eMedicine Specialties > Gastroenterology > Colon

Hirschsprung Disease

Author: Steven L Lee, MD, Chief, Pediatric Surgery, Department of Surgery, Kaiser-Permanente, Los Angeles Medical Center
Coauthor(s): Shant Shekherdimian, MD, Consulting Surgeon, Department of Surgery, Kaiser Foundation Hospital; Jeffrey J DuBois, MD,, Chief of Children's Surgical Services, Division of Pediatric Surgery, Kaiser Permanente, Women and Children's Center, Roseville Medical Center
Contributor Information and Disclosures

Updated: Dec 28, 2009

Introduction

Background

Hirschsprung disease is a developmental disorder of the enteric nervous system and is characterized by an absence of ganglion cells in the distal colon resulting in a functional obstruction.1

Hirschsprung disease. Contrast enema demonstratin...

Hirschsprung disease. Contrast enema demonstrating transition zone in the rectosigmoid region.

Hirschsprung disease. Contrast enema demonstratin...

Hirschsprung disease. Contrast enema demonstrating transition zone in the rectosigmoid region.



Although this condition was described by Ruysch in 1691 and popularized by Hirschsprung in 1886, the pathophysiology was not clearly determined until the middle of the 20th century, when Whitehouse and Kernohan described the aganglionosis of the distal intestine as the cause of obstruction in their series of patients.2

In 1949, Swenson described the first consistent definitive procedure for Hirschsprung disease, rectosigmoidectomy with coloanal anastomosis. Since then, other operations have been described, including the Duhamel and Soave techniques. More recently, advances in surgical technique, including minimally invasive procedures, and earlier diagnosis have resulted in decreased morbidity and mortality for patients with Hirschsprung disease.

Most cases of Hirschsprung disease are now diagnosed in the newborn period. Hirschsprung disease should be considered in any newborn who fails to pass meconium within 24-48 hours after birth. Although contrast enema is useful in establishing the diagnosis, full-thickness rectal biopsy remains the criterion standard. Once the diagnosis is confirmed, the basic treatment is to remove the poorly functioning aganglionic bowel and to create an anastomosis to the distal rectum with the healthy innervated bowel (with or without an initial diversion).

Pathophysiology

Congenital aganglionosis of the distal bowel defines Hirschsprung disease. Aganglionosis begins with the anus, which is always involved, and continues proximally for a variable distance. Both the myenteric (Auerbach) plexus and the submucosal (Meissner) plexus are absent, resulting in reduced bowel peristalsis and function. The precise mechanism underlying the development of Hirschsprung disease is unknown.

Enteric ganglion cells are derived from the neural crest. During normal development, neuroblasts will be found in the small intestine by the 7th week of gestation and will reach the colon by the 12th week of gestation.3 One possible etiology for Hirschsprung disease is a defect in the migration of these neuroblasts down their path to the distal intestine. Alternatively, normal migration may occur with a failure of neuroblasts to survive, proliferate, or differentiate in the distal aganglionic segment. Abnormal distribution in affected intestine of components required for neuronal growth and development, such as fibronectin, laminin, neural cell adhesion molecule (NCAM), and neurotrophic factors, may be responsible for this theory.4,5,6

Additionally, the observation that the smooth muscle cells of aganglionic colon are electrically inactive when undergoing electrophysiologic studies also points to a myogenic component in the development of Hirschsprung disease.7 Finally, abnormalities in the interstitial cells of Cajal, pacemaker cells connecting enteric nerves and intestinal smooth muscle, have also been postulated as an important contributing factor.8,9

Three neuronal plexus innervate the intestine: the submucosal (ie, Meissner) plexus, the intermuscular (ie, Auerbach) plexus, and the smaller mucosal plexus. All of these plexus are finely integrated and involved in all aspects of bowel function, including absorption, secretion, motility, and blood flow.

Normal motility is primarily under the control of intrinsic neurons. Bowel function is adequate, despite a loss of extrinsic innervation. These ganglia control both contraction and relaxation of smooth muscle, with relaxation predominating. Extrinsic control is mainly through the cholinergic and adrenergic fibers. The cholinergic fibers cause contraction, and the adrenergic fibers mainly cause inhibition.

In patients with Hirschsprung disease, ganglion cells are absent, leading to a marked increase in extrinsic intestinal innervation. The innervation of both the cholinergic system and the adrenergic system is 2-3 times that of normal innervation. The adrenergic (excitatory) system is thought to predominate over the cholinergic (inhibitory) system, leading to an increase in smooth muscle tone. With the loss of the intrinsic enteric inhibitory nerves, the increased tone is unopposed and leads to an imbalance of smooth muscle contractility, uncoordinated peristalsis, and a functional obstruction.

Frequency

United States

Hirschsprung disease occurs at an approximate rate of 1 case per 5400-7200 newborns.

