AUTHOR AND EDITOR INFORMATION

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
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INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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

Causes of Chronic Partial Intestinal Obstructions

Causes of Immediate Postnatal Small-Bowel Obstructions

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

Section 3 of 11  

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• Clinical
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• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
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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.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Inflammatory bowel disease
Intestinal pseudoobstruction

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• The following laboratory tests may be useful in patients with small-bowel obstruction:
• • Serum electrolyte level
  • BUN level
  • Creatinine level
  • Glucose level
  • CBC count
  • Urinalysis
  • ABG level
  • Stool for occult blood
• Routine laboratory studies usually do not help establish a diagnosis of malrotation with midgut volvulus, although leukocytosis with a left shift may develop late in the disease process.
• Potassium is an intracellular ion; thus, patients with incarcerated hernias or other conditions that lead to ischemic bowel may present with hyperkalemia.

Imaging Studies

• Plain abdominal radiography should be the initial radiologic study in suspected cases of small-bowel obstruction.
• • Obtain flat decubitus and upright radiographs of the abdomen.
  • Study radiographs for signs of dilated small-bowel loops and air-fluid levels produced by the layering of air and intestinal content.
  • Absent colonic or rectal gas also indicates a complete bowel obstruction.
  • The pattern of bowel gas on plain radiography can help differentiate between proximal and distal bowel obstructions. Drawing an imaginary line from the right upper quadrant to the left lower one is helpful in establishing the level of the obstruction. The jejunum corresponds to the left upper three fifths of the small bowel, whereas the right lower two fifths of it represents the ileum.
  • When intestinal perforation is suspected and the child cannot be placed in an upright position, a left lateral decubitus film with horizontal beam is helpful in diagnosing free intraperitoneal air because it facilitates identification of free air around the hepatic density.
• Contrast studies such as upper GI series and contrast enemas can help determine obstruction location. Contrast studies also reveal whether the obstruction is intrinsic or extrinsic to the bowel. Remember to always use hydrosoluble contrast to avoid severe barium peritonitis in patients with a perforation.
• Abdominal CT scanning should not be obtained when the diagnosis is evident on radiography because this would only delay treatment and subject the child to unnecessary radiation. CT scanning helps identify causes of chronic partial obstructions, as well as abscesses, tumors, and other causes of acute abdominal pain.
• Ultrasonographic examinations reveal many intestinal abnormalities, including tumors, mesenteric cysts, and intussusceptions.
• Intussusception imaging includes the following:
• • In approximately 60% of intussusception cases, plain abdominal radiography reveals the head of the intussusceptum projecting into the air-filled colon. Abdominal radiography may also reveal scattered air-fluid levels that suggest an ileus or partial obstruction. A left lateral decubitus film aids in the initial diagnosis of intussusception by revealing air or stool in the cecum and ascending colon.
  • Contrast radiography using a barium enema can be therapeutic as well as diagnostic. A classic sign is a coil spring appearance caused by the tracking of barium around the lumen of the edematous intestine. Air and water enemas have been used to reduce intussusception. Pneumatic reduction under fluoroscopic guidance and hydrostatic reduction under ultrasonographic monitoring are the preferred techniques. The aim should be a success rate of at least 90% in idiopathic intussusception.
