Showing posts with label bowel disorders. Show all posts
Showing posts with label bowel disorders. Show all posts
Monday, April 07, 2014
Thursday, April 03, 2014
Sunday, December 15, 2013
Intestinal obstructions
Intestinal obstruction is a partial or complete blockage of the bowel that prevents the contents of the intestine from passing through.
Causes, incidence, and risk factors
Obstruction of the bowel may due to:
- A mechanical cause, which means something is in the way
- Ileus, a condition in which the bowel doesn't work correctly but there is no structural problem
Paralytic ileus, also called pseudo-obstruction, is one of the major causes of intestinal obstruction in infants and children. Causes of paralytic ileus may include:
- Bacteria or viruses that cause intestinal infections (gastroenteritis)
- Chemical, electrolyte, or mineral imbalances (such as decreased potassium levels)
- Complications of abdominal surgery
- Decreased blood supply to the intestines (mesenteric ischemia)
- Infections inside the abdomen, such as appendicitis
- Kidney or lung disease
- Use of certain medications, especially narcotics
Mechanical causes of intestinal obstruction may include:
- Adhesions or scar tissue that forms after surgery
- Foreign bodies (eaten materials that block the intestines)
- Gallstones (rare)
- Hernias
- Impacted stool
- Intussusception (telescoping of one segment of bowel into another)
- Tumors blocking the intestines
- Volvulus (twisted intestine)
Symptoms
- Abdominal swelling (distention)
- Abdominal fullness, gas
- Abdominal pain and cramping
- Breath odor
- Constipation
- Diarrhea
- Inability to pass gas
- Vomiting
Signs and tests
During a physical exam, the health care provider may find bloating, tenderness, or hernias in the abdomen.
Tests that show obstruction include:
- Abdominal CT scan
- Abdominal x-ray
- Barium enema
- Upper GI and small bowel series
Treatment
Treatment involves placing a tube through the nose into the stomach or intestine to help relieve abdominal swelling (distention) and vomiting. Volvulus of the large bowel may be treated by passing a tube into the rectum.
Surgery may be needed to relieve the obstruction if the tube does not relieve the symptoms, or if there are signs of tissue death.
Expectations (prognosis)
The outcome depends on the cause of the blockage. Most of the time the cause is easily treated.
Complications
Complications may include or may lead to:
- Electrolyte (blood chemical and mineral) imbalances
- Dehydration
- Hole (perforation) in the intestine
- Infection
- Jaundice (yellowing of the skin and eyes)
If the obstruction blocks the blood supply to the intestine, it may cause infection and tissue death (gangrene). Risks for tissue death are related to the cause of the blockage and how long it has been present. Hernias, volvulus, and intussusception carry a higher gangrene risk.
In a newborn, paralytic ileus that destroys the bowel wall (necrotizing enterocolitis) is life-threatening and may lead to blood and lung infections.
Calling your health care provider
Call your health care provider if you:
- Cannot pass stool or gas
- Have a swollen abdomen (distention) that does not go away
- Keep vomiting
Prevention
Prevention depends on the cause. Treating conditions, such as tumors and hernias, that can lead to obstruction may reduce your risk of getting an obstruction.
Some causes of obstruction cannot be prevented.
References
- McKenzie S, Evers BM. Small intestine. In: Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 19th ed. St. Louis, Mo: WB Saunders; 2012:chap 50.
- Fry RD, Mahmoud N, Maron DJ, Bleier JIS. Colon and rectum. In: Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 19th ed. St. Louis, Mo: WB Saunders; 2012:chap 52.
- Turnage RH, Heldmann M. Intestinal obstruction. In: Feldman M, Friedman LS, Brandt LJ, eds. Sleisenger & Fordtran's Gastrointestinal and Liver Disease. 9th ed. Philadelphia, Pa: Saunders Elsevier; 2010:chap 119.
- Review Date: 7/25/2012.Reviewed by: Jacob L. Heller, MD, MHA, Emergency Medicine, Virginia Mason Medical Center, Seattle, Washington; and Joshua Kunin, MD, Consulting Colorectal Surgeon, Zichron Yaakov, Israel. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M. Health Solutions, Ebix, Inc.
Thursday, February 02, 2012
Thursday, January 26, 2012
About Adhesion Related Disorder ~ How can abdominal adhesions cause intestinal obstruction?
Abdominal Adhesions
On this page:
•What are abdominal adhesions?
•What causes abdominal adhesions?
•How can abdominal adhesions cause intestinal obstruction?
•How can abdominal adhesions cause female infertility?
•What are the symptoms of abdominal adhesions?
•What are the symptoms of an intestinal obstruction?
•How are abdominal adhesions and intestinal obstructions diagnosed?
•How are abdominal adhesions and intestinal obstructions treated?
•Can abdominal adhesions be prevented?
•Points to Remember
•Hope through Research
•For More Information
What are abdominal adhesions?
Abdominal adhesions are bands of tissue that form between abdominal tissues and organs. Normally, internal tissues and organs have slippery surfaces, which allow them to shift easily as the body moves. Adhesions cause tissues and organs to stick together.
The intestines are part of the digestive system. Abdominal adhesions can cause an intestinal obstruction.
Although most adhesions cause no symptoms or problems, others cause chronic abdominal or pelvic pain. Adhesions are also a major cause of intestinal obstruction and female infertility.
What causes abdominal adhesions?
Abdominal surgery is the most frequent cause of abdominal adhesions. Almost everyone who undergoes abdominal surgery develops adhesions; however, the risk is greater after operations on the lower abdomen and pelvis, including bowel and gynecological surgeries. Adhesions can become larger and tighter as time passes, causing problems years after surgery.
Surgery-induced causes of abdominal adhesions include
•tissue incisions, especially those involving internal organs
•the handling of internal organs
•the drying out of internal organs and tissues
•contact of internal tissues with foreign materials, such as gauze, surgical gloves, and stitches
•blood or blood clots that were not rinsed out during surgery
A less common cause of abdominal adhesions is inflammation from sources not related to surgery, including
•appendicitis—in particular, appendix rupture
•radiation treatment for cancer
•gynecological infections
•abdominal infections
Rarely, abdominal adhesions form without apparent cause.
How can abdominal adhesions cause intestinal obstruction?
Abdominal adhesions can kink, twist, or pull the intestines out of place, causing an intestinal obstruction. An intestinal obstruction partially or completely restricts the movement of food or stool through the intestines. A complete intestinal obstruction is life threatening and requires immediate medical attention and often surgery.
How can abdominal adhesions cause female infertility?
Abdominal adhesions cause female infertility by preventing fertilized eggs from reaching the uterus, where fetal development takes place. Adhesions can kink, twist, or pull out of place the fallopian tubes, which carry eggs from the ovaries—where eggs are stored and released—to the uterus.
What are the symptoms of abdominal adhesions?
Although most abdominal adhesions go unnoticed, the most common symptom is chronic abdominal or pelvic pain. The pain often mimics that of other conditions, including appendicitis, endometriosis, and diverticulitis.
What are the symptoms of an intestinal obstruction?
Symptoms of an intestinal obstruction include
•severe abdominal pain or cramping
•vomiting
•bloating
•loud bowel sounds
•swelling of the abdomen
•inability to pass gas
•constipation
A person with these symptoms should seek medical attention immediately.
How are abdominal adhesions and intestinal obstructions diagnosed?
No tests are available to diagnose adhesions, and adhesions cannot be seen through imaging techniques such as x rays or ultrasound. Most adhesions are found during exploratory surgery. An intestinal obstruction, however, can be seen through abdominal x rays, barium contrast studies—also called a lower GI series—and computerized tomography.
How are abdominal adhesions and intestinal obstructions treated?
Treatment for abdominal adhesions is usually not necessary, as most do not cause problems. Surgery is currently the only way to break adhesions that cause pain, intestinal obstruction, or fertility problems. More surgery, however, carries the risk of additional adhesions and is avoided when possible.
A complete intestinal obstruction usually requires immediate surgery. A partial obstruction can sometimes be relieved with a liquid or low-residue diet. A low-residue diet is high in dairy products, low in fiber, and more easily broken down into smaller particles by the digestive system.
Can abdominal adhesions be prevented?
Abdominal adhesions are difficult to prevent; however, surgical technique can minimize adhesions.
