eMedicine Specialties > Pediatrics: General Medicine > Gastroenterology

Small-Bowel Obstruction

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
Coauthor(s): 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; 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; Bruce Friedberg, MD, Staff Physician, Department of Emergency Medicine, Mount Diablo Medical Center; Mainor Antillon, MD, Director, Pancreaticobiliary Endoscopy and Endosonography Program, Department of Internal Medicine, Division of Gastroenterology, King-Drew Medical Center; Associate Clinical Professor, Department of Medicine, University of California at Los Angeles; Thomas Tsou, MD, Director of Fast Tract and Pediatrics, Associate Professor, Departments of Medicine and Emergency Medicine, Charles R Drew University and University of California at Los Angeles
Contributor Information and Disclosures

Updated: Nov 21, 2008

Introduction

Background

Small-bowel obstructions in pediatric patients are uncommon but 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 distension. 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.

Many different pathologic processes can cause 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.

Causes of Acute Intestinal Obstructions

Intussusceptions
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 intussusceptum) telescopes or invaginates into the lumen of another immediately adjacent distal segment (called intussuscipiens). The peak age of presentation is between 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.

Incarcerated hernias
Incarcerated hernias occur when the contents of a hernia sac cannot be reduced back into the abdominal cavity. Incarcerated hernias can be inguinal, femoral, or umbilical. Inguinal and femoral incarcerated hernias are most common in both sexes. The vast majority of inguinal hernias in children are indirect hernias. Most direct hernias in the pediatric population occur following repair of an indirect hernia. Femoral hernias, which tend to incarcerate, are extremely rare in children and are the only hernias that occur in girls more often than boys.
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 2 months.

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

Internal hernias are extremely rare and cause bowel obstruction in children. Hernias in the mesentery, mesocolon, mesosigmoid, and Winslow foramen1 and defects in the falciform ligament have been described.2
 
Malrotation of bowel with midgut volvulus
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. Malrotation is always present in patients with abdominal wall defects (gastroschisis, omphalocele) and patients with congenital diaphragmatic hernia. It is often associated with other congenital and acquired lesions of the 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.

Postoperative adhesions
Adhesive small-bowel obstruction is an annoying surgical complication. Its incidence seems to be lower after laparoscopic procedures than after laparotomy. Postoperative adhesions are responsible for about 7% of the intestinal obstructions in infants and children. A single adhesion causes most obstructions, regardless of the nature of the previous illness or type of abdominal surgery. Onset of obstructive symptoms can range from 2 days to 10 years postsurgery, although most adhesions (>50%) occur within the first 3-6 postoperative months, and few occur after 2 years.

Annular pancreas
This rare condition 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 malrotation abnormality.3 Nonfixed colonic and duodenal mesenteries lead to formation of potential hernia pouches, which transiently and recurrently entrap the bowel and cause partial obstructions. Their exact incidence is still unknown, but, fortunately, they are rather rare. The internal hernias may be right-sided or left-sided and can sometimes incarcerate and strangulate. The mesocolic hernia is not a malrotation anomaly per se but occurs in the presence of a rotational anomaly. Mesocolic hernias can also occur as a consequence of retroperitoneal surgery in cases in which a mesenteric defect is not properly closed during the procedure.

Necrotizing enterocolitis
Strictures from previous necrotizing enterocolitis (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. In 11-36% of patients, NEC can produce strictures that subsequently cause intestinal obstruction. Strictures usually occur within 1-6 months following an acute NEC episode. 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. The most common sites for these strictures are the terminal ileum and the colon.

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 (irresistible desire to pull out ones own hair) or trichophagia. 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 continent 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."

Duplication cysts
Duplications of the alimentary tract comprise a group of rare malformations that vary greatly in appearance, size, location, and symptoms. Foley et al reported on 12 cases of enteric duplications during an 11-year period. 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.

The 3 characteristics of alimentary tract duplications 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 one or more types of cells normally observed in the alimentary tract.

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, meconium ileus (MI), and extrinsic and 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, MI, volvulus, omphaloceles, gastroschisis). 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.

MI occurs almost exclusively in patients with cystic fibrosis (CF)—prevalence is 10-20% in US patients with CF—and is usually the earliest clinical manifestation of CF. MI is caused by hyperviscous secretions produced by the small intestinal mucous glands. MI 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 even perforate or develop a volvulus.

Duodenal atresia and stenosis are relatively rare causes of obstruction that occur at a rate of just 1 case per 10,000 live births. Duodenal obstructions in newborns may be partial or complete and they may be secondary to extrinsic or intrinsic abnormalities. In addition to atresia and stenosis, intrinsic duodenal obstructions in newborns may include duodenal webs or diaphragms. Duodenal atresia completely obliterates the duodenal lumen; duodenal stenosis only partially or incompletely obstructs the duodenal lumen.

