Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Intestinal Motility Disorders Clinical Presentation

  • Author: Nafisa K Kuwajerwala, MD; Chief Editor: Julian Katz, MD  more...
 
Updated: Dec 29, 2015
 

History

The clinical presentation of patients with intestinal motility disorders is protean and may range from simple nausea and indigestion to severe abdominal pain, vomiting, diarrhea, inability to eat, weight loss, and other symptoms. It should be kept in mind that during pregnancy, intestinal motility disorders may worsen as a consequence of uterine compression of intestinal loops.

Obtain a complete patient history, recording information about the following:

  • Feelings of abdominal discomfort, cramping, nausea or vomiting, pain, excessive gas, and rectal fullness
  • Frequency, amount, and timing of normal defecation and any recent change
  • Amount, consistency, and color of last passed feces
  • Type of diet, use of laxatives or enemas, and drug use

Chronic intestinal pseudo-obstruction

Patients with chronic intestinal pseudo-obstruction (CIP) generally experience abdominal distention, pain, dizziness, fatigue, nausea, and vomiting for several days or months before their condition is recognized.

One type of pain is directly related to intestinal distention and improves or temporarily disappears if intestinal distention decreases. A second type is probably secondary to smooth muscle spasm or visceral hyperalgesia and is independent of intestinal distention.

Abdominal distention ranges from almost none to the equivalent of a 9-month pregnancy, depending on the nature and extent of the underlying pathology. An audible succussion splash and loud borborygmi may be present. Pain and distention may be almost continuous or may be interrupted by periods of clinical improvement. The vomitus frequently consists of food ingested 12 or more hours previously and may be feculent.

In patients with predominant small intestinal involvement, bacterial overgrowth and stagnant loop syndrome often develop and may lead to steatorrhea and diarrhea. Predominant colonic involvement usually results in constipation, megacolon, or both. Patients with both types of involvement may cycle from diarrhea to constipation, depending on the severity of steatorrhea and the relative involvement of each organ.

Many patients have involvement of the esophagus, which may be asymptomatic or may produce dysphagia, chest pain, regurgitation, reflux, and heartburn. Visceral neuropathies may manifest as symptoms resembling achalasia or diffuse esophageal spasm.

Gastric involvement produces gastroparesis. The abdominal distention and pain produced by any combination of gastric, small intestine, and colonic involvement result in decreased food intake, weight loss, and malnutrition, especially when combined with malabsorption.

Patients with involvement limited to the colon and distal small bowel may have relatively normal weights because their unaffected proximal bowel allows for normal absorption. Patients may have a history of weight loss or previous abdominal operations with no obstructing lesion found, or they may have a family history positive for the condition.

Irritable bowel syndrome

Abdominal pain, nausea, and irregular bowel habits that intensify during stress are the most common symptoms in patients with irritable bowel syndrome (IBS).

Fecal incontinence

Fecal incontinence can be a life-threatening condition. In the mild form, patients may experience abdominal bloating and uproar, but in the severe form, they may experience serious abdominal pain. Patients may not experience symptoms if incontinence is related to a comorbid condition (eg, dementia, Parkinson disease, or a demyelinating disease of the spinal cord).

Constipation and fecal incontinence

Constipation can also be a life-threatening condition. Patients with constipation report abdominal discomfort, cramping, pain, rectal fullness, or, more rarely, nausea and vomiting.

Next

Physical Examination

The clinical picture of patients with intestinal motility disorders is protean and may vary greatly, depending on the specific condition present.

Always perform a digital rectal examination in any patient with an intestinal motility disorder to detect the presence of a mass (eg, feces, tumor, or a foreign body) or blood in the rectum.

Chronic intestinal pseudo-obstruction

Decreased or absent bowel sounds and progressive loss of bowel movements are the most common signs in patients with CIP.[11] Patients’ symptoms increase in the 4-7 days before clinical onset and recognition of the disorder.

Physical examination findings may include weight loss, cachexia, and abdominal distention. Patients with small intestinal involvement usually have a succussion splash located in the midabdomen, whereas patients with gastric involvement may have a splash in the left upper quadrant.

Hypertympany to percussion is usually present, and contracting bowel loops are occasionally observed pushing up against the abdominal wall. Bowel sounds are of no value in making a diagnosis of pseudo-obstruction.

Evidence of central and peripheral nervous system disease should be sought, and autonomic nervous system testing should be performed when indicated.

Involvement of the genitourinary system may be indicated by the presence of a palpable urinary bladder. Patients may have positive neurologic findings with signs of systemic disease (eg, progressive sclerosis, amyloidosis, or myxedema).

Irritable bowel syndrome

Patients with IBS commonly have bloating, heartburn, burping, vomiting, and difficulty swallowing. Symptoms can fluctuate, disappearing during sleep and occurring again during stressing occasions. Heartburn, burping, and difficulty swallowing are usually due to concomitant gastroesophageal reflux disease, a very common condition in such patients.