Laparoscopic surgery avoids opening up the abdomen with a large incision. Instead, the abdomen is inflated with gas while special surgical tools and a video camera are threaded through a few, small abdominal incisions. Inflating the abdomen gives the surgeon room to operate.
If a large abdominal incision is required, a special filmlike material (Seprafilm) can be inserted between organs or between the organs and the abdominal incision at the end of surgery. The filmlike material, which looks similar to wax paper, is absorbed by the body in about a week.
Other steps during surgery to reduce adhesion formation include using starch- and latex-free gloves, handling tissues and organs gently, shortening surgery time, and not allowing tissues to dry out.
Points to Remember
•Abdominal adhesions are bands of tissue that form between abdominal tissues and organs, causing tissues and organs to stick together.
•Although most adhesions cause no symptoms or problems, others cause chronic abdominal or pelvic pain, bowel obstruction, or female infertility.
•Abdominal surgery is the most frequent cause of abdominal adhesions.
•Abdominal adhesions can kink, twist, or pull the intestines out of place, causing an intestinal obstruction.
•A complete intestinal obstruction is life threatening and requires immediate medical attention and often surgery.
•Abdominal adhesions cause female infertility by preventing fertilized eggs from reaching the uterus, where fetal development takes place.
•No tests are available to diagnose adhesions, and adhesions cannot be seen through imaging techniques such as x rays or ultrasound.
•An intestinal obstruction can be seen through abdominal x rays, barium contrast studies—also called a lower GI series—and computerized tomography.
•Surgery is currently the only way to break adhesions that cause pain, intestinal obstruction, or fertility problems.
Hope through Research
The National Institute of Diabetes and Digestive and Kidney Diseases conducts and supports basic and clinical research into many digestive disorders.
Participants in clinical trials can play a more active role in their own health care, gain access to new research treatments before they are widely available, and help others by contributing to medical research. For information about current studies, visit http://www.clinicaltrials.gov/.
The U.S. Government does not endorse or favor any specific commercial product or company. Trade, proprietary, or company names appearing in this document are used only because they are considered necessary in the context of the information provided. If a product is not mentioned, the omission does not mean or imply that the product is unsatisfactory.
For More Information
American College of Gastroenterology
P.O. Box 342260
Bethesda, MD 20827–2260
Phone: 301–263–9000
Fax: 301–263–9025
Email: info@acg.gi.org
Internet: www.acg.gi.org
International Foundation for Functional Gastrointestinal Disorders
P.O. Box 170864
Milwaukee, WI 53217–8076
Phone: 1–888–964–2001 or 414–964–1799
Fax: 414–964–7176
Email: iffgd@iffgd.org
Internet: www.iffgd.org
You may also find additional information about this topic by visiting MedlinePlus at www.medlineplus.gov.
This publication may contain information about medications. When prepared, this publication included the most current information available. For updates or for questions about any medications, contact the U.S. Food and Drug Administration toll-free at 1–888–INFO–FDA (1–888–463–6332) or visit www.fda.gov. Consult your doctor for more information.
http://digestive.niddk.nih.gov/ddiseases/pubs/intestinaladhesions/
On this page:
•What are abdominal adhesions?
•What causes abdominal adhesions?
•How can abdominal adhesions cause intestinal obstruction?
•How can abdominal adhesions cause female infertility?
•What are the symptoms of abdominal adhesions?
•What are the symptoms of an intestinal obstruction?
•How are abdominal adhesions and intestinal obstructions diagnosed?
•How are abdominal adhesions and intestinal obstructions treated?
•Can abdominal adhesions be prevented?
•Points to Remember
•Hope through Research
•For More Information
What are abdominal adhesions?
Abdominal adhesions are bands of tissue that form between abdominal tissues and organs. Normally, internal tissues and organs have slippery surfaces, which allow them to shift easily as the body moves. Adhesions cause tissues and organs to stick together.
The intestines are part of the digestive system. Abdominal adhesions can cause an intestinal obstruction.
Although most adhesions cause no symptoms or problems, others cause chronic abdominal or pelvic pain. Adhesions are also a major cause of intestinal obstruction and female infertility.
What causes abdominal adhesions?
Abdominal surgery is the most frequent cause of abdominal adhesions. Almost everyone who undergoes abdominal surgery develops adhesions; however, the risk is greater after operations on the lower abdomen and pelvis, including bowel and gynecological surgeries. Adhesions can become larger and tighter as time passes, causing problems years after surgery.
Surgery-induced causes of abdominal adhesions include
•tissue incisions, especially those involving internal organs
•the handling of internal organs
•the drying out of internal organs and tissues
•contact of internal tissues with foreign materials, such as gauze, surgical gloves, and stitches
•blood or blood clots that were not rinsed out during surgery
A less common cause of abdominal adhesions is inflammation from sources not related to surgery, including
•appendicitis—in particular, appendix rupture
•radiation treatment for cancer
•gynecological infections
•abdominal infections
Rarely, abdominal adhesions form without apparent cause.
How can abdominal adhesions cause intestinal obstruction?
Abdominal adhesions can kink, twist, or pull the intestines out of place, causing an intestinal obstruction. An intestinal obstruction partially or completely restricts the movement of food or stool through the intestines. A complete intestinal obstruction is life threatening and requires immediate medical attention and often surgery.
How can abdominal adhesions cause female infertility?
Abdominal adhesions cause female infertility by preventing fertilized eggs from reaching the uterus, where fetal development takes place. Adhesions can kink, twist, or pull out of place the fallopian tubes, which carry eggs from the ovaries—where eggs are stored and released—to the uterus.
What are the symptoms of abdominal adhesions?
Although most abdominal adhesions go unnoticed, the most common symptom is chronic abdominal or pelvic pain. The pain often mimics that of other conditions, including appendicitis, endometriosis, and diverticulitis.
What are the symptoms of an intestinal obstruction?
Symptoms of an intestinal obstruction include
•severe abdominal pain or cramping
•vomiting
•bloating
•loud bowel sounds
•swelling of the abdomen
•inability to pass gas
•constipation
A person with these symptoms should seek medical attention immediately.
How are abdominal adhesions and intestinal obstructions diagnosed?
No tests are available to diagnose adhesions, and adhesions cannot be seen through imaging techniques such as x rays or ultrasound. Most adhesions are found during exploratory surgery. An intestinal obstruction, however, can be seen through abdominal x rays, barium contrast studies—also called a lower GI series—and computerized tomography.
How are abdominal adhesions and intestinal obstructions treated?
Treatment for abdominal adhesions is usually not necessary, as most do not cause problems. Surgery is currently the only way to break adhesions that cause pain, intestinal obstruction, or fertility problems. More surgery, however, carries the risk of additional adhesions and is avoided when possible.
A complete intestinal obstruction usually requires immediate surgery. A partial obstruction can sometimes be relieved with a liquid or low-residue diet. A low-residue diet is high in dairy products, low in fiber, and more easily broken down into smaller particles by the digestive system.
Can abdominal adhesions be prevented?
Abdominal adhesions are difficult to prevent; however, surgical technique can minimize adhesions.
Laparoscopic surgery avoids opening up the abdomen with a large incision. Instead, the abdomen is inflated with gas while special surgical tools and a video camera are threaded through a few, small abdominal incisions. Inflating the abdomen gives the surgeon room to operate.
If a large abdominal incision is required, a special filmlike material (Seprafilm) can be inserted between organs or between the organs and the abdominal incision at the end of surgery. The filmlike material, which looks similar to wax paper, is absorbed by the body in about a week.
Other steps during surgery to reduce adhesion formation include using starch- and latex-free gloves, handling tissues and organs gently, shortening surgery time, and not allowing tissues to dry out.
Points to Remember
•Abdominal adhesions are bands of tissue that form between abdominal tissues and organs, causing tissues and organs to stick together.
•Although most adhesions cause no symptoms or problems, others cause chronic abdominal or pelvic pain, bowel obstruction, or female infertility.
•Abdominal surgery is the most frequent cause of abdominal adhesions.
•Abdominal adhesions can kink, twist, or pull the intestines out of place, causing an intestinal obstruction.
•A complete intestinal obstruction is life threatening and requires immediate medical attention and often surgery.
•Abdominal adhesions cause female infertility by preventing fertilized eggs from reaching the uterus, where fetal development takes place.
•No tests are available to diagnose adhesions, and adhesions cannot be seen through imaging techniques such as x rays or ultrasound.
