frequent culprit that should be suspected in older children presenting with intussusception. Tumors causing intussusception primarily affect the duodenum and jejunum, and treatment includes surgical resection of the tumor once intussusception has been diagnosed.[9] Children undergoing extensive retroperitoneal dissections, such as that required for neuroblastoma or Wilms tumor resections, are also at risk of postoperative intussusceptions. These intussusceptions typically involve the small bowel alone and occur within 2 weeks after a previous laparotomy.[10]

Intussusception has also been described in patients with parasites, particularly Ascaris lumbricoides.[11] In Henoch-Schönlein purpura, mucosal hematomas are thought to act as lead points.[12]

Finally, 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, finding that 69% of them presented with at least one episode of intussusception, with 95% of those intussusceptions located in the small bowel and 92.5% requiring surgical correction.[13] Most polyps acting as lead points were larger than 10 mm; thus, the authors recommended endoscopic surveillance with resection of larger polyps (10-15 mm) to prevent intussusception in patients with PJS.[13] Similarly, familial polyposis coli and juvenile polyposis can also cause intussusceptions.

Incarcerated hernia

Inguinal hernias are very common in children and are more common in premature infants.[14] Hernias can cause small bowel obstruction when they become incarcerated, meaning the contents of the hernia sac cannot be reduced back into the abdominal cavity. Incarcerated hernias may contain small bowel, the appendix (Amyand hernia), omentum, or, rarely, a Meckel diverticulum (Littre hernia). In girls, the ovary and/or fallopian tube are frequently incarcerated. When a part of the bladder wall or bowel wall is contained in the hernia sac, it is called a sliding hernia. Incarceration is the most common complication associated with inguinal hernias, with the risk thought to be increased among premature infants.[15, 16]

Umbilical hernias are extremely common in children, and most close spontaneously. They very rarely incarcerate and therefore very rarely cause small bowel obstruction. Similarly, epigastric hernias are very common in children but rarely incarcerate. Femoral hernias do tend to incarcerate but are extremely rare in children.

Malrotation

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. 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. See the images below.

For unknown reasons, midgut rotation can arrest at any point, most commonly rotating 180° and leaving the cecocolic loop in the right upper quadrant. The duodenojejunal limb remains in a position of nonrotation, and the cecocolic limb has partial rotation (usually approximately 90° instead of 180°). The end result is that the cecum winds up in the mid-upper abdomen, and the abnormally positioned cecum is fixated to the right lateral abdominal wall by bands of peritoneum (Ladd bands). The Ladd bands cross the duodenum and can cause extrinsic compression and obstruction of the duodenum. This configuration leaves a narrow mesenteric root and creates a predisposition to clockwise volvulus of the midgut around an axis formed by the superior mesenteric artery. Midgut volvulus is a surgical emergency and can lead to complete necrosis of the midgut if not managed expeditiously (see the image below). The Ladd bands themselves can also obstruct the duodenum, which can create a more chronic, partially obstructive picture even in the absence of volvulus.

Postoperative adhesions

Adhesions following intra-abdominal surgery are a very common cause of small bowel obstruction, often occurring in areas of ischemia or serosal damage.[17] Laparotomy for inflammatory conditions renders a patient particularly prone to adhesive small bowel obstruction. Postsurgical onset of obstructive symptoms is variable.[18] The incidence of adhesive small bowel obstructions appears to be lower after laparoscopic procedures compared to open.[19]

Mesocolic (internal) hernia

Mesocolic (internal) hernias are rare rotational abnormalities in which nonfixed colonic and duodenal mesenteries allow formation of potential spaces for bowel herniation.[20, 21] Mesocolic hernias can be right-sided or left-sided and can occasionally incarcerate and strangulate. In addition, they can occasionally cause more chronic and intermittent partial obstructions. Iatrogenic internal hernias can also occur postoperatively if a mesenteric defect is not properly closed. See the image below.

Necrotizing enterocolitis

Necrotizing enterocolitis (NEC) is a common neonatal emergency that primarily affects premature neonates and low-birth-weight infants—it is associated with significant morbidity and mortality.[22] NEC can occasionally present with an obstructive picture in the acute setting. In addition, small bowel obstructions can present later after recovery from a prior episode of NEC. These obstructions are frequently caused by strictures. However, the most common location for NEC strictures is the colon.

