Pediatric Rectal Prolapse: Practice Essentials, Background, Anatomy (original) (raw)

Practice Essentials

Rectal prolapse refers to the circumferential extrusion of some or the entire rectal wall through the external anal sphincter. [1] Although, less common in Western societies, pediatric rectal prolapse is a relatively common benign disorder in children. However, without proper treatment, it can become a lifestyle limiting chronic condition. Most cases are self-limiting, with prompt resolution after conservative measures aimed at correcting the associated underlying process.

In children, rectal prolapse should always be considered a presenting sign of an underlying condition, and not a disease entity unto itself. Rectal prolapse starts as a mucosal extrusion from the mucocutaneous junction, which may eventually progress to full-thickness prolapse.

Rectal prolapse starts as a mucosal extrusion from the mucocutaneous junction, which may eventually progress to full-thickness prolapse. It is one of the first surgical entities ever described in medicine. (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 and Mummery [2] , who attributed the condition to malnutrition and careless nursing, but also acknowledged diarrheal disease 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.

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 to prolapse, as does childhood laxative usage. About 60%-70% of patients have fecal incontinence. [3] The prolapse can spontaneously reduce or may require digital reduction.

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Background

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, fallen out of use.

The most used classification for rectal prolapse was described in 1971 by Altemeier et al, who divided the entity into the following types [4] :

Type I Protrusion of redundant mucosa, termed false prolapse; 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, full-thickness rectal wall prolapse, associated with a sliding hernia of the Douglas pouch. It is the most frequent type.

Types II and III can be further subdivided into three degrees [5] :

First degree prolapse includes the mucocutaneous junction. The length of the protrusion from the anal verge usually is greater than 5cm.

Second degree prolapse occurs without involvement of the mucocutaneous junction. The length of the protrusion from the anal verge usually is between 2 and 5 cm.

Third degree prolapse is internal concealed or occult, and does not pass through the anal verge.

For the particular case of rectal prolapse occurring after the surgical correction of an anorectal malformation, [6] the entity can also be classified as:

Minimal, when the rectal mucosa was visible at the anal verge with Valsalva manoeuvre

Moderate, when there was a protrusion of the rectal mucosa inferior to 5 mm without the Valsalva manoeuvre; and

Evident, when the mucosal protrusion was greater than 5 mm without the Valsalva manoeuvre

The entity can also be categorized as circumferential,when it affects the rectum for 360o and hemi-circumferential, when the rectum is affected for less than 180o. [6] Most patients (77%) with rectal prolapse presenting after anorectoplasty can be successfully managed with conservative treatment. [6]

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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 [3] the external anal sphincter (EAS), which lies outside the IAS as an elliptic cylinder, 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 il

Levator ani muscle is shown in red. It includes ileococcygeus (stretches during defecation and labor), pubococcygeus (maintains integrity of pelvic floor), and puborectalis muscles (closes the anorectal canal as a sling).

Deep, superficial, and subcutaneous external sphin

Deep, superficial, and subcutaneous external sphincter.

Anatomy of internal and external anal sphincter me

Anatomy 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 to the submucosa, or the rectal wall to perirectal tissues.

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Pathophysiology

Children are predisposed to rectal prolapse due to anatomic considerations: A pelvic floor defect with levator ani muscle diastasis and a deep endopelvic fascia represent the pathophysiology of the disease. Patients with rectal prolapse have lost the normal semi-horizontal rectal position; they also have weak muscle insertions to the pelvic walls and sacrum, an abnormally deep Douglas pouch and Houston’s valves absence in approximately 75% of infants younger than 1 year of age. [7] A redundant rectosigmoid and weaker / wider anal sphincter are common.

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. [8] Whether this is a causative factor or a secondary finding is not clear, since the prolapse begins above the pelvic musculature. Most recently, information has suggested that rectal prolapse can be developed as a result of circumferential intussusception of the upper rectum and rectosigmoid colon. [7]

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

Cystic fibrosis (CF) deserves special attention as it may cause rectal prolapse in children. In the past, rectal prolapse was described in up to 20% of individuals with cystic fibrosis. However, current reports estimate an incidence of 3% of children with the disease. [18, 19] Potential mechanisms include bulky bowel movements, coughing paroxysms, and undernutrition. It is most frequently seen in toddlers, but it can occur at any age (triggered by cough). Clinical clues to cystic fibrosis include oily, malodorous, or floating stools; poor growth; wheezing or other respiratory symptoms; and digital clubbing. The absence of respiratory symptoms and normal findings upon physical examination do not necessarily exclude this diagnostic possibility. Sweat chloride test should be performed in order to rule out cystic fibrosis.