•An intestinal obstruction can be seen through abdominal x rays, barium contrast studies—also called a lower GI series—and computerized tomography.
•Surgery is currently the only way to break adhesions that cause pain, intestinal obstruction, or fertility problems.
Hope through Research
The National Institute of Diabetes and Digestive and Kidney Diseases conducts and supports basic and clinical research into many digestive disorders.
Participants in clinical trials can play a more active role in their own health care, gain access to new research treatments before they are widely available, and help others by contributing to medical research. For information about current studies, visit http://www.clinicaltrials.gov/.
The U.S. Government does not endorse or favor any specific commercial product or company. Trade, proprietary, or company names appearing in this document are used only because they are considered necessary in the context of the information provided. If a product is not mentioned, the omission does not mean or imply that the product is unsatisfactory.
For More Information
American College of Gastroenterology
P.O. Box 342260
Bethesda, MD 20827–2260
Phone: 301–263–9000
Fax: 301–263–9025
Email: info@acg.gi.org
Internet: www.acg.gi.org
International Foundation for Functional Gastrointestinal Disorders
P.O. Box 170864
Milwaukee, WI 53217–8076
Phone: 1–888–964–2001 or 414–964–1799
Fax: 414–964–7176
Email: iffgd@iffgd.org
Internet: www.iffgd.org
You may also find additional information about this topic by visiting MedlinePlus at www.medlineplus.gov.
This publication may contain information about medications. When prepared, this publication included the most current information available. For updates or for questions about any medications, contact the U.S. Food and Drug Administration toll-free at 1–888–INFO–FDA (1–888–463–6332) or visit www.fda.gov. Consult your doctor for more information.
http://digestive.niddk.nih.gov/ddiseases/pubs/intestinaladhesions/
Thursday, January 19, 2012
Barrier agents for adhesion prevention after gynaecological surgery.
Cochrane Database Syst Rev. 2008 Apr 16;(2):CD000475.
Barrier agents for adhesion prevention after gynaecological surgery.
Ahmad G, Duffy JM, Farquhar C, Vail A, Vandekerckhove P, Watson A, Wiseman D.
SourceStepping Hill Hospital, Obstetric & Gynaecology, 30 Badger Road, Altrincham, Cheshire, UK, WA14 5UZ. gaityahmad@hotmail.com
Abstract
BACKGROUND: Pelvic adhesion can form as a result of inflammation, endometriosis or surgical trauma. During pelvic surgery, strategies to reduce pelvic adhesion formation may include placing synthetic barrier agents such as oxidised regenerated cellulose, polytetrafluoroethylene or Fibrin sheets between the pelvic structures.
OBJECTIVES: To assess the effect of physical barriers used during pelvic surgery in women of reproductive age on pregnancy rates, pelvic pain, or postoperative adhesion reformation.
SEARCH STRATEGY: We searched the Cochrane Menstrual Disorders and Subfertility Group Trials Register (searched September 2007) which is based on regular searches of MEDLINE, EMBASE, CINAHL, PsycINFO and CENTRAL, plus handsearching of 20 relevant journals and conference proceedings, and searches of several key grey literature sources. In addition, companies were contacted for unpublished trials.
SELECTION CRITERIA: Any randomised controlled trials (RCTs) comparing the use of physical barriers versus no treatment or other physical barriers in the prevention of adhesions in women undergoing gynaecological surgery.
DATA COLLECTION AND ANALYSIS: Review authors assessed trial eligibility and quality.
MAIN RESULTS: Sixteen RCTs were included. Five trials randomised patients while the remainder randomised pelvic organs. Laparoscopy (six trials) and laparotomy (10 trials) were the primary surgical techniques. Indications for surgery included myomectomy (five trials), ovarian surgery (five trials), pelvic adhesions (four trials), endometriosis (one trial), and mixed (one trial). Eleven trials assessed Interceed versus no treatment, two assessed Interceed versus Gore-Tex, one trial assessed Gore-Tex versus no treatment, and one trial assessed Seprafilm versus no treatment. A single trial assessed Fibrin sheet versus no treatment. No studies reported pregnancy or reduction in pain as outcomes. The use of Interceed was associated with reduced incidence of pelvic adhesion formation, both new formation and reformation following laparoscopic surgery or laparotomy. However, this result should be interpreted with caution. Gore-Tex was more effective than no barrier or Interceed in preventing adhesion formation. There was only limited evidence that Seprafilm was effective in preventing adhesion formation following myomectomy and no evidence to support Fibrin sheet.
AUTHORS' CONCLUSIONS: The absorbable adhesion barrier Interceed reduces the incidence of adhesion formation following laparoscopy and laparotomy, but there are insufficient data to support its use to improve pregnancy rates. Gore-Tex may be superior to Interceed in preventing adhesion formation but its usefulness is limited by the need for suturing and later removal. There was no evidence of effectiveness of Seprafilm and Fibrin sheet in preventing adhesion formation.
Update of
Cochrane Database Syst Rev. 2000;(2):CD000475.
http://www.ncbi.nlm.nih.gov/pubmed/18425865
Barrier agents for adhesion prevention after gynaecological surgery.
Ahmad G, Duffy JM, Farquhar C, Vail A, Vandekerckhove P, Watson A, Wiseman D.
SourceStepping Hill Hospital, Obstetric & Gynaecology, 30 Badger Road, Altrincham, Cheshire, UK, WA14 5UZ. gaityahmad@hotmail.com
Abstract
BACKGROUND: Pelvic adhesion can form as a result of inflammation, endometriosis or surgical trauma. During pelvic surgery, strategies to reduce pelvic adhesion formation may include placing synthetic barrier agents such as oxidised regenerated cellulose, polytetrafluoroethylene or Fibrin sheets between the pelvic structures.
OBJECTIVES: To assess the effect of physical barriers used during pelvic surgery in women of reproductive age on pregnancy rates, pelvic pain, or postoperative adhesion reformation.
SEARCH STRATEGY: We searched the Cochrane Menstrual Disorders and Subfertility Group Trials Register (searched September 2007) which is based on regular searches of MEDLINE, EMBASE, CINAHL, PsycINFO and CENTRAL, plus handsearching of 20 relevant journals and conference proceedings, and searches of several key grey literature sources. In addition, companies were contacted for unpublished trials.
SELECTION CRITERIA: Any randomised controlled trials (RCTs) comparing the use of physical barriers versus no treatment or other physical barriers in the prevention of adhesions in women undergoing gynaecological surgery.
DATA COLLECTION AND ANALYSIS: Review authors assessed trial eligibility and quality.
MAIN RESULTS: Sixteen RCTs were included. Five trials randomised patients while the remainder randomised pelvic organs. Laparoscopy (six trials) and laparotomy (10 trials) were the primary surgical techniques. Indications for surgery included myomectomy (five trials), ovarian surgery (five trials), pelvic adhesions (four trials), endometriosis (one trial), and mixed (one trial). Eleven trials assessed Interceed versus no treatment, two assessed Interceed versus Gore-Tex, one trial assessed Gore-Tex versus no treatment, and one trial assessed Seprafilm versus no treatment. A single trial assessed Fibrin sheet versus no treatment. No studies reported pregnancy or reduction in pain as outcomes. The use of Interceed was associated with reduced incidence of pelvic adhesion formation, both new formation and reformation following laparoscopic surgery or laparotomy. However, this result should be interpreted with caution. Gore-Tex was more effective than no barrier or Interceed in preventing adhesion formation. There was only limited evidence that Seprafilm was effective in preventing adhesion formation following myomectomy and no evidence to support Fibrin sheet.
AUTHORS' CONCLUSIONS: The absorbable adhesion barrier Interceed reduces the incidence of adhesion formation following laparoscopy and laparotomy, but there are insufficient data to support its use to improve pregnancy rates. Gore-Tex may be superior to Interceed in preventing adhesion formation but its usefulness is limited by the need for suturing and later removal. There was no evidence of effectiveness of Seprafilm and Fibrin sheet in preventing adhesion formation.
Update of
Cochrane Database Syst Rev. 2000;(2):CD000475.
http://www.ncbi.nlm.nih.gov/pubmed/18425865
Thursday, December 15, 2011
What is ovarian remnant syndrome?
Q:What is ovarian remnant syndrome?