Meckel diverticulum

Meckel diverticulum is the most common small bowel congenital malformation, with an estimated incidence of 1.2% in autopsy studies.[23] It is characterized by a true diverticulum (including the four layers of the intestinal wall) arising from an incompletely obliterated omphalomesenteric duct (see the image below).

Although mostly asymptomatic, Meckel diverticulum can cause symptoms in the setting of gastrointestinal bleeding from heterotopic gastric mucosa within the diverticulum or with the development of Meckel diverticulitis. The diverticulum itself does not typically cause obstruction. However, Meckel diverticulum can act as a lead point for intussusception. In addition, an omphalomesenteric duct remnant or band is occasionally associated with the diverticulum and can act as point of obstruction, volvulus, or internal herniation.

Enteric duplication

Duplications of the alimentary tract make up a group of rare malformations that vary greatly in appearance, size, location, and symptoms. They have been reported to occur anywhere along the gastrointestinal tract, 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.[24] These cystic structures generally cause symptoms through mass effect, and duplications can cause partial or complete small bowel obstructions (see the image below).

Jejunoileal atresia

Jejunoileal atresia is believed to result from intrauterine mesenteric vascular accidents. 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 (see the images below). Jejunoileal atresias are classified into the following four types based upon anatomic characteristics:

• Type 1: No discontinuity in the bowel, obstruction from a diaphragm or web, no mesenteric defect

• Type 2: Discontinuous bowel connected with a fibrous cord, no mesenteric defect

• Type 3a: Presence of a gap between discontinuous bowel with a mesenteric defect

• Type 3b (“apple peel” or “Christmas tree” atresia): Presence of a large gap and mesenteric defect between a discontinuous proximal atresia and distal small bowel that is shortened and coiled around its mesentery

• Type 4: Presence of multiple atresias, often appearing as a “string of sausages”

Duodenal obstructions

Duodenal obstructions in newborns may be partial or complete and secondary to extrinsic or intrinsic abnormalities. Duodenal atresia and stenosis are intrinsic obstructions believed to be caused by failure of recanalization of the duodenum after the embryologic cord stage. Duodenal atresia and stenosis are relatively rare causes of obstruction. Duodenal atresia has a high rate of associated anomalies.

The anatomic classification of duodenal atresia is as follows:

• Type I: Luminal web or membrane

• Type II: Complete atresia connected by a fibrous cord

• Type III: Complete atresia with a mesenteric gap between the affected intestinal segments

Annular pancreas

Annular pancreas is a rare congenital anomaly that causes an extrinsic duodenal obstruction. It 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. These lesions may coexist with duodenal atresia and stenosis.[25] An annular pancreas can be asymptomatic, or it can cause external compression on the second portion of the duodenum, which creates a partial or complete obstruction.

Meconium ileus

Meconium ileus occurs almost exclusively in neonates with cystic fibrosis and is usually its earliest clinical manifestation. The disease is caused by the accumulation of hyperviscous and thickened meconium that obstructs the distal small intestine and colon. Dilatation of the involved and obstructed bowel segment can also lead to volvulus or perforation (complicated meconium ileus). A similar pathologic process that causes distal small bowel obstruction can occur in older children with cystic fibrosis, referred to as distal intestinal obstruction syndrome (DIOS).

Hirschsprung disease

Hirschsprung disease is a functional distal bowel obstruction resulting from the abnormal development of the enteric nervous system and ensuing aganglionosis of the distal gut. It is an uncommon cause of small bowel obstruction, as the transition between ganglionic and aganglionic bowel is most commonly located in the colon. However, in cases of total colonic Hirschsprung disease, the transition does occur within the small intestine, with a resulting obstruction at that level.

Congenital obstructions

Malrotation of the bowel with midgut volvulus occurs at a rate of 1 case per 6000 live births.[26] 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, atresias are almost equally divided between the jejunum (51%) and ileum (49%).

Jejunoileal atresia is twice as common as duodenal atresia and also occurs more commonly 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.[27, 28] The incidence of alimentary tract duplications is 1 case per 4500 population.