International

The exact worldwide frequency is unknown, although international studies have reported rates ranging from approximately 1 case per 1500 newborns to 1 case per 7000 newborns.10,11

Mortality/Morbidity

  • Approximately 20% of infants will have one or more associated abnormality involving the neurological, cardiovascular, urological, or gastrointestinal system.12
  • Hirschsprung disease has been found to be associated with the following:
    • Down syndrome
    • Neurocristopathy syndromes
    • Waardenburg-Shah syndrome
    • Yemenite deaf-blind syndrome
    • Piebaldism
    • Goldberg-Shprintzen syndrome
    • Multiple endocrine neoplasia type II
    • Congenital central hypoventilation syndrome
  • Untreated aganglionic megacolon in infancy may result in a mortality rate of as much as 80%. Operative mortality rates for any of the interventional procedures are very low. Even in cases of treated Hirschsprung disease, the mortality rate may be as high as 30% as a result of enterocolitis.
  • Possible complications of surgery include anastomotic leak (5%), anastomotic stricture (5-10%), intestinal obstruction (5%), pelvic abscess (5%), and wound infection (10%). Long-term complications include ongoing obstructive symptoms, incontinence, chronic constipation, enterocolitis, and late mortality, mostly affecting patients with long-segment disease. Although many patients will encounter one or more of these problems postoperatively, long-term follow-up studies have shown that greater than 90% of most children experience significant improvement and will do relatively well.13 Patients with an associated syndrome and those with long-segment disease have been found to have poorer outcomes.14,15,16

Race

Hirschsprung disease has no racial predilection.

Sex

Hirschsprung disease occurs more often in males than in females, with a male-to-female ratio of approximately 4:1. However, with long-segment disease, the incidence increases in females.

Age

Hirschsprung disease is uncommon in premature infants.

  • The age at which Hirschsprung disease is diagnosed has progressively decreased over the past century. In the early 1900s, the median age at diagnosis was 2-3 years; from the 1950s to 1970s, the median age was 2-6 months.
  • Currently, approximately 90% of patients with Hirschsprung disease are diagnosed in the newborn period.17

Clinical

History

  • Approximately 10% of patients have a positive family history. This is more common in patients with longer segment disease.
  • Hirschsprung disease should be considered in any newborn with delayed passage of meconium or in any child with a history of chronic constipation since birth. Other symptoms include bowel obstruction with bilious vomiting, abdominal distention, poor feeding, and failure to thrive.
  • Prenatal ultrasound demonstrating bowel obstruction is rare, except in cases of total colonic involvement.18
  • Older children with Hirschsprung disease have usually had chronic constipation since birth. They may also show evidence of poor weight gain.
  • Older presentation is more common in breastfed infants who will typically develop constipation around the time of weaning.
  • Despite significant constipation and abdominal distension, children with Hirschsprung disease rarely develop encopresis. In contrast, children with functional constipation or stool-withholding behaviors more commonly develop encopresis.
  • About 10% of children may present with diarrhea caused by enterocolitis, which is thought to be related to stasis and bacterial overgrowth. This may progress to colonic perforation, causing life-threatening sepsis.19
  • In a study of 259 consecutive patients, Menezes et al reported that 57% of patients presented with intestinal obstruction, 30% with constipation, 11% with enterocolitis, and 2% with intestinal perforation.20

Physical

  • Physical examination in the newborn period is usually not diagnostic, but it may reveal a distended abdomen and/or spasm of the anus.
  • A low imperforate anus with a perineal opening may have a similar presentation to that of a patient with Hirschsprung disease. Careful physical examination differentiates the two.
  • In older children, however, a distended abdomen resulting from an inability to release flatus is not uncommon.

Causes

See Pathophysiology.

More on Hirschsprung Disease

Overview: Hirschsprung Disease
Differential Diagnoses & Workup: Hirschsprung Disease
Treatment & Medication: Hirschsprung Disease
Follow-up: Hirschsprung Disease
Multimedia: Hirschsprung Disease
References
Further Reading

References

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Further Reading

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Keywords

Hirschsprung disease, Hirschsprung's disease, megacolon, colonic aganglionosis, ultrashort-segment Hirschsprung disease, congenital aganglionosis, aganglionic megacolon, acquired megacolon, congenital dilation of the colon, congenital megacolon, aganglionic megacolon, meconium, anorectal reflex, chronic constipation, enterocolitis, rectosigmoid colon aganglionosis, total colonic aganglionosis,
 
trisomy 21, Down syndrome, bowel obstruction, bilious vomiting, abdominal distention, poor feeding, failure to thrive, myenteric plexus, Auerbach plexus, submucosal plexus, Meissner plexus, colonic lavage, full-thickness rectal biopsy, simple suction rectal biopsy, anorectal manometry, diverting colostomy, Swenson procedure, Duhamel procedure, Soave procedure, anorectal myomectomy

Contributor Information and Disclosures

Author

Steven L Lee, MD, Chief, Pediatric Surgery, Department of Surgery, Kaiser-Permanente, Los Angeles Medical Center
Steven L Lee, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American College of Surgeons, American Pediatric Surgical Association, Association for Academic Surgery, Society of American Gastrointestinal and Endoscopic Surgeons, and Society of Laparoendoscopic Surgeons
Disclosure: Nothing to disclose.

Coauthor(s)

Shant Shekherdimian, MD, Consulting Surgeon, Department of Surgery, Kaiser Foundation Hospital
Disclosure: Nothing to disclose.

Jeffrey J DuBois, MD,, Chief of Children's Surgical Services, Division of Pediatric Surgery, Kaiser Permanente, Women and Children's Center, Roseville Medical Center
Jeffrey J DuBois, MD, is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American College of Surgeons, American Pediatric Surgical Association, and California Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Vivek V Gumaste, MD, Associate Professor of Medicine, Mt Sinai School of Medicine; Adjunct Clinical Assistant, Mt Sinai Hospital; Director, Division of Gastroenterology, City Hospital Center
Vivek V Gumaste, MD is a member of the following medical societies: American College of Gastroenterology and American Gastroenterological Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Oscar S Brann, MD, FACP, Associate Clinical Professor, Department of Medicine, University of California at San Diego; Consulting Staff, Mecklenburg Medical Group
Oscar S Brann, MD, FACP is a member of the following medical societies: American Gastroenterological Association
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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