A: Ovarian remnant syndrome (ORS) occurs if any ovarian tissue is left after surgery to remove both ovaries and fallopian tubes, called a bilateral salpingo-oophorectomy. The syndrome occurs if this ovarian tissue causes severe pelvic pain and/or a pelvic mass.
The condition typically occurs because of the surgical technique used to remove the ovaries. Although ORS is considered fairly rare, its incidence appears to have increased in the past 40 years, possibly related to the increased use of laparoscopic surgeries.These surgeries allow the surgeon to operate through two or three tiny incisions instead of a large abdominal incision.
Certain factors increase the risk of incomplete ovarian removal, including a history of endometriosis, pelvic inflammatory disease, previous abdominal or pelvic surgeries and pelvic adhesions. Adhesions are scar tissue that forms after pelvic or abdominal surgery and "sticks" to organs and other tissue. Adhesions make it difficult for the surgeon to completely identify and remove the ovaries because of the fibrous tissue that binds an ovary with the other structures or with the peritoneum, the membrane that covers the inside of the abdomen and pelvis.
If any ovarian tissue is left in your pelvis, it can, in some instances, continue to produce hormones.
The most common symptoms of ovarian remnant syndrome are constant, chronic pelvic pain, difficult or painful intercourse, cyclic pelvic pain, and painful urination and bowel movements.
The condition is diagnosed based on a careful medical history. One sign that there may be residual ovarian tissue is if after your ovaries were removed, you didn't immediately start hormone therapy but didn't experience menopausal symptoms, such as hot flashes. This would suggest that you may still be producing estrogens. An alternative situation is if after surgery, you started hormone therapy and then discontinued it for some reason but didn't experience these symptoms.
Your doctor may also perform an ultrasound, CT scan or MRI to identify any ovarian tissue or pelvic mass and may measure blood levels of follicle-stimulating hormone (FSH) and estradiol. Estradiol is produced by the ovaries and FSH by the pituitary gland in response to hormonal signals from the ovaries. Levels of estradiol should be very low and levels of FSH should be very high after both ovaries have been removed.
If your doctor does find ovarian tissue remnants, you may be treated with medication to suppress any ovarian function, surgery to remove the tissue, or, as a last resort, radiation to destroy the tissue.
http://www.healthywomen.org/content/ask-expert/1761/ovarian-remnant-syndrome?context=womentalk/ask-the-expert&context_title=ask-the-expert
A: Ovarian remnant syndrome (ORS) occurs if any ovarian tissue is left after surgery to remove both ovaries and fallopian tubes, called a bilateral salpingo-oophorectomy. The syndrome occurs if this ovarian tissue causes severe pelvic pain and/or a pelvic mass.
The condition typically occurs because of the surgical technique used to remove the ovaries. Although ORS is considered fairly rare, its incidence appears to have increased in the past 40 years, possibly related to the increased use of laparoscopic surgeries.These surgeries allow the surgeon to operate through two or three tiny incisions instead of a large abdominal incision.
Certain factors increase the risk of incomplete ovarian removal, including a history of endometriosis, pelvic inflammatory disease, previous abdominal or pelvic surgeries and pelvic adhesions. Adhesions are scar tissue that forms after pelvic or abdominal surgery and "sticks" to organs and other tissue. Adhesions make it difficult for the surgeon to completely identify and remove the ovaries because of the fibrous tissue that binds an ovary with the other structures or with the peritoneum, the membrane that covers the inside of the abdomen and pelvis.
If any ovarian tissue is left in your pelvis, it can, in some instances, continue to produce hormones.
The most common symptoms of ovarian remnant syndrome are constant, chronic pelvic pain, difficult or painful intercourse, cyclic pelvic pain, and painful urination and bowel movements.
The condition is diagnosed based on a careful medical history. One sign that there may be residual ovarian tissue is if after your ovaries were removed, you didn't immediately start hormone therapy but didn't experience menopausal symptoms, such as hot flashes. This would suggest that you may still be producing estrogens. An alternative situation is if after surgery, you started hormone therapy and then discontinued it for some reason but didn't experience these symptoms.
Your doctor may also perform an ultrasound, CT scan or MRI to identify any ovarian tissue or pelvic mass and may measure blood levels of follicle-stimulating hormone (FSH) and estradiol. Estradiol is produced by the ovaries and FSH by the pituitary gland in response to hormonal signals from the ovaries. Levels of estradiol should be very low and levels of FSH should be very high after both ovaries have been removed.
If your doctor does find ovarian tissue remnants, you may be treated with medication to suppress any ovarian function, surgery to remove the tissue, or, as a last resort, radiation to destroy the tissue.
http://www.healthywomen.org/content/ask-expert/1761/ovarian-remnant-syndrome?context=womentalk/ask-the-expert&context_title=ask-the-expert
Monday, October 17, 2011
Functional Bowel Disorders
Functional Bowel Disorders
Michael Snyder, MD
Clinical Instructor
Colon and Rectal Surgery
University of Texas at Houston Health Center
Clinical Associate Professor
Baylor College of Medicine
Houston, Texas
http://www.fascrs.org/physicians/education/core_subjects/2005/functional_bowel_disorders/
Functional bowel disorders are syndromes characterized by chronic gastrointestinal tract symptoms in patients without significant infectious, metabolic or anatomical abnormalities. Functional gastrointestinal disorders can affect the entire digestive tract from the mouth to the anus. The two most common functional disorders seen by the colon and rectal surgeon are irritable bowel syndrome (IBS) and functional constipation which affect the mid to lower gastrointestinal tract.
Irritable Bowel Syndrome
Irritable Bowel Syndrome (IBS), the most frequent condition diagnosed in most gastroenterology practices, is responsible for over three million office visits annually. Depending on the diagnostic inclusion criteria, the prevalence of IBS in the United States is between six and twenty percent (1). Female predominance is as high as 2:1 in some studies. While it is primarily a disorder of younger people in the third or fourth decade of life, up to 23% of patients with IBS have symptoms that persist into old age. A new diagnosis of IBS should be made cautiously in patients older than 60, however, because this age group has an increased incidence of other colonic disorders with similar symptoms. Since there has never been a well-designed study on the natural history of IBS, the reasons for the female predominance are unclear. Whether this represents a true difference or is secondary to health care seeking behavior is uncertain. IBS is a chronic disorder with at least 75% of patients having persistent symptoms five years or more after the diagnosis is first considered (2).
The understanding of the pathophysiology of IBS has evolved significantly over the past half century. Originally IBS was thought to represent a nervous disorder with augmented gastrointestinal motility occurring in patients under stress. Recent research has shown that IBS is a complex multifaceted disorder. Abnormalities in intestinal motility in conjunction with heightened visceral sensory input and processing are important aspects of the disease. In many patients with IBS, abdominal pain in the immediate postprandial period is associated with either rhythmic contractions or high amplitude prolonged contractions. These alterations in the migratory motor complex can either delay or accelerate intestinal transit (3). In addition, increased sensitivity to pain in the gastrointestinal tract has been demonstrated in patients with IBS. Several studies have suggested that patients with IBS may process sensory input from the gastrointestinal tract differently and have an exaggerated response to intestinal distention (4). Finally, two studies have demonstrated that infectious gastroenteritis may increase the possibility of developing IBS later in life (5,6), presumably by damaging the enteric nerves responsible for peristalsis.
IBS is defined by abdominal discomfort associated with altered bowel habits. As there are no biochemical or structural markers, IBS is diagnosed by the absence of organic disease and the presence of a constellation of symptoms. The Rome II diagnostic criteria divide IBS into three relatively equal groups depending on the presence of diarrhea, constipation, or alternating diarrhea and constipation. These criteria for IBS require at least twelve weeks duration of symptoms in one year that need not be consecutive. Symptoms defining IBS are abdominal pain or discomfort relieved with defecation or associated with a change in the frequency or appearance of the stool. Nine symptoms supporting the diagnosis of IBS include (a greater than 25% occurrence of): 1) Fewer than three bowel movements per week, 2) More than three bowel movements per day, 3) Hard or lumpy stools, 4) Loose (mushy) or watery stools. 5) Straining during bowel movement, 6) Urgency, 7) Passing mucous during bowel movement, 9) Abdominal fullness, bloating or swelling. IBS with diarrhea is associated with one or more of the supportive symptoms numbered 2,4 or 6 and none of 1, 3 or 5. IBS with constipation is associated with one or more of the supportive symptoms numbered1,3 or 5 and none of 2, 4 or 6 (7). An individual patient may change from one diagnostic group to the other during the treatment of this, so symptom based management is currently recommended.