Sex-related differences

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. Most other causes of small bowel obstruction equally affect both sexes. Malrotation of the bowel with midgut volvulus can affect either sex. Neither duplication cysts nor jejunoileal atresia exhibit a sexual predilection.

Age-related differences

Adhesive small bowel obstruction can occur among patients of any age who have had prior abdominal surgery. Certain causes of small bowel obstruction, however, are more likely to present and be diagnosed within certain age groups.

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 children aged 5-10 months; the 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. Jejunoileal atresia causes obstruction in the immediate postnatal period.

Patients with duodenal atresia typically present in the first 24 hours of life. However, patients with duodenal stenosis may remain asymptomatic until later in childhood; symptom onset depends upon the degree of stenosis.

For annular pancreas, the age of onset of obstructive symptoms also varies. On occasion, symptoms do not develop until adulthood. However, many pediatric patients present in the newborn period with complete duodenal obstruction, often after the first feeding.

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" (DIOS).

Necrotizing enterocolitis is primarily a disease seen in premature infants. However, approximately 10% of cases occur in term infants.

Mortality and morbidity in pediatric small bowel obstruction depend on the type of lesion that causes the intestinal blockage and the time elapsed before diagnosis and definitive treatment, which affects the extent to which bowel is compromised. Mortality is generally low for most diagnoses with early identification and treatment.

Clinical factors that appear to be useful for identifying strangulated small bowel obstruction include two or more of the following: intractable continuous abdominal pain, tachycardia, leukocytosis, abdominal distention with ultrasonographically proven ascites or wall thickness and reduced wall contrast enhancement.[29] If left untreated, strangulated obstructions can be lethal. Mortality rates may reach 65% if more than 75% of the small bowel is necrotic at the time of laparotomy. With extensive bowel loss, children can suffer from malnutrition due to short-bowel syndrome.[30]

Strictures and adhesions are late complications of treated obstructions. Other long-term outcomes are largely dependent on the underlying etiology of the small bowel obstruction. Long-term survival in patients with duodenal atresia or stenosis is approximately 86%, and most of the morbidity and mortality is related to cardiac anomalies. 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) carries a mortality of 15-30%.[31] Mortality is higher in surgically treated infants, reaching up to 50%, and depends on the extent of bowel involvement. Infants with pan-intestinal involvement show a 33% survival, compared with 69.5% survival for multifocal disease. Isolated NEC has an 88% survival.[32] Wright et al reported a particularly high (80%) mortality among premature neonates undergoing surgery for NEC.[33] Survivors of NEC frequently have 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 relatively high and increased among those with a greater extent of bowel resection.[34]

The first goal when evaluating children with abdominal pain is to identify life-threatening conditions that require emergent interventions. Bilious vomiting in a neonate is considered malrotation with midgut volvulus until proven otherwise and warrants emergent surgical evaluation. Nonemergent causes of abdominal pain can be identified through deliberate evaluation, beginning with a careful history.

The typical symptoms of small bowel obstruction are abdominal pain, distention, and vomiting. A history of repetitive intermittent abdominal pain with vomiting suggests a chronic, partial small bowel obstruction. Other signs and symptoms that occasionally accompany small bowel obstruction include anorexia, diarrhea (sometimes early in the course of the obstruction), obstipation (common with complete obstructions), hematochezia, and fever (worrisome sign associated with bowel strangulation and necrosis).

Obtain as much history as possible from the child. Seek an accurate chronology of the events. Asking when the child was last completely healthy may help provide an accurate assessment of the child's pathophysiology. In young children, feeding intolerance is often the first change noted by caregivers. 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 typically described as crampy 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 may occur later in the disease course, when strangulation, perforation, or both have occurred. Vomiting caused by a proximal obstruction is usually of gastric content, or it is bilious if the obstruction is distal to the ampulla of Vater. In distal obstructions, vomiting may be feculent.

Obtain a complete past medical history, specifically including information on birth history and any history of trauma, malignancy, radiation, and abdominal surgery.

Additional details regarding the history for frequently encountered diagnoses are provided below.

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. 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 become bloody and mucoid over time.

