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Pediatric Small-Bowel Obstruction Clinical Presentation

  • Author: Jaime Shalkow, MD, FACS; Chief Editor: Carmen Cuffari, MD  more...
 
Updated: Dec 11, 2015
 

History

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

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

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

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

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

Other issues to focus on include the following:

  • 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

The first goal when evaluating children with abdominal pain is to identify life-­threatening conditions that require emergent interventions. Once this has been accomplished, other causes of abdominal pain can often be identified through deliberate evaluation, with careful attention to the clinical features of the illness (such as the child's age and gender, history of trauma, pattern of the pain, related symptoms, physical findings, and selected diagnostic studies).

Children with abdominal pain frequently have fever. Vomiting is frequently reported among children with abdominal pain. Volvulus must always be quickly excluded as the cause of bilious emesis in a neonate. With intussusception, vomiting (initially non­bilious, but becoming bilious as the obstruction progresses) may occur following episodes of pain.[68]

Intussusception

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

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

Hernia

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

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

Internal hernias are usually asymptomatic and when symptoms occur, they include vague abdominal symptoms such as diffuse pain, discomfort, and vomiting. Only severe cases present symptoms of intestinal obstruction.[26]

Acute midgut volvulus

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

Adhesion

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

Spontaneous remission of symptoms in patients with adhesive obstructions is reported to be 47-65%, contradicting the common approach with early surgical intervention, which is reported to be 85% in the United States.[33]

Duplication

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

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

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

Intestinal atresia and stenosis

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

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

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

Annular pancreas

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

Necrotizing enterocolitis

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

Cecal volvulus

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

Meconium ileus

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

Next

Physical Examination

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

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

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

Bowel sounds can be characterized as follows:

  • 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. (Careful physical examination is most useful in the diagnosis of an incarcerated hernia.) Perform a pelvic examination to exclude a genitourinary pathology as the cause of the obstruction.

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

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

The diagnosis of intestinal malrotation should be suspected in any infant who presents with bilious emesis, acute duodenal obstruction, or abdominal tenderness associated with hemodynamic instability. In young premature infants, NEC may be difficult to distinguish from malrotation.

The most common symptom is abdominal pain. Vomiting is also frequently present, but not necessarily bilious; both abdominal pain and vomiting may be intermittent. Other, less common presentations include failure to thrive, solid food intolerance, malabsorption, chronic diarrhea from protein-­losing enteropathy, pancreatitis, peritonitis, biliary obstruction, motility disorders, and chylous ascites. Older children and adults with chronic symptoms may have been previously diagnosed with other chronic GI disorders, such as allergy, irritable colon, functional abdominal pain, or cyclic vomiting syndrome.[28]

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

Patients with NEC have a wide variation in clinical presentation, from feeding intolerance to shock; however, specific clinical signs that should raise high suspicion include abdominal distention, bluish discoloration of the abdominal wall, and blood in the stool. Refer to the Bell’s staging criteria, which are still widely used to classify the staging of NEC; the criteria provide a clinical and radiographic assessment of the disease.[69] See the image below.

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

During rectal examination, keep the following in mind:

  • Check for gross or occult bleeding that suggests strangulation
  • The absence of stool in the vault may help to 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)
Previous
 
 
Contributor Information and Disclosures
Author

Jaime Shalkow, MD, FACS Director, National Pediatric Cancer Program, National Center for Pediatric and Adolescent Health (CeNSIA); Attending Pediatric Surgical Oncologist, Cancer Center at the American British Cowdray Medical Center

Jaime Shalkow, MD, FACS is a member of the following medical societies: American College of Surgeons, International Society of Paediatric Surgical Oncology, Pacific Association of Pediatric Surgery, Mexican Association of Pediatric Surgery, Mexican Society of Oncology, Mexican Association of Pediatrics

Disclosure: Nothing to disclose.

Coauthor(s)

Adrian Florens, MD, FAAP Neonatologist, KIDZ Medical Services; Clinical Instructor of Pediatrics, Florida International University and Florida Atlantic University

Adrian Florens, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Eduardo Fastag Guttman, MD Medical Assistant Physician, Anesthesiology Integral

Disclosure: Nothing to disclose.

Issac Octavio Vargas Olmos Universidad Anahuac, Mexico

Disclosure: Nothing to disclose.