Patients prone to diarrhea find that the first stool in the morning is usually normal in consistency. Subsequent bowel movements, however, become more watery and mucoid, and are associated with intestinal cramps, rectal urgency and bloating. Symptoms are relieved with the passage of stool but often quickly return. Patients prone to constipation also note mucous either in the stool or separately. The stool consistency is often hard, and/or rocky. Many patients strain to complete defecation or experience incomplete evacuation. Fecal incontinence occurs in up to 20% of patients with IBS, primarily in those with concomitant diarrhea. This is possibly due to repetitive reflex relaxation of the sphincter mechanism associated with colonic spasms.
The evaluation of patients who fall into one of the Rome II criteria is limited as long as no "alarm" symptoms or signs are noted. These "alarm" symptoms or signs include hematochezia, weight loss greater than ten pounds, family history of colon cancer, recurring fever, anemia, and severe chronic diarrhea. Routine colonoscopy for colon cancer screening is no different than the general population. Based on the best current data, the probability of colorectal cancer, inflammatory bowel disease and infectious diarrhea is less than 1% among IBS patients without "alarm" symptoms or signs (8). As this is similar to that of healthy patients undergoing screening, the routine use of endoscopy, radiologic tests, or microbiological evaluation is unnecessary. The only exception occurs in those patients with IBS and diarrhea. The incidence of celiac sprue in these patients is 5% and routine testing of these patients should certainly be considered (9).
Because the precise etiology of IBS is unknown, and there is a lack of objective biochemical markers, treatment of IBS has focused upon the relief of symptoms. Treatment of IBS is indicated when the symptoms of IBS significantly decrease the quality of life. It should result in improvement of global IBS symptoms such as abdominal pain, bloating and altered bowel habits.
For patients with IBS and constipation initial treatment involves increasing both the amount of daily fiber to 25-30gms and water intake to 64oz a day. For many patients with mild symptoms this may be all that is required. If dietary changes are insufficient, fiber supplements such as methylcellulose or psyllium are added. While these products act as hydrophilic agents to bind water and prevent excessive dehydration, they do not relieve abdominal pain and may accentuate bloating. Other laxatives such as polyethylene glycol solutions have been used with some success, but also do not address the abdominal discomfort. Tegaserod, a selective serotonin type 4 receptor agonist, binds to the enteric receptors initiating the peristaltic reflex. Four randomized controlled trials have compared tegaserod 6mg b.i.d. to placebo and found significant global symptom relief in women with IBS and constipation. The use of tegaserod in men or in patients with alternating diarrhea and constipation is not established (10).
For patients with IBS and diarrhea, loperamide has been studied in randomized control trials and found to decrease stool frequency, improve stool consistency, but have no effect on abdominal pain or bloating. Low doses of tricyclic antidepressants may also decrease the frequency of diarrhea. In those women who fail to respond to this conservative therapy and who have severe diarrhea predominant IBS, the serotonin type 3-receptor antagonist alosetron may be used. Five randomized controlled studies have demonstrated efficacy. Side effects include constipation (25%) and ischemic colitis (84 cases in the literature)(10).
Therapy for the abdominal discomfort associated with IBS has been disappointing until recently. Traditionally, antispasmodic agents have been prescribed. Dicyclomine and hyoscyamine are the two agents available in the United States. The only trial to demonstrate efficacy of either medication was associated with a 70% rate of anticholinergic side effects (10). Since these side effects include constipation, the two antispasmodic medications should be used cautiously in IBS patients with constipation. Antispasmodic medications should be taken 30-60 minutes prior to a meal to prevent postprandial abdominal pain and bloating. Currently, however, the most effective and preferred medication for abdominal pain and bloating is the previously mentioned serotonin type 4 receptor agonist, tegaserod.
Other therapies for IBS include behavioral modification and investigational drugs. Anxiety and depression are noted in up to 20% of IBS patients. Behavioral therapy for IBS has been evaluated in sixteen randomized controlled studies. While none of these examined global IBS improvement, most studies demonstrated that attenuation of individual IBS symptoms correlated with a reduction in anxiety and depression. In patients with sleep disorders, the administration of melatonin significantly diminished abdominal pain and rectal urgency (11). Other medications with visceral analgesic properties are being investigated to include the kappa opioid agonist fedotozine and neurokinin receptor antagonists. Probiotics are also being evaluated because of promising results controlling flatulence in a controlled trial.
Constipation
Constipation, a common disorder seen by both primary care and specialty physicians, is responsible for more than 2.5 million annual office visits. Many people do not seek medical care and instead self medicate with a multitude of over the counter and alternative medications. Constipation is a symptom of many diseases and the medications used to treat them. It is interchangeably used to describe patients with stool that is difficult to pass, passes infrequently, or has a hard consistency. Because of a lack of consensus defining constipation in the literature, the International Congress of Gastroenterology formulated the Rome II criteria. They defined constipation as abdominal discomfort of at least twelve weeks duration in the previous twelve months (need not be consecutive) having two or more of the following symptoms; 1) Straining more than 25% of the time, 2) Lumpy or hard stools more than 25% of the time, 3) Anorectal blockage, 4) Incomplete evacuation, 5) Need for manual maneuvers, and 6) Less than three stools per week. In these patients loose stools may not be present and there should not be sufficient criteria for the diagnosis of irritable bowel syndrome (12).
The physiology of constipation primarily encompasses the transit of stool through the colon, rectum and anus. Stool enters the colon as a liquid and becomes solid during passage to the rectosigmoid. Segmental and high amplitude propagating contractions are the two major contractile activities in the colon. The propagating contractions are responsible for the movement of stool to the anal sphincter, which regulates eventual stool evacuation. These propagating contractions originate from pacemakers found in the muscle layer of the colon called the interstial cells of Cajal (13). The loss or inactivity of these cells may play a role in patients with slow transit constipation.
Defecation is the evacuation of stool from the rectum and is determined by the propulsive force of the stool and the resistance of the anus. It is triggered by distention of the rectum by stool. Propulsive force consists of voluntary increases in intra-abdominal pressure and involuntary high amplitude contractions of the rectum. Resistance to defecation decreases with voluntary straightening of the anorectal angle in conjunction with relaxation of the external sphincter and involuntary relaxation of the internal anal sphincter.
The etiology of constipation may be primary or secondary. The more common secondary causes of constipation are listed in Table 1. Many patients have multiple factors that may contribute to their constipation. Notably, medications, including over-the-counter and herbal preparations, are a factor in up to 40% of patients (14).
The evaluation of constipated patients begins with a thorough history and physical exam to identify one of the numerous secondary causes of constipation. A colonoscopy or combined sigmoidoscopy and barium enema should be considered to identify malignant or anatomical abnormalities in the colon and rectum. A careful examination of the perineum and anus will help exclude anatomical outlet obstruction, the presence of a rectocele and abnormal perineal descent. Laboratory testing includes thyroid functions and electrolytes to help diagnose metabolic and endocrine abnormalities contributing to the constipation.
If the initial evaluation does not reveal a secondary cause for the constipation, a transit study is recommended to objectively measure the severity, and helps establish the primary cause of the constipation. The initial study called a SitzMark test is performed with radio-opaque markers that are swallowed. Abdominal radiographs are obtained on days 3 and 5. The radiograph on day 3 confirms the patient ingesting the markers. The presence of more than 25% of the markers in the colon at day 5 is indicative of a positive test. Markers evenly spread throughout the colon are consistent with slow transit constipation, while those that congregate in the rectosigmoid are indicative of an outlet obstruction. A negative SitzMark test with fewer than 25% of the markers on day 5 is suggestive of normal transit constipation or a patient who is not compliant with the instructions regarding no laxative use during the testing.
Further evaluation of outlet obstruction consists of anal manometry and defecography. Anal manometry permits documentation of the anorectal inhibitory reflex to rule out a short segment Hirschrprung’s disease. In addition, normal manometric sphincter pressures during simulated defecation are useful in excluding outlet obstruction. Defecography is particularly useful in the diagnosis of intra-anal prolapse, rectoceles, and other pelvic floor abnormalities. Barium paste is placed into the rectum and the act of defecation is visualized. Anorectal angle visualization, perineal descent and the nonemptying of rectoceles can be objectively measured.
