Pediatric Rectal Prolapse 

  • Author: Jaime Shalkow, MD; Chief Editor: Carmen Cuffari, MD   more...
 
Updated: Dec 7, 2011
 

Background

Pediatric rectal prolapse is uncommon in Western societies. Most cases are self-limiting, characterized by prompt resolution with institution of conservative measures aimed at correcting associated underlying problems. Rectal prolapse in children is thought to begin as mucosal prolapse starting at the mucocutaneous junction, which may eventually progress to full-thickness prolapse. In the pediatric population, rectal prolapse should always be considered as a presenting sign of an underlying condition and not a discrete disease entity unto itself.

Prolapse of the rectum is one of the first surgical entities described in the medical profession. It can be defined as the protrusion of a few or all layers of the rectal wall through the anal sphincter (see the image below).

Image of young patient with full-thickness rectal Image of young patient with full-thickness rectal prolapse with multiple circular folds seen on exposed mucosa.

Rectal prolapse and its etiology were first described in 1912 by Moschcowitz. Rectal prolapse in childhood was first highlighted in 1939 by Lockhart-Mummery,[1] who attributed the condition to malnutrition and careless nursing but also acknowledged diarrheal and wasting illnesses as contributing factors. Lockhart-Mummery’s preferred operative treatment was linear cauterization of the prolapsed rectum, with recurrences treated by 5% phenol injection.

In adults, rectal prolapse is 6 times more frequent in females than in males. Almost all patients have a history of constipation (75%), which stretches the pelvic floor and the anal sphincter mechanism, predisposing them to rectal prolapse.

In children, the incidence is higher during the first year of life, after which it becomes increasingly infrequent. It is slightly more common in boys than in girls. Whether prolapse in children is predominantly mucosal prolapse (procidentia) rather than full-thickness prolapse is controversial.

Loss of the normal sacral curvature that causes a vertical tube between the rectum and the anal canal has been described as a causative factor. Straining during defecation predisposes children with constipation, diarrhea, or parasitosis and children who use laxatives to prolapse. About 60-70% of the patients have fecal incontinence.[2] The prolapse can spontaneously reduce, or it can be digitally reduced.

One classification of rectal prolapse divides the entity into true prolapse (protrusion of all layers of the rectum) and procidentia (herniation of only the mucosa). However, this classification is confusing and nonspecific and therefore should be abandoned.

The classification most widely used at present for rectal prolapse was described in 1971 by Altemeier et al, who divided the entity into the following 3 types[3] :

  • Type I - Protrusion of redundant mucosa, termed false prolapse; it is usually associated with hemorrhoids
  • Type II - Intussusception without sliding hernia of the cul-de-sac; it occupies the rectal ampulla but does not continue through the anal canal; the most common symptom is fecal incontinence, but solitary ulcers in the anterior rectal mucosa can be seen
  • Type III - Complete prolapse, including full-thickness rectal wall prolapse; it is associated with a sliding hernia of the Douglas pouch and is the most frequent type
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Anatomy

The anal canal extends cephalad from the anal verge to the anorectal ring. The rectum extends from this point to the sacral promontory.

Upon histologic examination, the anal canal consists of mucosa, submucosa, and 2 muscular layers: the internal anal sphincter (IAS), which is a continuation of the circular muscle of the rectum, and (2) the external anal sphincter (EAS), which lies outside the IAS as an elliptic cylinder and is continuous with the puborectalis muscle superiorly. The surgical anal canal includes this entire muscular sphincter mechanism (see the images below).

Levator ani muscle is shown in red. It includes ilLevator ani muscle is shown in red. It includes ileococcygeus (stretches during defecation and labor), pubococcygeus (maintains integrity of pelvic floor), and puborectalis (closes anorectal canal as sling) muscles. Deep, superficial, and subcutaneous external sphinDeep, superficial, and subcutaneous external sphincter. Anatomy of internal and external anal sphincter meAnatomy of internal and external anal sphincter mechanisms.