Most cases of childhood rectal prolapse occur in children younger than 4 years, with the highest incidence during 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, a relatively low position of the rectum in relation to other pelvic organs, increased mobility of the sigmoid colon, relative lack of support by the levator ani muscle, loose attachment of the rectal mucosa to the underlying muscularis, and absence of Houston valves, seen in about 75% of infants.

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Etiology

Several predisposing factors have been identified, chronic constipation and straining being most common (52%). Other causes include diarrhea (15%), [9] rectal parasites, [20] malnutrition, [7] neuromuscular and pelvic nerve disorders, myelomeningocele, bladder and cloacal exstrophy, Hirschsprung disease, behavioral and psychological disorders, [21] high anorectal malformations, [22] cystic fibrosis, chronic respiratory infections and cough, [23] lymphoid hyperplasia, rectal polyps, and shigellosis. [24] Rectal prolapse has also been described in a case of Clostridium difficile –associated pseudomembranous colitis in a child. [22]

Hill et al. evaluated 39 patients for associated behavioral/psychiatric disorders. Of these, they identified 21 (54%) children with one or more behavioral or psychological disorders (ADHD, anxiety disorder, depression, encopresis/stool withholding). They concluded there’s a high rate (over 50%) incidence of behavioral and psychological disorders in older (3-18 years) children presenting with rectal prolapse. However, there is scant published literature identifying a high rate of BPD in prolapsed children. [25]

Broden and Snellman demonstrated by cineradiography, that the entity implies a circumferential intussusception of the rectum, with its origin three inches above the anal margin. [26]

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Epidemiology

In adults, rectal prolapse is six times more common in females than in males. 75% of patients have history of constipation, which stretches the pelvic floor and the anal sphincter mechanism, predisposing them to the disease.

In children, 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 and usually occurs between infancy and 4 years of age.

Rentea and St. Peter, proposed the following risk factors for rectal prolapse [7] :

As mentioned before, the cystic fibrosis group deserves special interest. An earlier review of CF revealed that 23% of patients with CF experienced rectal prolapse and that 78% of these patients experiencing rectal prolapse before the diagnosis of CF. This led to the recommendation that CF should be considered in a child with rectal prolapse of unknown etiology. [1]

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Prognosis

Most cases reduce spontaneously. Otherwise, venous stasis, edema, and ulceration ensure. Longstanding or frequent recurrent prolapse episodes lead to proctitis.

Approximately 10% of patients who experience rectal prolapse as children continue to be symptomatic into adulthood. Over 90% of children who prolapsed during the first 3 years of life, respond to conservative treatment by age 6. It is important to achieve this early because the more episodes of rectal prolapse, especially, those cases that do not reduce spontaneously or have difficult reduction, demonstrate a lesser response to conservative management. [27] Spontaneous resolution is much less likely in children who develop their first episode of prolapse after age 4 years. After a surgical rectopexy, continence is achieved in 92% of patients. Resective procedures demonstrate lower recurrence rates.

Recovery of continence after surgery is not immediate, it may take up to a year.

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, with excision of the prolapsed mucosa. [24]

Hight et al recommend linear cauterization of the rectal mucosa, with a 98% success rate in 72 patients. [28]

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Author

Jaime Shalkow, MD, FACS Pediatric Surgical Oncologist, ABC Cancer Center; Associated Researcher, Anahuac University, Mexico

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

Disclosure: Nothing to disclose.

Coauthor(s)

Pablo Magaña Mainero, MD General and Laparoscopic Surgeon, ABC Medical Center; Assistant Director, General Hospital of Mexico “Dr Eduardo Liceaga”, Mexico

Pablo Magaña Mainero, MD is a member of the following medical societies: American College of Surgeons, Mexican Association for Endoscopic Surgery, Mexican Association of General Surgery, Mexican Hepato Pancreato Biliary Association

Disclosure: Nothing to disclose.

Andrés Olivares Ronces, MD Assistant Surgeon, Centro Médico ABC Campus Observatorio, 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. for: Abbott Nutritional, Abbvie, speakers' bureau.

Additional Contributors

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.

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.

Issac Octavio Vargas Olmos Universidad Anahuac, Mexico

Disclosure: Nothing to disclose.

Shahida Bibi, MD Resident Physician, Department of Surgery, Bronx-Lebanon Hospital Center

Disclosure: Nothing to disclose.

Acknowledgements

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.