There are three types of primary constipation that are important to recognize. The first type, colonic inertia, is associated with a lack of urgency and intractability resulting in many patients having several days to weeks between bowel movements. Daily use of stimulant laxatives is typical and evacuation is uncommon without medication. While the etiology is idiopathic in nature, the patients are overwhelmingly young women. Increasing dietary fiber or fiber supplements may make symptoms of bloating and abdominal cramps worse. SitzMark studies are often markedly positive demonstrating a characteristic pattern of markers relatively evenly spaced throughout the colon. It is important to rule out coexisting outlet obstruction with defecography and/or anal manometry. The second type, normal transit constipation, is characterized by evacuation frequency and stool consistency that is within the normal range, but the patients feel constipated. Bowel management regimens and reassurance are often all that is necessary to treat these patients. The third type, anismus or obstructed defecation, is characterized by the sensation of incomplete evacuation and the need to strain to produce a stool. SitzMark studies may be positive with most markers present in the rectosigmoid. Physical examination along with defecography and/or anal manometry is critical in determining both the exact etiology and response to therapy.
Treatment of functional constipation begins with dietary manipulation consisting of a high fiber diet (25-30gm/day) and augmented water intake (64oz/day). Most patients can be effectively managed with dietary measures alone or in conjunction with occasional laxative or enema use. For those patients who fail dietary measures, treatment with mild stimulating or osmotic laxatives can be safely done. Polyethylene glycol (PEG) is a poorly absorbed large polymer with substantial osmotic activity. When used in a solution that does not contain any salt, PEG can be ingested in large amounts without any harmful effect. PEG also binds water to the stool improving the consistency in many constipated patients. Other osmotic agents include non-absorbed carbohydrates such as lactulose. These agents also bind water and soften the stool. Complications include fermentation with consequent bloating, flatus and abdominal cramping.
Additional therapies for refractory constipation have attempted to address the lack of normal high amplitude contractions in the colon found in patients with slow transit constipation. The selective serotonin type 4 receptor agonist, tegaserod, is currently recommended for women with IBS and constipation. It acts by stimulating the serotonin type 4 receptors with a pronounced enterokinetic effect. Constipation was improved in 5-19% of women compared to placebo (15). Previous serotonin type 4 agonists such as cisipride and prucalopride also induced strong contractions of the proximal colon, but because of cardiac arrhythmias and carcinogenesis respectively, they have been withdrawn from the market. Another way to recreate the high amplitude contractions appears to be colonic pacing. In a small study pacing induced rectal evacuation in two-thirds of patients with total colonic inertia (16). Further studies will determine if it will become a replacement for extirpative surgical intervention.
Other medical approaches to stimulating the enteric neural plexuses include serotonin reuptake inhibitors, cholecystokinnin antagonists, antimuscarinic agents and serotonin type 1-receptor agonists. All these agents are currently being investigated and are not yet commercially available.
The surgical approach to constipation is one of last resort. Obstructive defecation is initially treated with biofeedback that improves symptoms in up to 70% of patients, although a rare patient may benefit from internal sphincterotomy. In patients with slow transit constipation refractory to medical therapy, attempt at segmental resection of the colon is unsuccessful. Total abdominal colectomy with ileorectal anastomosis is the preferred operation. Relief of abdominal pain and return to normal bowel function occur in up to 90% of patients with total abdominal colectomy. Risks of the surgery include ileus in approximately one-third of patients, small bowel obstruction, diarrhea, and possible incontinence (17).
Conclusion
Functional bowel diseases such as IBS and constipation are common disorders. The Rome II criteria permit more objective diagnosis and patient stratification. Therapy is determined by the major symptom or symptom complex. Therapy is often simply dietary modification, but may require medications, biofeedback and rarely surgery. As more knowledge about the enteric neural pathways and the influence of various neurotransmitters on bowel motility is discovered, focused treatment regimens with fewer side effects should be possible.
Table 1. Common Causes of Constipation
Dietary
Low fiber diet, inadequate fluid intake, ingestion of stool hardening foods.
Functional
Inadequate toilet facilities, depression, psychosis, ignoring need for bowel movement, immobility.
Endocrine, Metabolic
Diabetes mellitus, hypothyroidism, hypoparathyroidism, pregnancy, hypopituitarism, hypokalemia, hypercalcemia.
Neuropathy
Cerebrovascular accident, Parkinson’s disease, multiple sclerosis, trauma, cerebral or spinal tumors, colonic inertia, Ogilvie’s syndrome, Hirschprung’s disease, Chagas’ disease.
Medication
Analgesics, anticonvulsants, antihistamines, antihypertensives, diuretics, chemotherapeutics, anticholinergics, metal ions and minerals.
Structural
Neoplasm, diverticular disease, inflammatory bowel disease, volvulus, ischemic colitis, endometriosis, anastomotic stricture.
Anal Outlet
Thrombosed hemorrhoids, anal fissure, rectal prolapse, proctitis, rectocele, nonrelaxing puborectalis, hypertrophic internal anal sphincter.
Bibliography
1.Olden, KW. Diagnosis of irritable bowel syndrome. Gastroenterology. 2002;122:1701-14.
2.Harvey RF, Mauad EC, Brown AM. Prognosis in the irritable bowel syndrome: a five year prospective study. Lancet. 1987;1:963-5.
3.Kellow JE, Phillips SF, Miller IJ, et al. Dysmotility of the small intestine in irritable bowel syndrome. Gut. 1988;29:1236-43.
4.Mertz H, Morgan V, Tanner G, et al. Regional cerebral activation in irritable bowel syndrome and control subjects with painful and non-painful rectal distention. Gastroenterology. 200;118:842-8.
5.Gwee KA, Leong YL, Graham C, et al. Psychometric scores and the persistence of irritable bowel after infectious diarrhoea. Lancet. 1996;347:150-3.
6.Rodriguez LA, Ruigomez A. Increased risk of irritable bowel syndrome after bacterial gastroenteritis. BMJ. 1999;318:565-6.
7.Thompson WG, Longstreth GF, Drossman DA, et al. Functional bowel disorders and functional abdominal pain. Gut.1999;45(suppl II):1143-7.
8.American College of Gastroenterology Functional Gastrointestinal Disorders Task Force. Evidence-based position statement on the management of irritable bowel syndrome in North America. Am J Gastroenterol. 2002;97:11(suppl):S1-5.
9.Sanders DS, Carter MJ, Hurlstone DP, et al. Association of adult celiac disease with irritable bowel syndrome: a case control study in patients fulfilling ROME II criteria referred to secondary care. Lancet. 2001;358:1604-8.
10.Brandt LJ, Bjorkman D, Fennerty MB, et al. Systematic review on the management of irritable bowel syndrome in North America. Am J Gastroenterol. 2002;97:11(suppl):S7-26.
11.Bowser A. Melatonin relieves IBS symptoms in patients with sleep disorders. Gastroenterology & Endoscopy News. 2005;56:12.
12.Thompson WG, Longstreth GF, Drossman DA, Heaton KW, et al. Functional bowel disorders and functional abdominal pain. Gut. 1999;45(suppl 2):1143-7.
13.Ward SM. Interstial cells of Cajal in enteric neurotransmission. Gut. 2000;47(suppl 4):iv40-3.
14.Adeniji OA, DiPalma JA. Prevalence of medication-associated constipation. Am J Gastroenterol. 2001;96:SI40.
15.American Gastroenterological Association Clinical Practice Committee. AGA technical review on irritable bowel syndrome. Gastroenterology 2002;123:2108-31.
16.Shafik A, Shafik AA, El-Sibai O, Ahmed I. Colonic pacing; a therapeutic option for the treatment of constipation due to total colonic inertia.
17.Lubowski DZ, Chen FC, Kennedy ML, King DW. Results of colectomy for slow transit constipation. Dis Colon Rectum. 1999;39:23-9.