The classic triad described for intussusception (colicky abdominal pain, a sausage-shaped, palpable abdominal mass, and currant-jelly stools [see the following image]), is actually found in only 20% of cases. Postoperative intussusception occurs within 2-3 weeks after an extensive retroperitoneal dissection (Wilms tumor or neuroblastoma resection, etc). 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 distention, and irritability.

Hernia

An incarcerated hernia presents with signs and symptoms of intestinal obstruction (assuming the incarcerated organ is intestine), along with a tender and edematous mass at the site of herniation. A swollen, erythematous mass that becomes erythematous to violaceous and is exquisitely tender usually indicates a strangulated hernia. Fever and toxicity suggest necrosis of the incarcerated organ and possible perforation.

Internal hernias are usually asymptomatic, but when symptoms occur they are often vague. Repeated episodes of colicky abdominal pain and vomiting are common. These symptoms spontaneously subside when the hernia spontaneously reduces. Patients with incarcerated hernias have continuous pain, abdominal distention, fever, nausea, and vomiting.[35]

Malrotation with midgut volvulus

The hallmark of acute midgut volvulus is the sudden onset of bilious vomiting. A careful history may reveal prior feeding problems, with transient episodes of bilious vomiting or failure to thrive. 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.

Postoperative adhesions

Adhesive small bowel obstructions usually cause sudden onset of crampy abdominal pains, followed by anorexia, nausea, and bilious vomiting. Bowel movements and passage of flatus typically cease shortly after symptom onset.

Enteric duplications

The presentation of duplication cysts primarily depends on the type of mucosal lining and cyst location. Some small intestine duplications contain gastric mucosa and manifest with peptic ulceration leading to gastrointestinal hemorrhage. Other cystic duplications may enlarge sufficiently to cause obstructive symptoms; in addition, these cysts may also act as the lead point for an intussusception.

Intestinal atresia and stenosis

Because most atresias (including duodenal atresias) are postampullary, bilious vomiting is the most common presentation. Abdominal distention may be notably absent in more proximal atresias; distention becomes more apparent in infants with more distal obstructions such as ileal atresia.

Necrotizing enterocolitis

The presenting clinical features of necrotizing enterocolitis (NEC) are nonspecific and variable; they include lethargy, temperature instability, feeding intolerance, and abdominal distention. Other common symptoms include bilious vomiting, gross or occult rectal bleeding, abdominal tenderness, and discoloration of the abdominal wall (see the image below). The Bell staging criteria are used to classify the severity of NEC using clinical and radiographic criteria.[36]

Meconium ileus

Infants with meconium ileus typically present with signs of a distal bowel obstruction (usually the terminal ileum), including vomiting (usually bile-stained), failure to pass meconium in the first 48 hours of life, and abdominal distention.

On examination, children with small bowel obstructions frequently have abdominal distention. This finding may be notably absent, however, in more proximal obstructions. The abdomen may be tympanic to percussion. On auscultation, obstructions often produce active, high-pitched, and hyperactive bowel sounds with occasional rushes. In infants with thin abdominal walls, peristaltic waves within the bowel proximal to the obstruction can occasionally be visualized on the abdomen.

Abdominal tenderness varies but is typically not dramatic in the absence of compromised bowel. Patients who present late with necrotic bowel and/or perforation will develop signs of peritonitis on examination. In addition, these children may exhibit signs of inadequate perfusion, such as poor capillary refill, tachycardia, decreased urine output, mental status changes, and hypotension as a result of volume depletion from vomiting and third spacing of fluid into the bowel lumen.

Examination must include a careful assessment for signs of hernias that could be the culprit for the obstruction. Depending on the clinical scenario and level of concern for a very distal obstruction, a digital rectal examination may also be warranted.

With intussusception, physical examination occasionally reveals a tender, sausage-shaped mass. Because most intussusceptions are ileocolic, patients may also present with the Dance sign (empty or retracted right lower quadrant).

After a careful history and physical examination are complete, the following laboratory tests may be useful in patients with small bowel obstruction:

• Basic metabolic panel

• Complete blood cell (CBC) count

• Urinalysis and urine culture

• Blood culture

• Arterial blood gas (ABG) level

• Stool for occult blood

A leukocytosis with a left shift may develop late in the disease process when bowel has been compromised; alternatively, this finding could suggest another disease process such as appendicitis or sepsis that is mimicking some signs of small bowel obstruction. Thrombocytopenia often accompanies severe necrotizing enterocolitis; a more than 30% drop in platelet count is associated with increased morbidity and mortality, as well as length of hospital stay.[37]

The basic metabolic panel is a helpful marker of a child’s level of volume depletion, a common finding in children with small bowel obstruction.