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. The incidence is about 1 per 7000 live births. About 50% of these patients have major associated anomalies (eg, Down syndrome, malrotation, congenital heart disease, renal anomalies, other small-bowel atresias, biliary atresia). Polyhydramnios occurs in approximately 40% of patients, and this clinical finding suggests a more proximal intestinal obstruction in the fetus. Duodenal atresia is believed to be caused by a failure of revacuolization of the duodenal lumen at 8-10 weeks' gestation. In prior stages of fetal development, the duodenal lumen is obliterated by the proliferating layers of duodenal wall.

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 blood stream, 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 in 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.
Most intussusceptions are idiopathic. A lead point is identified in only 2-8% of cases.

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. Because of the seasonal incidence that seems to follow peak viral illness seasons, these lead points may be enlarged lymphoid tissue from proliferation of Peyer patches.

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

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.

Frequency

United States

Malrotation of the bowel with midgut volvulus occurs at a rate of 1 case per 600 infants. Jejunoileal atresia and stenosis have a combined reported incidence of 1 case per 330-1500 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 10,000 live births. The incidence of alimentary tract duplications is 1 case per 4,500 population.

Mortality/Morbidity

Mortality and morbidity 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.

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 over the past 2 decades, 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 one year is approximately 92% in patients with uncomplicated MI and 89% in those with complicated disease.

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.

Sex

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 boys. Malrotation of the bowel with midgut volvulus can affect either sex. Neither duplication cysts nor jejunoileal atresia and stenosis exhibit a sexual predilection.

Age

Intussusception can occur at any time in life, yet 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 affects stressed premature infants who weigh less than 2000 g. Full-term newborns with polycythemia or congenital heart disease have higher risk for NEC, 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.

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.

MI 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."

Clinical

History

Obtain as much history as possible from the child. Younger children for example, 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 an emergent surgical evaluation.

Focus on the following issues:

  • Abdominal pain
    • Pain 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 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.
  • Nausea and vomiting
    • Vomiting is a classic symptom of mechanical obstruction.
    • Emesis caused by a proximal obstruction is usually of gastric content, or bilious if the obstruction is distal to the ampulla of Vater; in distal ileal obstructions, vomit is feculent.
  • Anorexia: Anorexia is an early and frequent sign.
  • Diarrhea: Diarrhea may occur early in the course of the obstruction.
  • Obstipation: This is a late sign of complete obstruction.
  • Fever: Fever can occur late in the disease process and is associated with bowel strangulation and necrosis.
  • General historical points: 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. In addition to the general guidelines above, the following evidence may suggest the specific cause of a small-bowel obstruction:
    • 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 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 or neuroblastoma). It is usually an ileoileal intussusception, and affected patients lack the palpable mass and rectal bleeding.
    • 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.
    • 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 proximal 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.
    • Postoperative adhesive small-bowel obstructions usually cause a sudden cramplike abdominal pain, followed by anorexia, nausea, and vomiting. Bowel movements typically cease shortly after symptom onset.
    • Presentation of duplication cysts primarily depends on the type of mucosal lining and 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 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. History of polyhydramnios on prenatal ultrasound (28%), prematurity (35%), or low birth weight (25-50%) can be helpful hints in the diagnosis.
    • 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.
    • The clinical features of necrotizing enterocolitis (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.
    • 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.
    • The presenting symptoms of cecal volvulus include pain, distention, constipation or obstipation, and vomiting.
    • 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.
    • In patients with meconium ileus (MI), 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.
    • 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.

Physical

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.
  • Patients who develop peritonitis obviously have severe pain and rebound tenderness.
  • The abdomen may be tympanic to percussion.
  • Bowel sounds include the following:
    • Mechanical obstructions produce active, high-pitched, hyperactive bowel sounds with occasional rushes.
    • Peristalsis may be increased in the upper abdomen (above the obstruction; termed "fighting peristalsis") and decreased in the lower abdomen.
    • With time, peristaltic waves and bowel sounds diminish or disappear.
  • During abdominal examinations, look for hernias in the groin, femoral triangle, and obturator foramina.
  • Perform a pelvic examination to exclude a genitourinary pathology as the cause of the obstruction.
  • Rectal examination includes the following:
    • Check for gross or occult bleeding that suggests strangulation.
    • The absence of stool in the vault may help confirm a diagnosis of bowel obstruction, although its presence does not eliminate a more proximal obstruction.
    • In proximal obstructions, patients may be able to evacuate preexisting rectal contents.
    • Massive diarrhea after rectal examination of an empty rectal vault is suggestive of colonic aganglionosis (ie, Hirschsprung disease).
  • 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).
  • Careful physical examination is most useful in the diagnosis of an incarcerated hernia.
  • 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.