Michael Snyder, MD
Clinical Instructor
Colon and Rectal Surgery
University of Texas at Houston Health Center
Clinical Associate Professor
Baylor College of Medicine
Houston, Texas
http://www.fascrs.org/physicians/education/core_subjects/2005/functional_bowel_disorders/
Functional bowel disorders are syndromes characterized by chronic gastrointestinal tract symptoms in patients without significant infectious, metabolic or anatomical abnormalities. Functional gastrointestinal disorders can affect the entire digestive tract from the mouth to the anus. The two most common functional disorders seen by the colon and rectal surgeon are irritable bowel syndrome (IBS) and functional constipation which affect the mid to lower gastrointestinal tract.
Irritable Bowel Syndrome
Irritable Bowel Syndrome (IBS), the most frequent condition diagnosed in most gastroenterology practices, is responsible for over three million office visits annually. Depending on the diagnostic inclusion criteria, the prevalence of IBS in the United States is between six and twenty percent (1). Female predominance is as high as 2:1 in some studies. While it is primarily a disorder of younger people in the third or fourth decade of life, up to 23% of patients with IBS have symptoms that persist into old age. A new diagnosis of IBS should be made cautiously in patients older than 60, however, because this age group has an increased incidence of other colonic disorders with similar symptoms. Since there has never been a well-designed study on the natural history of IBS, the reasons for the female predominance are unclear. Whether this represents a true difference or is secondary to health care seeking behavior is uncertain. IBS is a chronic disorder with at least 75% of patients having persistent symptoms five years or more after the diagnosis is first considered (2).
The understanding of the pathophysiology of IBS has evolved significantly over the past half century. Originally IBS was thought to represent a nervous disorder with augmented gastrointestinal motility occurring in patients under stress. Recent research has shown that IBS is a complex multifaceted disorder. Abnormalities in intestinal motility in conjunction with heightened visceral sensory input and processing are important aspects of the disease. In many patients with IBS, abdominal pain in the immediate postprandial period is associated with either rhythmic contractions or high amplitude prolonged contractions. These alterations in the migratory motor complex can either delay or accelerate intestinal transit (3). In addition, increased sensitivity to pain in the gastrointestinal tract has been demonstrated in patients with IBS. Several studies have suggested that patients with IBS may process sensory input from the gastrointestinal tract differently and have an exaggerated response to intestinal distention (4). Finally, two studies have demonstrated that infectious gastroenteritis may increase the possibility of developing IBS later in life (5,6), presumably by damaging the enteric nerves responsible for peristalsis.
IBS is defined by abdominal discomfort associated with altered bowel habits. As there are no biochemical or structural markers, IBS is diagnosed by the absence of organic disease and the presence of a constellation of symptoms. The Rome II diagnostic criteria divide IBS into three relatively equal groups depending on the presence of diarrhea, constipation, or alternating diarrhea and constipation. These criteria for IBS require at least twelve weeks duration of symptoms in one year that need not be consecutive. Symptoms defining IBS are abdominal pain or discomfort relieved with defecation or associated with a change in the frequency or appearance of the stool. Nine symptoms supporting the diagnosis of IBS include (a greater than 25% occurrence of): 1) Fewer than three bowel movements per week, 2) More than three bowel movements per day, 3) Hard or lumpy stools, 4) Loose (mushy) or watery stools. 5) Straining during bowel movement, 6) Urgency, 7) Passing mucous during bowel movement, 9) Abdominal fullness, bloating or swelling. IBS with diarrhea is associated with one or more of the supportive symptoms numbered 2,4 or 6 and none of 1, 3 or 5. IBS with constipation is associated with one or more of the supportive symptoms numbered1,3 or 5 and none of 2, 4 or 6 (7). An individual patient may change from one diagnostic group to the other during the treatment of this, so symptom based management is currently recommended.
Patients prone to diarrhea find that the first stool in the morning is usually normal in consistency. Subsequent bowel movements, however, become more watery and mucoid, and are associated with intestinal cramps, rectal urgency and bloating. Symptoms are relieved with the passage of stool but often quickly return. Patients prone to constipation also note mucous either in the stool or separately. The stool consistency is often hard, and/or rocky. Many patients strain to complete defecation or experience incomplete evacuation. Fecal incontinence occurs in up to 20% of patients with IBS, primarily in those with concomitant diarrhea. This is possibly due to repetitive reflex relaxation of the sphincter mechanism associated with colonic spasms.
The evaluation of patients who fall into one of the Rome II criteria is limited as long as no "alarm" symptoms or signs are noted. These "alarm" symptoms or signs include hematochezia, weight loss greater than ten pounds, family history of colon cancer, recurring fever, anemia, and severe chronic diarrhea. Routine colonoscopy for colon cancer screening is no different than the general population. Based on the best current data, the probability of colorectal cancer, inflammatory bowel disease and infectious diarrhea is less than 1% among IBS patients without "alarm" symptoms or signs (8). As this is similar to that of healthy patients undergoing screening, the routine use of endoscopy, radiologic tests, or microbiological evaluation is unnecessary. The only exception occurs in those patients with IBS and diarrhea. The incidence of celiac sprue in these patients is 5% and routine testing of these patients should certainly be considered (9).
Because the precise etiology of IBS is unknown, and there is a lack of objective biochemical markers, treatment of IBS has focused upon the relief of symptoms. Treatment of IBS is indicated when the symptoms of IBS significantly decrease the quality of life. It should result in improvement of global IBS symptoms such as abdominal pain, bloating and altered bowel habits.
For patients with IBS and constipation initial treatment involves increasing both the amount of daily fiber to 25-30gms and water intake to 64oz a day. For many patients with mild symptoms this may be all that is required. If dietary changes are insufficient, fiber supplements such as methylcellulose or psyllium are added. While these products act as hydrophilic agents to bind water and prevent excessive dehydration, they do not relieve abdominal pain and may accentuate bloating. Other laxatives such as polyethylene glycol solutions have been used with some success, but also do not address the abdominal discomfort. Tegaserod, a selective serotonin type 4 receptor agonist, binds to the enteric receptors initiating the peristaltic reflex. Four randomized controlled trials have compared tegaserod 6mg b.i.d. to placebo and found significant global symptom relief in women with IBS and constipation. The use of tegaserod in men or in patients with alternating diarrhea and constipation is not established (10).
For patients with IBS and diarrhea, loperamide has been studied in randomized control trials and found to decrease stool frequency, improve stool consistency, but have no effect on abdominal pain or bloating. Low doses of tricyclic antidepressants may also decrease the frequency of diarrhea. In those women who fail to respond to this conservative therapy and who have severe diarrhea predominant IBS, the serotonin type 3-receptor antagonist alosetron may be used. Five randomized controlled studies have demonstrated efficacy. Side effects include constipation (25%) and ischemic colitis (84 cases in the literature)(10).
Therapy for the abdominal discomfort associated with IBS has been disappointing until recently. Traditionally, antispasmodic agents have been prescribed. Dicyclomine and hyoscyamine are the two agents available in the United States. The only trial to demonstrate efficacy of either medication was associated with a 70% rate of anticholinergic side effects (10). Since these side effects include constipation, the two antispasmodic medications should be used cautiously in IBS patients with constipation. Antispasmodic medications should be taken 30-60 minutes prior to a meal to prevent postprandial abdominal pain and bloating. Currently, however, the most effective and preferred medication for abdominal pain and bloating is the previously mentioned serotonin type 4 receptor agonist, tegaserod.
Other therapies for IBS include behavioral modification and investigational drugs. Anxiety and depression are noted in up to 20% of IBS patients. Behavioral therapy for IBS has been evaluated in sixteen randomized controlled studies. While none of these examined global IBS improvement, most studies demonstrated that attenuation of individual IBS symptoms correlated with a reduction in anxiety and depression. In patients with sleep disorders, the administration of melatonin significantly diminished abdominal pain and rectal urgency (11). Other medications with visceral analgesic properties are being investigated to include the kappa opioid agonist fedotozine and neurokinin receptor antagonists. Probiotics are also being evaluated because of promising results controlling flatulence in a controlled trial.
Constipation
Constipation, a common disorder seen by both primary care and specialty physicians, is responsible for more than 2.5 million annual office visits. Many people do not seek medical care and instead self medicate with a multitude of over the counter and alternative medications. Constipation is a symptom of many diseases and the medications used to treat them. It is interchangeably used to describe patients with stool that is difficult to pass, passes infrequently, or has a hard consistency. Because of a lack of consensus defining constipation in the literature, the International Congress of Gastroenterology formulated the Rome II criteria. They defined constipation as abdominal discomfort of at least twelve weeks duration in the previous twelve months (need not be consecutive) having two or more of the following symptoms; 1) Straining more than 25% of the time, 2) Lumpy or hard stools more than 25% of the time, 3) Anorectal blockage, 4) Incomplete evacuation, 5) Need for manual maneuvers, and 6) Less than three stools per week. In these patients loose stools may not be present and there should not be sufficient criteria for the diagnosis of irritable bowel syndrome (12).