The many and varied procedures described for the treatment of rectal prolapse attempt to create a fixation of the anorectal mucosa and/or wall to the submucosa and/or perirectal tissues.

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Pathophysiology

A pelvic floor defect with levator ani muscle diastasis and a deep endopelvic fascia have been described. Patients with rectal prolapse have lost the normal semihorizontal rectal position; they also have weak insertions to the pelvic walls and sacrum, an abnormally deep Douglas pouch, a redundant rectosigmoid, and a weaker and wider anal sphincter.

The normal resting tone of the anal sphincter decreases in response to rectal distention. In 1962, Porter found that patients with rectal prolapse have a profound and lengthy response and weakened tone of the levator ani muscles.[4] Whether this is a causative factor or a secondary finding is not known, because the prolapse begins above the pelvic musculature.

Rectal prolapse has been associated with a myriad of conditions, including the following:

  • Increased intra-abdominal pressure due to straining (as often occurs in toilet training and constipation)
  • Parasitic disease (eg, trichuriasis, or whipworm) and neoplastic disease
  • Malnutrition (loss of ischiorectal fat pad) - Worldwide, this is possibly the most common condition associated with pediatric rectal prolapse; the loss of ischiorectal fat reduces perirectal support
  • Ulcerative colitis
  • Ehlers-Danlos syndrome
  • Meningomyelocele
  • Pertussis
  • Surgical repair of an anorectal malformation
  • Fecal incontinence and diarrhea[5, 6]
  • Chronic constipation[7]
  • Neuromuscular disorders
  • Mental challenge[8]
  • Poor sacral root innervation (as observed in patients with spina bifida)
  • Bladder or cloacal exstrophy[9]
  • Scleroderma[10]
  • Hirschsprung disease (especially in the ultrashort aganglionic segment, which acts as a subocclusion, favoring the appearance of rectal prolapse)[11]
  • Rectal polyps (in which the polyp acts as a leading point for the intussusception)[12]
  • Cystic fibrosis[13]
  • Shigellosis in neonates[14]

Cystic fibrosis deserves a special mention; rectal prolapse is found in as many as one fifth of cystic fibrosis patients and is the presenting symptom in one third. Potential mechanisms in which this condition predisposes an individual to prolapse include voluminous or bulky bowel movements, coughing paroxysms, and undernutrition.[15]

Other implicated entities include lymphoid hyperplasia of the distal colon, which also acts as a leading point for the rectal intussusception,[16] parasites and infectious agents,[17, 18, 19] and HIV infection.[20]

Most cases of childhood prolapse occur in patients younger than 4 years, with the highest incidence in the first year of life. Anatomic considerations related to this early presentation include the vertical course of the rectum along the straight surface of the sacrum and coccyx, the relatively low position of the rectum in relation to other pelvic organs, the increased mobility of the sigmoid colon, the relative lack of support by the levator ani muscle, the loose attachment of the rectal mucosa to the underlying muscularis, and the absence of Houston valves in about 75% of infants.

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Etiology

The exact etiology of rectal prolapse in children is unknown. However, several predisposing factors have been identified. The most common underlying condition is chronic constipation and straining (52%).

Other causes include diarrhea (15%),[5] rectal parasites[21] (the most common cause of rectal prolapse in the developing world), neuromuscular disorders, pelvic nerve disorders, myelomeningocele, bladder and cloacal exstrophy, Hirschsprung disease, high anorectal malformations, cystic fibrosis, chronic respiratory infections and coughing,[22] lymphoid hyperplasia, rectal polyps, and shigellosis.

Broden and Snellman proposed a theory to explain the etiology of rectal prolapse.[23] They cineradiographically demonstrated that the entity implies a circumferential intussusception of the rectum, with its origin 3 inches above the anal margin.

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Epidemiology

Pediatric rectal prolapse is an uncommon entity in the United States and other industrialized countries.[24] It was more common 50 years ago than it is now, and this decreased occurrence is thought to be due to improved nutrition and hygiene in industrialized countries. Pediatric rectal prolapse is more common in tropical and underdeveloped countries, where diarrhea and parasitic infection play much greater roles.