Many obstructive processes in children can be identified with plain radiographs. A flat decubitus and upright radiograph of the abdomen can reveal dilated small bowel loops and air-fluid levels that are produced by the layering of air and intestinal contents. Absent colonic or rectal gas may also be present in a complete obstruction. The pattern of bowel gas on plain radiography can help to differentiate between proximal and distal bowel obstructions. In lieu of an upright radiograph, a left lateral decubitus film can also be obtained to demonstrate air-fluid levels or, in the case of perforation, to identify free intraperitoneal air.

Ultrasonography can identify many intestinal abnormalities causing obstruction, including tumors, mesenteric cysts, and intussusceptions. Contrast studies such as an upper gastrointestinal (GI) series or contrast enema can also be used to diagnose an obstruction and determine the obstruction location. Contrast studies may also help reveal whether the obstruction is intrinsic or extrinsic to the bowel.

Abdominal computed tomography (CT) scanning is occasionally necessary to identify the specific cause of a small bowel obstruction, in particular in the evaluation of chronic partial obstructions and to rule out other etiologies that may mimic small bowel obstruction.

Finally, magnetic resonance imaging (MRI) can also be used to evaluate small bowel obstructive processes. For example, small bowel strictures in patients with inflammatory bowel disease are often diagnosed using magnetic resonance enterography (MRE).

Additional details regarding the imaging for frequently encountered diagnoses are provided below.

Intussusception

Plain abdominal radiography can be useful in the diagnosis of intussusception.[38, 39] X-rays can suggest a soft-tissue mass projecting toward the right upper quadrant or reveal the intussusceptum projecting into the air-filled colon. Abdominal radiography may also reveal scattered air-fluid levels that suggest partial obstruction.

The diagnosis is typically confirmed with ultrasonography, which reveals a "target" sign that corresponds to the echogenic appearance of the intussusceptum in the intussuscipiens. The reliability and accuracy of ultrasonography may help avoid unnecessary radiologic studies or surgical intervention.[40] See the images below.

Abdominal CT scanning and MRI are usually unnecessary to make the diagnosis of intussusception. Contrast radiography can be diagnostic as well as therapeutic (see Treatment).

Incarcerated hernia

Incarcerated hernias are diagnosed clinically, and no imaging studies are required. Air-fluid levels are often visible on plain radiography when obtained. The bowel may be visible within the inguinal canal and scrotum. Ultrasonography may reveal the incarcerated viscera in the inguinal canal or umbilical ring and can be useful in difficult cases (see the image below).

Malrotation of the bowel with midgut volvulus

Volvulus is typically identified using plain radiography, an upper GI series, or CT scanning.[41]

Plain abdominal radiography may reveal air-fluid levels, especially in the stomach and duodenum, or the abdomen may appear gasless on abdominal plain radiography. Distended loops of small bowel are only occasionally visible because the point of obstruction is proximal.

An upper GI series is the classic study to diagnose malrotation with or without volvulus. The duodenum usually has a "C" shape, and the duodenojejunal junction is localized to the left of the midline.[42] In malrotation, the duodenum lacks this normal shape and does not cross the midline. Duodenal obstructions can also be identified. The classic patterns of volvulus are the "bird beak," in cases involving complete duodenal obstruction, or the "corkscrew,” in cases involving incomplete obstruction.

Malrotation can also be identified on ultrasonograms and CT scans. Ultrasonographic findings suggestive of malrotation include the following[43] :

• Third part of the duodenum not in the normal retromesenteric position (ie, located between the superior mesenteric artery [SMA] and the aorta in the retroperitoneal space)

• Abnormal position of the superior mesenteric vein (either anterior or to the left of the SMA [the superior mesenteric vein is normally located to the right of the SMA])

• The "whirlpool" sign of volvulus caused by the vessels twisting around the base of the mesenteric pedicle

• Dilated duodenum (suggesting duodenal obstruction by Ladd bands)

Finally, contrast enema findings may provide indirect evidence of malrotation by revealing an ectopically placed right colon and cecum. However, a high or mobile cecum is common in many asymptomatic patients, and a significant number of patients with malrotation will have a normal contrast enema.