  • Ultrasonography is useful in some cases and may have high sensitivity in as many as 75% of patients. The characteristic finding is a target or bull's eye configuration, consisting of 2 rings of low echogenicity that are separated by an intermediate hyperechoic ring visible on a cross-sectional image of intussuscepted bowel.
• Incarcerated hernia imaging includes the following:
• • In complete bowel obstruction, air-fluid levels are visible on plain radiography.
  • The bowel may be visible within the inguinal canal and scrotum.
  • Ultrasonography may reveal the incarcerated viscera in the inguinal canal or the umbilical ring and can be useful in difficult cases.
  • A careful physical examination is more helpful than imaging studies for the diagnosis of incarcerated inguinal or umbilical hernias. Incarcerated hernias are diagnosed clinically, and no imaging studies are required. Determining the level of the obstruction is not that important because the treatment does depend on this finding.
• Imaging for malrotation of the bowel with midgut volvulus includes the following: Plain abdominal radiography sometimes reveals a double-bubble sign that depicts air-fluid levels in both the stomach and in the distended duodenum. The abdomen often appears gasless on abdominal plain radiography. Distended loops of small bowel are only occasionally visible because the point of obstruction is proximal, in the third portion of the duodenum.
• Definitive diagnosis of midgut volvulus requires contrast studies. Barium enema findings may provide indirect evidence by revealing an ectopically placed right colon and cecum, but a high or mobile cecum is common in many asymptomatic infants. In fact, 10-15% of patients with malrotation have barium enema findings that appear normal. An upper GI series is a quicker and more direct approach with high sensitivity and accuracy, making it the criterion standard study for malrotation with or without volvulus. The duodenum usually has a "C" shape, and the duodenojejunal junction is localized to the left of the midline. In malrotation, the duodenum lacks its normal shape and does not cross the midline. Duodenal obstructions due to volvulus, Ladd bands, or angulation are evident. The classic patterns of volvulus are the "bird beak" in cases involving complete duodenal obstruction, or the "corkscrew in cases involving incomplete obstruction.
• Imaging for postoperative adhesive small-bowel obstruction includes the following:
• • Supine and upright abdominal radiography reveals dilated gas-filled loops of small intestine with multiple air-fluid levels scattered throughout the abdomen above the obstruction site. Air in the colon usually indicates a partial obstruction, although determining whether a gas-filled loop is the colon or small bowel is difficult in infants. Demonstrating gas in the rectum is the only way to be certain of gas in the colon.
  • Oral administration of water soluble contrast media (Gastrografin) with subsequent abdominal radiography is useful in deciding whether to perform early operation in cases in which the obstruction cannot be determined to be partial or complete.^{4, 5} If the contrast is found in the large bowel 6-8 hours after administration, the obstruction is presumed to be partial, and the patient can be conservatively managed without an immediate operation. The technique has been successfully used in children.
• Imaging for duplication cysts is as follows:
• • Plain radiography usually reveals a soft-tissue mass within the abdomen that displaces the adjacent bowel and causes the obstruction.
  • An upper GI contrast series may reveal stenosis or extrinsic compression by a mass.
  • Technetium scanning can be used to image duplications that contain ectopic gastric mucosa.
  • For most abdominal duplications, ultrasonography is more expedient and provides greater detail than conventional contrast radiography. Ultrasonography reveals either a sonolucent mass that has good through transmission because of its clear fluid content, or an echogenic mass secondary to hemorrhage that has inspissated material within the duplication. Intraabdominal enteric duplication cysts are increasingly likely to be prenatally detected.
• Imaging for annular pancreas is as follows:
• • Although an annular pancreas is often not diagnosed until surgery, plain abdominal radiography may reveal the double-bubble sign characteristic of duodenal obstruction.
  • An upper GI series reveals a diminished duodenal lumen.
  • Ultrasonography provides a reliable method to help diagnose duodenal obstruction, even prenatally in pregnancies complicated by polyhydramnios in the third trimester. It is also a good study to rule out hypertrophic pyloric stenosis as a differential diagnosis.
• Imaging for necrotizing enterocolitis (NEC) includes the following:
• • 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 ground-glass appearance, which suggests free intraperitoneal fluid, is sometimes encountered.
  • Pneumatosis intestinalis is the radiographic hallmark; its presence indicates gas in the bowel wall. Portal venous gas is an ominous sign, and pneumoperitoneum indicates a bowel perforation. Pneumatosis intestinalis and portal venous gas (pylephlebitis) are easily detected using ultrasonography.
• Mesocolic hernia imaging is as follows:
• • An upper GI study with small bowel follow-through during a hernia episode can support the diagnosis. This study usually reveals the intestines bunched together as if enveloped by a sac.
  • Abdominal CT scanning may reveal a mesocolic hernia during nonherniating periods.
• Cecal volvulus imaging is as follows:
• • Plain abdominal radiography may reveal a large air-filled loop of colon that occupies the right lower quadrant, in addition to depicting a typical small-bowel obstruction.
  • The characteristic barium enema finding is a bird-beak–shaped deformity, coupled with nonvisualization of the cecum.
• Jejunoileal atresia and stenosis imaging involves the following:
• • Radiographic findings often reveal thumb-sized intestinal loops and air-fluid levels. A loop of small bowel proximal to the atresia may become grossly distended and filled with fluid, producing the appearance of a mass.
  • A contrast enema is usually indicated to confirm the diagnosis. The preferred methodology is a water-soluble enema, which aids in distinguishing between small- and large-bowel distention, determining the presence or absence of a microcolon, and locating the position of the cecum relative to possible abnormalities of intestinal rotation and fixation.
  • An upper GI series reveals the level of obstruction with a grossly distended proximal bowel. Care must be taken to avoid contrast aspiration.
• Meconium disease imaging studies are as follows:
• • Abdominal radiographic studies reveal multiple air-fluid levels consistent with small-bowel obstruction. The presence of calcifications throughout the peritoneum suggests a prenatal perforation and meconium peritonitis or meconium pseudocyst.
  • The inspissated meconium often has a ground-glass appearance on radiography. A "soap-bubble" image in the right lower quadrant is characteristic.
  • A contrast enema is diagnostic and, in many cases, therapeutic for both MI and meconium plug syndrome. In most cases, the contrast enema reveals a microcolon (nonused colon) and meconium pellets in either the terminal ileum (MI) or the colon (meconium plug syndrome). Gastrografin is the agent of choice. Its osmotic properties pull water into the lumen, which may unplug the intestine.
• Duodenal atresia and stenosis imaging studies involve the following:
• • Abdominal radiography usually confirms a duodenal atresia diagnosis. Gas and air-fluid levels are present in the stomach and the dilated duodenal bulb (ie, double-bubble sign), but no air is present in the distal GI tract. These radiographic findings confirm a diagnosis of duodenal obstruction, making further studies unnecessary.
  • An upper GI series adds no information and creates the potential hazard of vomiting with barium aspiration. If the patient has vomited or has been decompressed using a nasogastric (NG) tube prior to abdominal radiography, the stomach and duodenum may be collapsed, making the correct diagnosis difficult. In such cases, a small amount of air (ie, 10-15 mL) may be injected into the stomach through the NG tube, and radiography may be repeated.
  • Upper GI studies are useful in the late diagnosis of duodenal web and stenosis.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