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, Royal College of Physicians and Surgeons of Canada

Disclosure: Received honoraria from Prometheus Laboratories for speaking and teaching; Received honoraria from Abbott Nutritionals for speaking and teaching.

Additional Contributors

Joyce Vazquez-Braverman, MD Instructor of ACLS, BLS, and Heartsavers, American Heart Assocation

Joyce Vazquez-Braverman, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Acknowledgements

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.

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

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

Disclosure: Nothing to disclose.

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.

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

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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

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Small-bowel obstruction visible on plain radiograph caused by intussusception in a 5-month-old patient.
Barium enema revealing a coil spring appearance caused by the tracking of barium around the lumen of the edematous intestine in intussusception.
Small-bowel obstruction caused by an incarcerated inguinal hernia in a 2-month-old infant with bilateral inguinal hernias as well as an umbilical hernia.
Radiograph depicting the double-bubble sign characteristic of duodenal atresia.
Upper GI contrast study demonstrating a jejunal atresia with a proximal dilated atretic bowel and lack of passage of contrast into the distal small bowel.
Surgical photograph of the patient in the previous image depicting the proximal dilated atretic jejunum.
Upper GI contrast study showing a malrotation with lack of normal C-shaped duodenum and the small bowel "hanging" on the right side of the abdomen.
Contrast enema with an abnormally located cecum in a patient with malrotation.
Surgical photograph of necrotic bowel in a patient with midgut volvulus.
Necrotic bowel after surgical reduction of an intussusception.
Surgical photograph of a transition zone in an infant with small bowel obstruction.
Incarcerated left inguinal hernia.
Mesocolic hernia.
Surgical image of a laparotomy on a 7-month-old girl with ileocolic intussusception. An edematous and erythematous cecal appendix was found to be acting as a lead point.
Surgical image of a laparotomy on a 2-day-old female patient with congenital small bowel obstruction. A type I jejunal atresia without mesenteric gap and a grossly dilated proximal intestine is seen.
A barium enema on a 1-year-old male patient depicts an ileocolic intussusception.
Clinical photograph of a 5-month-old male patient with characteristic currant-jelly stools due to intussusception.
Plain abdominal film on a 3-day-old newborn depicting the classic double-bubble sign for duodenal atresia.
Contrast-enhanced upper gastrointestinal film showing a duodenal atresia on a 2-day-old newborn.
Surgical photograph of a 3-year-old male patient with an obstructive, noncommunicating ileal duplication.
Plain abdominal film of a 6-year-old male patient with MRCP (mental retardation and cerebral palsy), with organo-axial gastric volvulus. Note the grossly dilated and obstructed stomach. A gastrostomy feeding tube can be seen in place. Surgical staplers from a previous laparoscopic fundoplication are seen near the diaphragmatic crura.
Surgical photograph of an 8-month-old patient with ileocolic intussusception.
Plain abdominal film of a premature baby born at 28 weeks of gestation with necrotizing enterocolitis. Note the "railroad sign" (pneumatosis intestinalis) in the hepatic flexure and soap-bubbles in the descending colon.
Clinical image of a micro-premature baby boy with discoloration on the right lower quadrant of the abdomen, due to intestinal perforation secondary to necrotizing enterocolitis. An umbilical catheter is in place.
Plain abdominal film on a premature baby girl with necrotizing enterocolitis. Note the air in the biliary tree and the grossly dilated bowel.
Surgical photograph of a 1-year-old male patient who previously underwent a right radical nephrectomy for Wilms tumor. He presented to the emergency department with signs of a mechanical small bowel obstruction. A transition zone is clearly seen at the point where the small bowel is trapped on an internal hernia through a mesenteric gap.
Image of intussusception by ultrasound on a 9-month-old male patient.
Surgical photograph of an 8-month-old boy with intussusception. The surgeon's finger is inserted into the intussusceptum, and the intussuscipiens is seen entering the distal bowel. No leading point was identified.
Surgical photograph depicting loops of bowel passing through a mesenteric defect. The bowel segment proximal to the obstruction is dilated, purplish, distended and hypoperistaltic. The bowel distal to the obstruction is decompressed and normal-looking.
Surgical photograph of a newborn with a type III jejunal atresia. Note the dilated proximal bowel pouch, the mesenteric V-shaped defect, and the thin, nondilated distal jejunum.
Surgical photograph of a Meckel diverticulum.
 
 
 
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