Postoperative adhesive small bowel obstruction

Supine and upright abdominal radiography reveals dilated, gas-filled loops of small intestine with air-fluid levels. If the diagnosis is in question or if there is concern for compromised bowel that would preclude a trial of nonoperative management, a CT scan can be obtained to provide additional data for decision making.

Duplication cysts

Enteric duplication cysts are increasingly detected prenatally.[44] Plain radiography may reveal a soft-tissue mass within the abdomen that displaces the adjacent bowel. An upper GI contrast series may reveal stenosis or extrinsic compression from the 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. Although typically unnecessary, enteric duplications can also be visualized on CT scan or MRI.

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 occasionally encountered.[45] Pneumatosis intestinalis is the radiographic hallmark; its presence indicates gas in the bowel wall. Portal venous gas is an ominous sign suggesting more advanced disease, and pneumoperitoneum indicates a bowel perforation. Pneumatosis intestinalis and portal venous gas can also be detected using ultrasonography; color Doppler ultrasonography may be a more accurate method of diagnosing bowel necrosis than plain abdominal radiography.[46]

See the images below.

Mesocolic hernia

An upper GI study with small bowel follow-through may support the diagnosis of mesocolic hernia. However, abdominal CT scanning is the diagnostic imaging study of choice.[35]

Jejunoileal atresia and stenosis

Plain radiography demonstrates dilated intestinal loops and air-fluid levels proximal to the level of obstruction. In many cases, plain radiography is sufficient to make the diagnosis. A contrast enema may also be helpful to obtain, however, especially when plain radiography suggests a more distal bowel obstruction and colonic obstruction must be ruled out. A contrast enema can distinguish between small and large bowel distention, determine the presence or absence of a microcolon, and locate the position of the cecum with regard to possible abnormalities of intestinal rotation and fixation. Even when plain radiography more clearly demonstrates a small intestinal atresia, a preoperative contrast enema is often desired to obviate the need for a full examination of the colon intraoperatively (when it has already been shown to be normal on contrast enema). An upper GI series can reveal the level of obstruction with grossly distended proximal bowel. However, contrast aspiration is a significant risk, and this study is not routinely necessary. See the image below.

Duodenal atresia and stenosis

Abdominal radiography usually confirms a duodenal atresia diagnosis by showing a dilated stomach and proximal duodenum (ie, the double-bubble sign), with little to no air present in the distal GI tract. With this classic appearance, no further studies are necessary.

The double-bubble sign characteristic of duodenal obstruction can also be seen in cases of annular pancreas. If the child 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.

An upper GI series is rarely necessary in neonates and creates unnecessary risk of contrast aspiration from vomiting. Upper GI studies are more useful in the later diagnosis of a duodenal web or stenosis. See the images below.

Meconium disease

Abdominal radiographic studies reveal multiple air-fluid levels consistent with a distal (usually at the terminal ileum) 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. The contrast enema reveals a microcolon (nonused colon) and varying degrees of obstruction of refluxing contrast material into the small intestine caused by meconium pellets in the terminal ileum.

Children with small bowel obstructions are admitted to the hospital for close monitoring even if initial nonoperative management is chosen.

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

• Stabilize the patient and monitor ABCs (airway, breathing, circulation).

• Replace fluid losses with diligent intravenous (IV) resuscitation, using isotonic sodium chloride solution or lactated Ringer's solution.

• Administer nothing by mouth (NPO).

• Early gastric decompression with a nasogastric (NG) tube.

• Administer broad-spectrum antibiotics when necrosis or perforation is suspected.

Consultations

When small bowel obstruction is suspected in a pediatric patient, consult with a pediatric or general surgeon, depending on availability. Consider early transfer of care to a children’s center fully resourced to provide optimal care to children.[47]

Other considerations

Specific approaches to different causes of small bowel obstruction are discussed below.