• General principles in small-bowel obstruction treatment
• • Stabilize the patient and monitor ABCs.
  • Replace fluids with diligent intravenous resuscitation, using isotonic sodium chloride solution or lactated Ringer solution.
  • Early bowel decompression with an nasogastric (NG) tube decreases the chance of bowel necrosis and perforation.
  • Administer broad-spectrum antibiotics when necrosis or perforation is suspected.
• Intussusception
• • Stabilize the patient's ABCs and replace large fluid losses. Administer nothing by mouth (NPO) to the child and place an NG tube to decompress the obstruction from above. The use of antibiotics is appropriate for management of bacterial translocation.
  • Barium, water, or air enema reduction is appropriate after surgical consultation if symptom duration is less than 24 hours and if the patient has no signs of peritonitis. Enemas successfully reduce 80-95% of all intussusceptions, with better success rates in short-duration intussusceptions.
  • Children whose symptoms persist longer than 24 hours, or have signs of peritonitis, should not be considered candidates for enema reduction. Stabilize these children and immediately transport them to the operating room because untreated intussusception is almost always fatal. The recurrence rate is higher after radiographic than after surgical reduction. Surgery is also indicated for patients whose intussusception cannot be reduced after 2 enema attempts.
• Adhesive small-bowel obstruction
• • Only about 6-7% of children with adhesive small-bowel obstruction require immediate laparotomy. Approximately one half of these patients respond to medical treatment, which includes NPO, intravenous fluids, NG decompression, and antibiotics. Children younger than 1 year tend to respond poorly to conservative management. No single agent or treatment has proven effective in preventing adhesion formation after a laparotomy.
  • The use of water-soluble contrast via NG tube may decrease the need for surgery in some patients. Water-soluble contrast media (Gastrografin) cause redistribution of intravascular and extracellular fluid into the intestinal lumen because of their hyperosmolarity. As a result, these media decrease intestinal wall edema and act as a direct stimulant to intestinal peristalsis
• Incarcerated hernia
• • Stabilize the patient's ABCs and focus on replacing the large fluid losses.
  • Nonoperative reduction of a nonstrangulated hernia is possible in approximately 95-98% of cases. Facilitate the reduction by sedating the patient and placing the patient in a mild Trendelenburg position. Gentle traction on the hernia and the contents of the sac usually suffices to reduce the volume and rapidly retract the contents of the sac into the abdominal cavity.
  • The only contraindication to nonoperative reduction is a long-standing incarceration with evidence of peritoneal irritation.
  • Antibiotic therapy is usually unwarranted, but critically ill infants with perforation and peritonitis require coverage for aerobic gram-negative organisms and anaerobic infections.
• Necrotizing enterocolitis (NEC)
• • NEC management involves cessation of enteral feeds, gastric decompression on low continuous suction with a sump-type tube, fluid management to correct hypovolemia, parenteral nutrition with a centrally located intravenous catheter once fluid resuscitation is complete, and antibiotic therapy.
  • Direct antimicrobial therapy is aimed at enteric bacteria (eg, Escherichia coli, Klebsiella species, Enterococcus species, anaerobic colonic flora, [Clostridia species]).
  • Serial abdominal examinations are preferably performed by the same examiner.
  • Obtain radiographs of the abdomen, including cross-table lateral films, every 6-8 hours for the first 48 hours.
  • Obtain blood, urine, sputum, and CSF cultures, if indicated.
• Meconium disease
• • Treatment of MI requires evacuating the meconium. Nonsurgical methods relieve the obstructions of more than 50% of patients.
  • The therapy of choice for uncomplicated MI is nonoperative hyperosmolar enema (Gastrografin or Omnipaque), with enterotomy and irrigation reserved for enema failures. Dilute Gastrografin with N-acetylcysteine may also be administered using an NG tube from above to help loosen the meconium. Distal intestinal obstruction syndrome may be treated in the same way.
  • Complicated cases (meconium peritonitis, meconium pseudocyst, perforation, intestinal atresia) require exploration and bowel resection with primary anastomosis or stoma creation.
  • Meconium plug syndrome is usually relieved with rectal stimulation (suppositories, washouts, or contrast enemas).