In the pediatric population, rectal prolapse is most common in patients younger than 4 years; the highest incidence is in the first year of life. Incidence is evenly distributed between males and females in the pediatric population. This is in contrast to the adult population, in whom rectal prolapse is 6 times more common in women. No racial predilection is noted in the pediatric population.

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Prognosis

Most prolapses spontaneously reduce. Failure to reduce may lead to venous stasis, edema, and possibly ulceration. Long-standing or frequent recurrent prolapse may lead to proctitis.

Approximately 10% of patients who experience rectal prolapse as children continue to experience it in their adult lives. Approximately 90% of children aged 9 months to 3 years who experience rectal prolapse respond to conservative management by age 6 years. Spontaneous resolution is much less likely in children who first experience prolapse when they are older than 4 years.

After a surgical rectopexy, continence can be achieved in as many as 92% of patients. Resective procedures are associated with decreased recurrence rates. Recovery of continence after surgery is not immediate and may take as long as 12 months.

Nwako et al reported a 100% success rate with the Lockhart-Mummery procedure, which involves packing the presacral space with gauze through a posterior approach and excision of the prolapsed mucosa.[25]

Hight et al recommend linear rectal cauterization of the anorectal mucosa; they achieved a 98% success rate in 72 patients.[26]

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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

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

Disclosure: Nothing to disclose.

Coauthor(s)

Brian F Gilchrist, MD  Surgeon-in-Chief of Pediatric Surgery, The Floating Hospital for Children at Tufts-New England Medical Center; Associate Professor, Department of Surgery, Tufts University School of Medicine

Brian F Gilchrist, MD is a member of the following medical societies: American College of Surgeons, American Pediatric Surgical Association, and Society for Surgery of the Alimentary Tract

Disclosure: Nothing to disclose.

Jose Ignacio Guzman, MD  Medical Staff, Medical and Surgical Patient Care, General Hospital of Mexico; Medical Staff, Pediatric Surgical Oncology, National Institute of Pediatrics, 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, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Additional Contributors

Robert Baldassano, MD Director, Center for Pediatric Inflammatory Bowel Disease, Children's Hospital of Philadelphia; Professor, Department of Pediatrics, Division of Gastroenterology and Nutrition, University of Pennsylvania School of Medicine

Robert Baldassano, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Deborah F Billmire, MD Associate Professor, Department of Surgery, Indiana University Medical Center

Deborah F Billmire, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American College of Surgeons, American Pediatric Surgical Association, Phi Beta Kappa, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Rebeccah Brown, MD Associate Director of Trauma Services, Associate Professor, Department of Clinical Surgery and Pediatrics, Cincinnati Children's Hospital Medical Center and University of Cincinnati Hospital

Rebeccah Brown, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, and American Medical Women's Association

Disclosure: Nothing to disclose.

Frank Cunningham, Jr, MD, FAAP, FACEP Director, Division of Emergency Pediatrics, Assistant Professor, Department of Pediatrics, University of Medicine and Dentistry of New Jersey

Frank Cunningham, Jr, MD, FAAP, FACEP is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Joel A Friedlander, DO, MBe Instructor, Department of Pediatrics, University of Pennsylvania School of Medicine; Fellow, Pediatric Gastroenterology, Division of Gastroenterology, Hepatology and Nutrition, Children's Hospital of Philadelphia

Joel A Friedlander, DO, MBe is a member of the following medical societies: American Academy of Pediatrics, American Association for the Study of Liver Diseases, American College of Osteopathic Pediatricians, American Gastroenterological Association, American Medical Association, American Osteopathic Association, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Leon M Garner, DO, MPH Staff Physician, Department of Emergency Medicine, North Broward Medical Center

Leon M Garner, DO, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and American College of Osteopathic Emergency Physicians

Disclosure: Nothing to disclose.