Intussusception

Initial management of an ileocolic intussusception is a trial at reduction using an air or contrast enema, which is successful in approximately 90% of cases.[48, 49] Repeat enemas are useful and can be considered when the first enema is unsuccessful but did achieve some partial reduction.[41] Although some centers still elect to admit children for observation after a successful enema reduction, discharge from the emergency department after successful reduction has also been shown to be safe.[50]

Children who are systemically ill with signs of peritonitis are not candidates for enema reduction and should be expeditiously taken to surgery. Surgery is also indicated for patients whose intussusception cannot be reduced with enemas. See the image below.

Adhesive small bowel obstruction

A high level of concern for compromised bowel mandates operative exploration. In most patients with adhesive small bowel obstruction, however, such signs are not present, and a trial of nonoperative management with NPO, IV fluids, and NG decompression is appropriate. This management alone will result in resolution of many adhesive small bowel obstructions in children.[18]

The administration of a water-soluble contrast medium (such as Gastrografin) via NG tube, followed by abdominal radiography to assess the contrast progression, is useful in deciding early whether or not surgical intervention will be required. The passage of contrast material into the colon is predictive of resolution with nonoperative management, and administration of contrast medium may also decrease the need for surgery in some patients. This approach has been successfully used in children.[51]

Incarcerated hernia

In the absence of signs of strangulation, an attempt should be made to reduce the incarcerated hernia to relieve the associated obstruction. Sedation and placing the patient in a slight Trendelenburg position can be helpful. After reduction, semi-elective repair is typically performed 24-48 hours after reduction to allow the edema to subside. If reduction cannot be obtained or in the setting of strangulation, surgery is required.

Necrotizing enterocolitis

Treatment for early and uncomplicated necrotizing enterocolitis (NEC) is medical with broad-spectrum antibiotics, cessation of enteral feeds, and NG decompression. However, medical treatment may fail to improve the patient’s condition, or severe complications may develop that require surgical consultation. Infants who develop small bowel obstruction from NEC, either acutely from a necrotic portion of intestine or from a stricture that develops after a prior episode of NEC, generally fall into this group that requires surgical intervention.

Meconium ileus

The therapy of choice for uncomplicated meconium ileus is the administration of hyperosmolar contrast enema, which is both diagnostic and therapeutic in the majority of patients. In some cases, N -acetylcysteine can be added to the enema solution or can be administered using an NG tube from above to help loosen the meconium. Surgical intervention is required for complicated cases (volvulus, perforation, necrosis, associated atresia) and those obstructions that are not relieved with enemas.

Intussusception

When reduction of intussusception via air or contrast enemas is unsuccessful, surgery is required. In addition, children with signs of compromised bowel should proceed directly to the operating room. The procedure can be performed safely via laparotomy or via laparoscopy.[52, 53] Surgery consists of reduction of the intussusception, followed by an evaluation of the viability of the bowel, with bowel resection and primary anastomosis as indicated.

Incarcerated hernia

After reducing the hernia, elective repair is possible 24-48 hours after the edema subsides. For patients whose incarcerated hernias cannot be reduced or for patients with signs of strangulation, immediate surgery is required.

Malrotation of the bowel with midgut volvulus

Rapid diagnosis and surgery for malrotation with midgut volvulus is vital to preserve intestinal viability.[54] Clinical judgment trumps imaging, and there should be no delay in proceeding with emergent exploration to obtain confirmatory imaging when clinical findings suggest midgut volvulus.

Surgery consists of a Ladd procedure, which includes evisceration and inspection of the mesenteric root, derotation of the volvulus, lysis of Ladd bands, opening of the visceral peritoneum that covers the mesentery to maximally widen the mesenteric pedicle, and replacing the small bowel into the right side of the abdomen and the large bowel into the left side. It also typically includes an appendectomy, because the appendix will otherwise be located in an unusual place. The Ladd procedure can also be performed laparoscopically, although this is rarely used in the setting of acute volvulus.[55] 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. When large segments of bowel have questionable viability, temporary abdominal closure with a second look in 24-48 hours is advisable.