Causes

  • Intussusception
    • Although the cause of intussusception is unknown in 90-95% of children, a viral etiology is suspected because of its seasonal predisposition for spring and autumn, as well as higher incidence of adenoid hypertrophy in children who suffered 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 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.
    • Intussusception is a well-described complication of patients with Meckel diverticulum, Waugh syndrome, cocaine abuse, laxative use, and even antibiotic use, presumably due to motility derangements caused by some of these agents.
    • In Henoch-Schönlein purpura, mucosal hematomas are thought to act as lead points.
    • Peutz-Jeghers syndrome is a rare cause of intussusception in older children; in this condition, hamartomatous polyps act as the lead point. 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.
    • As mentioned above, extensive retroperitoneal dissections are known to predispose children to postoperative intussusceptions, probably because of intestinal dysmotility in these patients.
    • Blunt abdominal trauma has also been known to cause intussusception.
  • Incarcerated 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 or nonreducible hernias may contain small bowel, cecal appendix (Amiand hernia), omentum, or, rarely, Meckel diverticulum (Littre hernia). In girls, the ovary, fallopian tube, or both is 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%).
  • Malrotation of the bowel with midgut volvulus
    • 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 anatomical and pathologic findings, but the actual rotation movements have not been seen in human embryos. Recent evidence suggests that, at least in rats, the midgut never rotates around the superior mesenteric artery and the final normal position and fixation of the midgut is probably due to differential growth of specific intestinal segments, rather than to rotation movements.
  • Jejunoileal atresia: 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 determine 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.
  • Postoperative adhesive small-bowel obstruction
  • Duplication cysts: 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.
  • Annular pancreas: 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.
  • Necrotizing enterocolitis: The primary infectious process likely results in enteroinvasion, release of inflammatory mediators, toxin production, ileus, gas production, bowel distension, increased intraluminal pressure, and vascular compromise, which causes loss of mucosal integrity, and bacterial translocation, which results in a systemic inflammatory response.
  • Mesocolic hernia
  • Cecal volvulus
  • Meconium disease
    • MI is caused by intestinal and pancreatic dysfunction, which results from the autosomal recessive disease cystic fibrosis (CF). MI is the result of the accumulation of sticky and inspissated intraluminal meconium.
    • Meconium plug syndrome or meconium obstruction does not appear to be associated with CF or Hirschsprung disease in extremely low birth weight infants.
  • Duodenal atresia and stenosis
    • 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.
    • The 3 basic morphologic features of duodenal atresias are as follows:
      • Type I atresias are characterized by luminal webs or membranes.
      • Type II is characterized by a complete atresia connected by a fibrous cord.
      • Type III is characterized by complete atresia with a mesenteric gap between the affected intestinal segments.

More on Small-Bowel Obstruction

Overview: Small-Bowel Obstruction
Differential Diagnoses & Workup: Small-Bowel Obstruction
Treatment & Medication: Small-Bowel Obstruction
Follow-up: Small-Bowel Obstruction
Multimedia: Small-Bowel Obstruction
References
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Further Reading

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Keywords

small-bowel obstruction, small bowel obstruction, SBO, intussusception, incarcerated hernia, malrotation of the bowel with midgut volvulus, postoperative adhesive small bowel obstruction, duplication cysts, annular pancreas, necrotizing enterocolitis, NEC, mesocolic hernia, cecal volvulus, jejunoileal atresia and stenosis, meconium Ileus

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Contributor Information and Disclosures

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)

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.

Bruce Friedberg, MD, Staff Physician, Department of Emergency Medicine, Mount Diablo Medical Center
Bruce Friedberg, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

Mainor Antillon, MD, Director, Pancreaticobiliary Endoscopy and Endosonography Program, Department of Internal Medicine, Division of Gastroenterology, King-Drew Medical Center; Associate Clinical Professor, Department of Medicine, University of California at Los Angeles
Disclosure: Nothing to disclose.

Thomas Tsou, MD, Director of Fast Tract and Pediatrics, Associate Professor, Departments of Medicine and Emergency Medicine, Charles R Drew University and University of California at Los Angeles
Thomas Tsou, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Jorge H Vargas, MD, Clinical Professor of Pediatrics, Division of Pediatric Gastroenterology, Hepatology & Nutrition
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
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Managing Editor

B U K 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 U K 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
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CME Editor

Steven M Schwarz, MD, FAAP, FACN, AGAF, Professor of Pediatrics, State University of New York, Downstate Medical Center College of Medicine; Distinguished Lecturer, New York Medical College, School of Public Health
Steven M Schwarz, MD, FAAP, FACN, AGAF is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American College of Physician Executives, American Gastroenterological Association, American Pediatric Society, Gastroenterology Research Group, New York Academy of Medicine, North American Society for Pediatric Gastroenterology and Nutrition, and Society for Pediatric Research
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Chief Editor

Carmen Cuffari, MD, Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine
Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, and Royal College of Physicians and Surgeons of Canada
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