The physiology of constipation primarily encompasses the transit of stool through the colon, rectum and anus. Stool enters the colon as a liquid and becomes solid during passage to the rectosigmoid. Segmental and high amplitude propagating contractions are the two major contractile activities in the colon. The propagating contractions are responsible for the movement of stool to the anal sphincter, which regulates eventual stool evacuation. These propagating contractions originate from pacemakers found in the muscle layer of the colon called the interstial cells of Cajal (13). The loss or inactivity of these cells may play a role in patients with slow transit constipation.
Defecation is the evacuation of stool from the rectum and is determined by the propulsive force of the stool and the resistance of the anus. It is triggered by distention of the rectum by stool. Propulsive force consists of voluntary increases in intra-abdominal pressure and involuntary high amplitude contractions of the rectum. Resistance to defecation decreases with voluntary straightening of the anorectal angle in conjunction with relaxation of the external sphincter and involuntary relaxation of the internal anal sphincter.
The etiology of constipation may be primary or secondary. The more common secondary causes of constipation are listed in Table 1. Many patients have multiple factors that may contribute to their constipation. Notably, medications, including over-the-counter and herbal preparations, are a factor in up to 40% of patients (14).
The evaluation of constipated patients begins with a thorough history and physical exam to identify one of the numerous secondary causes of constipation. A colonoscopy or combined sigmoidoscopy and barium enema should be considered to identify malignant or anatomical abnormalities in the colon and rectum. A careful examination of the perineum and anus will help exclude anatomical outlet obstruction, the presence of a rectocele and abnormal perineal descent. Laboratory testing includes thyroid functions and electrolytes to help diagnose metabolic and endocrine abnormalities contributing to the constipation.
If the initial evaluation does not reveal a secondary cause for the constipation, a transit study is recommended to objectively measure the severity, and helps establish the primary cause of the constipation. The initial study called a SitzMark test is performed with radio-opaque markers that are swallowed. Abdominal radiographs are obtained on days 3 and 5. The radiograph on day 3 confirms the patient ingesting the markers. The presence of more than 25% of the markers in the colon at day 5 is indicative of a positive test. Markers evenly spread throughout the colon are consistent with slow transit constipation, while those that congregate in the rectosigmoid are indicative of an outlet obstruction. A negative SitzMark test with fewer than 25% of the markers on day 5 is suggestive of normal transit constipation or a patient who is not compliant with the instructions regarding no laxative use during the testing.
Further evaluation of outlet obstruction consists of anal manometry and defecography. Anal manometry permits documentation of the anorectal inhibitory reflex to rule out a short segment Hirschrprung’s disease. In addition, normal manometric sphincter pressures during simulated defecation are useful in excluding outlet obstruction. Defecography is particularly useful in the diagnosis of intra-anal prolapse, rectoceles, and other pelvic floor abnormalities. Barium paste is placed into the rectum and the act of defecation is visualized. Anorectal angle visualization, perineal descent and the nonemptying of rectoceles can be objectively measured.
There are three types of primary constipation that are important to recognize. The first type, colonic inertia, is associated with a lack of urgency and intractability resulting in many patients having several days to weeks between bowel movements. Daily use of stimulant laxatives is typical and evacuation is uncommon without medication. While the etiology is idiopathic in nature, the patients are overwhelmingly young women. Increasing dietary fiber or fiber supplements may make symptoms of bloating and abdominal cramps worse. SitzMark studies are often markedly positive demonstrating a characteristic pattern of markers relatively evenly spaced throughout the colon. It is important to rule out coexisting outlet obstruction with defecography and/or anal manometry. The second type, normal transit constipation, is characterized by evacuation frequency and stool consistency that is within the normal range, but the patients feel constipated. Bowel management regimens and reassurance are often all that is necessary to treat these patients. The third type, anismus or obstructed defecation, is characterized by the sensation of incomplete evacuation and the need to strain to produce a stool. SitzMark studies may be positive with most markers present in the rectosigmoid. Physical examination along with defecography and/or anal manometry is critical in determining both the exact etiology and response to therapy.
Treatment of functional constipation begins with dietary manipulation consisting of a high fiber diet (25-30gm/day) and augmented water intake (64oz/day). Most patients can be effectively managed with dietary measures alone or in conjunction with occasional laxative or enema use. For those patients who fail dietary measures, treatment with mild stimulating or osmotic laxatives can be safely done. Polyethylene glycol (PEG) is a poorly absorbed large polymer with substantial osmotic activity. When used in a solution that does not contain any salt, PEG can be ingested in large amounts without any harmful effect. PEG also binds water to the stool improving the consistency in many constipated patients. Other osmotic agents include non-absorbed carbohydrates such as lactulose. These agents also bind water and soften the stool. Complications include fermentation with consequent bloating, flatus and abdominal cramping.
Additional therapies for refractory constipation have attempted to address the lack of normal high amplitude contractions in the colon found in patients with slow transit constipation. The selective serotonin type 4 receptor agonist, tegaserod, is currently recommended for women with IBS and constipation. It acts by stimulating the serotonin type 4 receptors with a pronounced enterokinetic effect. Constipation was improved in 5-19% of women compared to placebo (15). Previous serotonin type 4 agonists such as cisipride and prucalopride also induced strong contractions of the proximal colon, but because of cardiac arrhythmias and carcinogenesis respectively, they have been withdrawn from the market. Another way to recreate the high amplitude contractions appears to be colonic pacing. In a small study pacing induced rectal evacuation in two-thirds of patients with total colonic inertia (16). Further studies will determine if it will become a replacement for extirpative surgical intervention.
Other medical approaches to stimulating the enteric neural plexuses include serotonin reuptake inhibitors, cholecystokinnin antagonists, antimuscarinic agents and serotonin type 1-receptor agonists. All these agents are currently being investigated and are not yet commercially available.
The surgical approach to constipation is one of last resort. Obstructive defecation is initially treated with biofeedback that improves symptoms in up to 70% of patients, although a rare patient may benefit from internal sphincterotomy. In patients with slow transit constipation refractory to medical therapy, attempt at segmental resection of the colon is unsuccessful. Total abdominal colectomy with ileorectal anastomosis is the preferred operation. Relief of abdominal pain and return to normal bowel function occur in up to 90% of patients with total abdominal colectomy. Risks of the surgery include ileus in approximately one-third of patients, small bowel obstruction, diarrhea, and possible incontinence (17).
Conclusion
Functional bowel diseases such as IBS and constipation are common disorders. The Rome II criteria permit more objective diagnosis and patient stratification. Therapy is determined by the major symptom or symptom complex. Therapy is often simply dietary modification, but may require medications, biofeedback and rarely surgery. As more knowledge about the enteric neural pathways and the influence of various neurotransmitters on bowel motility is discovered, focused treatment regimens with fewer side effects should be possible.
Table 1. Common Causes of Constipation
Dietary
Low fiber diet, inadequate fluid intake, ingestion of stool hardening foods.
Functional
Inadequate toilet facilities, depression, psychosis, ignoring need for bowel movement, immobility.
Endocrine, Metabolic
Diabetes mellitus, hypothyroidism, hypoparathyroidism, pregnancy, hypopituitarism, hypokalemia, hypercalcemia.
Neuropathy
Cerebrovascular accident, Parkinson’s disease, multiple sclerosis, trauma, cerebral or spinal tumors, colonic inertia, Ogilvie’s syndrome, Hirschprung’s disease, Chagas’ disease.
Medication
Analgesics, anticonvulsants, antihistamines, antihypertensives, diuretics, chemotherapeutics, anticholinergics, metal ions and minerals.
Structural
Neoplasm, diverticular disease, inflammatory bowel disease, volvulus, ischemic colitis, endometriosis, anastomotic stricture.
Anal Outlet
Thrombosed hemorrhoids, anal fissure, rectal prolapse, proctitis, rectocele, nonrelaxing puborectalis, hypertrophic internal anal sphincter.
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