Postoperative adhesive small bowel obstruction

Signs of compromised bowel such as fever, tachycardia, and peritonitis mandate surgical exploration, as does failure of nonoperative management to relieve the obstruction. Adhesiolysis is the treatment of choice. In general, only the adhesion causing the obstruction needs to be resolved, as 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. Adhesiolysis can be achieved with laparotomy or laparoscopy.[56] Some patients will require bowel resection because of perforation or necrosis.

Duplication cysts

The treatment for enteric duplications is surgical excision, either via laparotomy or laparoscopy. Duplications of the small intestine often require resection and anastomosis. See the image below.

Necrotizing enterocolitis

Indications for surgery in necrotizing enterocolitis (NEC) include pneumoperitoneum (the only absolute indication); a fixed, dilated bowel loop; abdominal wall discoloration; and clinical deterioration or lack of improvement with nonoperative management. The presence of portal venous gas suggests advanced disease but does not by itself mandate surgical intervention, unless the child clinically requires it. See the image below.

Surgical management of NEC that is causing small bowel obstruction consists of laparotomy with resection of any necrosed bowel, followed by primary anastomosis or creation of an ostomy.[32]

Mesocolic hernia

In symptomatic patients with mesocolic or other internal hernias, prompt surgical exploration to reduce the hernia and repair the defect is imperative. These patients often have a delayed diagnosis and present as a surgical emergency with acute bowel obstruction and intestinal ischemia.[35] See the image below.

Jejunoileal atresia and stenosis

Patients with jejunoileal atresia typically undergo surgical resection of the atretic segment, followed by an end-to-end anastomosis. The proximal, dilated bowel may need to be tapered to fit the smaller distal intestine. Surgeons should take care to preserve as much intestinal length as possible to prevent short-bowel syndrome, especially in patients with multiple atresias. Small intestinal atresias have classically been repaired through a transverse supraumbilical incision, although single jejunoileal atresias have also been successfully approached through a smaller periumbilical incision.[57]

Duodenal obstructions

The treatment for duodenal obstructions is a linear or diamond-shaped duodenoduodenostomy. Duodenojejunostomy is another option. A duodenal web, although less common, can be treated with duodenotomy and excision of the web, with or without duodenoplasty.[58]

Surgical management for annular pancreas is similar to that for duodenal atresia, with diamond-shaped duodenoduodenostomy being the preferred approach.

Meconium ileus

Surgical management is necessary for cases of complicated meconium ileus and when enemas are unsuccessful in relieving the obstruction. For uncomplicated cases, enterotomy and irrigation to remove the thickened meconium and meconium pellets may be sufficient. Catheter or tube enterostomy can be considered to allow for postoperative administration of N-acetylcysteine, which can also be provided via nasogastric tube postoperatively.

Complicated cases (volvulus, perforation, necrosis, associated atresia) require not only clearance of the meconium but also care of the associated complication, typically intestinal resection with primary anastomosis or stoma creation.[59]

Meckel diverticulum/band

Surgical resection of the diverticulum and lysis of any associated bands is the proper treatment in symptomatic patients. The minimally invasive approach is reasonable even in small children.[60, 61]

Immediately administer empiric broad-spectrum antibiotics when managing a pediatric small bowel obstruction in which compromised bowel with necrosis or perforation is suspected. Infants with necrotizing enterocolitis are treated with antibiotics regardless of whether or not their disease progresses to requiring surgery. In addition, perioperative prophylactic antibiotics should be given whenever there is reasonable expectation of intraoperative entry into the gastrointestinal tract (making the wound classification at minimum "clean contaminated"). The exact antibiotics utilized vary between institutions based upon local antibiograms and provider preferences.

Class Summary

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

Clindamycin (Cleocin)

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)

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)

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)

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

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)

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

Ampicillin (Ampi, Omnipen, Penglobe)

Ampicillin is a broad-spectrum penicillin. It interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms. Ampicillin is an alternative to amoxicillin when patients are unable to take medication orally.

Ticarcillin and clavulanate potassium (Timentin)

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.

Piperacillin/tazobactam (Zosyn)

The combination of piperacillin/tazobactam comprises an antipseudomonal penicillin plus a beta-lactamase inhibitor. This agent inhibits biosynthesis of cell wall mucopeptide synthesis by binding to one or more of the penicillin-binding proteins and is effective during active-multiplication stage.