Surgical Care

• Intussusception: Intussusception can be reduced by radiographic means in 80-95% of patients. Surgical reduction is indicated when symptoms have been present for more than 24 hours, in the presence of shock that cannot be corrected, when a lead point has been identified, when necrosis or perforation are present, or if the intussusception is irreducible by radiographic means.
• Incarcerated hernia: After reducing the hernia, elective repair is possible 24-48 hours after the edema subsides. For patients whose hernias cannot be reduced and for patients with strangulation, immediate surgery is mandatory to prevent the incarceration from progressing to perforation and frank peritonitis.
• Malrotation of the bowel with midgut volvulus
• • Preserving intestinal viability requires rapid diagnosis and surgery for malrotation with midgut volvulus. Initiate NG suction and intravenous hydration when entertaining the possibility of midgut volvulus. If abdominal plain radiographic findings confirm the diagnosis, defer contrast studies and take the child directly to the operating room.
  • A Ladd procedure is the preferred treatment. It includes evisceration and inspection of the mesenteric root, derotation of the volvulus (which has always been reported to occur in a clockwise direction), lysis of Ladd bands with kocherization of the duodenum along the right abdominal gutter, opening of the visceral peritoneum that covers the mesentery, and replacing the small bowel into the right side of the abdomen and the large bowel into the left side (in a position of nonrotation). It also includes an appendectomy (usually an inversion appendectomy) because the cecum and appendix are located in an unusual place. The procedure can also be laparoscopically performed.
  • Any frankly necrotic bowel should be resected and end-to-end anastomosis performed unless the peritoneal cavity is grossly contaminated or the condition of the patient does not allow it; in such cases, stomas should be created.
• Postoperative adhesive small-bowel obstruction: A possible diagnosis of adhesive small-bowel obstruction requires prompt surgical consultation because delay can lead to intestinal necrosis. Patients usually present with a single-point obstruction. Adhesiolysis is the treatment of choice. This can be achieved laparoscopically or with laparotomy. Some patients require bowel resection because of perforation or necrosis.
• Duplication cysts
• • The treatment for duplications is surgical excision, even in an asymptomatic patient who is incidentally diagnosed. The prevalence of gastric mucosa suggests that the duplications should not be left indefinitely. The procedure may depend on the location of the cyst.
  • In esophageal duplications, the cyst is excised, and a mucosectomy is performed if the muscular layer shared with the esophagus is left behind. The entire muscular wall can be excised with the cyst, taking care not to penetrate the esophageal mucosa.
  • Duplications of the small intestine usually require resection and anastomosis. In rectal duplications, only the mucosal lining usually needs to be excised because the duplication and normal rectum share the muscularis layer. If malignant degeneration is suspected, total excision including the normal rectum may be necessary. Infected duplications may require initial drainage, followed by a staged resection. Laparoscopically assisted resection of ileocecal duplications is safe and effective.
• Annular pancreas: Surgical management is similar to that of duodenal atresia. Diamond-shaped duodenoduodenostomy is the preferred approach (Kimura procedure).
• Necrotizing enterocolitis: Indications for surgery include pneumoperitoneum, fixed dilated bowel loop, abdominal wall discoloration, or children whose conditions deteriorate or show no improvement with conservative therapy. Portal venous air suggests extensive intestinal necrosis but does not indicate that celiotomy is necessary.
• Mesocolic hernia: Surgically reduce the hernia and repair the potential hernia pouch, either electively (for reducible hernias) or emergently (for incarcerated hernias.)
• Cecal volvulus: Surgical reduction of the cecal volvulus and pexy to the lateral peritoneal wall is usually required, in addition to fluid resuscitation, bowel decompression, and ABC monitoring.
• Jejunoileal atresia and stenosis: Surgical resection of the atretic segment is followed by end-to-end anastomosis. The proximal dilated bowel may need to be tapered to fit the smaller distal intestine. Care should be taken to preserve as much intestinal length as possible in order to prevent short bowel syndrome, mainly in patients with multiple atresias. These have classically been repaired through transverse supraumbilical incision, although single jejunoileal atresias have been successfully approached through a smaller periumbilical incision (as the one described for hypertrophic pyloric stenosis).
• Meconium ileus: Surgical management by either primary resection and anastomosis or an ileostomy is sometimes required.
• Duodenal atresia and stenosis: The usual treatment for duodenal atresia is a linear or diamond-shaped duodenoduodenostomy (Kimura procedure). Duodenojejunostomy is another option. A duodenal web is much rarer and can be treated with duodenotomy and excision of the web, with or without duodenoplasty.

Consultations

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

Diet

• Administer NPO.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Bowel obstructions often require surgical interventions, but start antibiotic administration in the emergency department (ED) first. Antibiotic coverage must include gram-negative aerobic and gram-negative anaerobic organisms. (The following list of antibiotics is not all-inclusive.)

Drug Category: Antibiotics

Therapy must cover all likely pathogens in the clinical setting.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• Patients with partial small-bowel obstructions can be nonoperatively treated with adequate fluid resuscitation and nasoenteric suctioning.
• Patients who do not respond to nonoperative treatment within 12-24 hours require surgical treatment.
• After nonoperative hernia reduction, elective repair may be accomplished 24-48 hours after the edema subsides.
• Admit any child with an intussusception that is successfully reduced with a barium enema for observation because this condition has a high reoccurrence rate, especially in the first 24 hours.

Further Outpatient Care

• Close follow-up observation is mandatory for patients whose partial small-bowel obstructions are nonoperatively treated and who are stable for discharge.
• Inst