Harsh Grewal, MD, FACS, FAAP Professor of Surgery and Pediatrics, Temple University School of Medicine; Chief, Section of Pediatric Surgery, Temple University School of Medicine

Harsh Grewal, MD, FACS, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Surgeons, American Pediatric Surgical Association, Association for Surgical Education, Children's Oncology Group, Eastern Association for the Surgery of Trauma, International Pediatric Endosurgery Group, Society of American Gastrointestinal and Endoscopic Surgeons, Society of Laparoendoscopic Surgeons, and SouthwesternSurgical Congress

Disclosure: Nothing to disclose.

Marc S Lessin, MD Consulting Surgeon, Children's Surgical Associates, PC

Marc S Lessin, MD is a member of the following medical societies: American College of Surgeons and American Pediatric Surgical Association

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.

Maria Rebello Mascarenhas, MBBS Associate Professor of Pediatrics, University of Pennsylvania School of Medicine; Section Chief of Nutrition, Division of Gastroenterology and Nutrition, Director, Nutrition Support Service, Children's Hospital of Philadelphia

Maria Rebello Mascarenhas, MBBS is a member of the following medical societies: American Gastroenterological Association, American Society for Parenteral and Enteral 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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Image of young patient with full-thickness rectal prolapse with multiple circular folds seen on exposed mucosa.
Photograph of severe rectal prolapse with clinically significant edema and mucosal ulceration.
Picture of infant with full-thickness rectal prolapse. Severe edema and abundant mucus are seen on mucosal surface.
Levator ani muscle is shown in red. It includes ileococcygeus (stretches during defecation and labor), pubococcygeus (maintains integrity of pelvic floor), and puborectalis (closes anorectal canal as sling) muscles.
Deep, superficial, and subcutaneous external sphincter.
Anatomy of internal and external anal sphincter mechanisms.
Image demonstrates mucosal prolapse, with radial folds seen on mucosa.
Diagram depicting clinical difference between true (full-thickness) prolapse (left), including all layers of rectum and with circular folds seen on prolapsed intestine, and procidentia, or mucosa-only prolapse (right), in which radial folds are seen in mucosa.
Thiersch procedure. Perianal subcutaneous sutures create mechanical barrier for prolapse.
Lomas and Cooperman modified Thiersch procedure by performing right anterior and left posterior radial incisions, encircling anus with Marlex mesh stripe, and tying it around finger placed on anal canal. Care must be taken to avoid perforating posterior vaginal wall or anterior rectal wall. Skin is closed, with mesh left subcutaneously.
Ripstein procedure is designed to maintain normal posterior rectal curvature by attaching it to presacral fascia, thus avoiding straight tube that intussuscepts during straining. (A) Rectum is mobilized down to coccyx. (B) Marlex mesh is placed around rectum while this is tensed upward and sutured to presacral fascia with nonabsorbable material. Mesh loop must be loose enough to prevent postoperative constipation. (C) Sagittal view shows suspended rectum. (D) Peritoneum is closed with a continuous absorbable suture.
Intraoperative photograph of 12-year-old girl with recurrent rectal prolapse and mucosal ulceration with profuse bleeding. She had long sigmoid colon, which was resected; end-to-end anastomosis was performed. This photograph depicts anastomosed rectum fixed to presacral fascia with mesh. Nonabsorbable sutures retain mesh to serosa. Note that mesh is slightly loose to allow for child's growth. Uterus and its ligaments can be seen in front of rectum. Iliac vessels remain intact on each side.
Ivalon sponge procedure. (A) Rectum is mobilized. Meticulous hemostasis is mandatory to prevent hematoma that predisposes patient to prosthetic material infection. (B) Ivalon rectangular sponge made of polyvinyl alcohol is sutured to sacral periosteum. (C) Rectum is retracted upward, and sponge is wrapped around it and tied to anterior surface. Portion of anterior rectal wall is left free to prevent luminal obliteration. (D) Peritoneum is closed with continuous absorbable suture.
 
 
 
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