Fecal incontinence

In the first stage of the disease, passing gas more than the normal 14-23 times a day characterizes fecal incontinence. In the second stage, liquid incontinence occurs, and patients are unaware that stools are being passed (stage of passive fecal incontinence). In the third stage, which is more severe, involuntary passage of feces through normal sphincter muscles occurs (stage of urge incontinence).

Constipation

The pattern of at least 3 stools per week and no more than 3 per day is considered normal defecation. Any reduction in the frequency of defecation may be considered constipation. Abdominal colicky pains are frequent in these patients.

Previous
Next

Complications

Complications of intestinal motility disorders vary greatly, depending on the specific type of disorder under consideration.

Intestinal pseudo-obstruction is often associated with a high mortality (15-30%), in most cases due to delayed diagnosis.

Constipation may have a severe complication, impaction. If this condition is not recognized early, the patient may die. Impaction is the collection of dry and hardened feces in the rectum or colon. Symptoms of impaction may be similar to those of constipation or may be unrelated to the gastrointestinal system.

If abdominal distention occurs, movements of the diaphragm are compromised and cause insufficient aeration with subsequent hypoxia and left ventricular dysfunction. In addition, hypoxia can precipitate angina or tachycardia. When a vasovagal response begins, the patient may have hypotension. Patients with impaction may experience vomiting, diarrhea, and resultant dehydration. They may present in an acutely confused and disoriented state, with tachycardia, fever, and altered blood pressure.

IBS is not usually associated with complications. Fecal incontinence may cause psychological problems in affected patients.

Previous
 
 
Contributor Information and Disclosures
Author

Nafisa K Kuwajerwala, MD Staff Surgeon, Breast Care Center, William Beaumont Hospital

Nafisa K Kuwajerwala, MD is a member of the following medical societies: American College of Surgeons, American Society of Breast Surgeons, American Society of Breast Disease

Disclosure: Nothing to disclose.

Coauthor(s)

Vivek V Gumaste, MD Associate Professor of Medicine, Mount Sinai School of Medicine of New York University; Adjunct Clinical Assistant, Mount Sinai Hospital; Director, Division of Gastroenterology, City Hospital Center at Elmhurst; Program Director of GI Fellowship (Independent Program); Regional Director of Gastroenterology, Queens Health Network

Vivek V Gumaste, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association

Disclosure: Nothing to disclose.

Luigi Santacroce, MD Assistant Professor, Medical School, State University at Bari, Italy

Disclosure: Nothing to disclose.

Venkata Subramanian Kanthimathinathan, MD Fellow in Bariatric/Advanced Laparoscopic Surgery, University of Missouri Healthcare

Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD Clinical Professor of Medicine, Drexel University College of Medicine

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law, Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Acknowledgements

Silvia Gagliardi, MD Consulting Staff, Department of Surgery, Medical Center Vita, Italy

Disclosure: Nothing to disclose.

Douglas M Heuman, MD, FACP, FACG, AGAF Chief of GI, Hepatology, and Nutrition at North Shore University Hospital/Long Island Jewish Medical Center; Professor, Department of Medicine, Hofstra North Shore-LIJ School of Medicine

Douglas M Heuman, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, and American Gastroenterological Association

Disclosure: Novartis Grant/research funds Other; Bayer Grant/research funds Other; Otsuka Grant/research funds None; Bristol Myers Squibb Grant/research funds Other; Scynexis None None; Salix Grant/research funds Other; MannKind Other

Sandeep Mukherjee, MB, BCh, MPH, FRCPC Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center

Sandeep Mukherjee, MB, BCh, MPH, FRCPC is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Merck Honoraria Speaking and teaching; Ikaria Pharmaceuticals Honoraria Board membership

Shivkumar Prabhu, MD Consulting Staff, Department of Internal Medicine, St John Detroit Riverview Hospital

Disclosure: Nothing to disclose.

Daniel Schafer Department of Surgery, University of Nebraska Medical Center

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Di Lorenzo C, Youssef NN. Diagnosis and management of intestinal motility disorders. Semin Pediatr Surg. 2010 Feb. 19(1):50-8. [Medline].

  2. Keller J, Layer P. Intestinal and anorectal motility and functional disorders. Best Pract Res Clin Gastroenterol. 2009. 23(3):407-23. [Medline].

  3. Venkatasubramani N, Sood MR. Motility disorders of the gastrointestinal tract. Indian J Pediatr. 2006 Oct. 73(10):927-30. [Medline].

  4. Ouyang A, Locke GR 3rd. Overview of neurogastroenterology-gastrointestinal motility and functional GI disorders: classification, prevalence, and epidemiology. Gastroenterol Clin North Am. 2007 Sep. 36(3):485-98, vii. [Medline].

  5. Rao SS. Constipation: evaluation and treatment of colonic and anorectal motility disorders. Gastroenterol Clin North Am. 2007 Sep. 36(3):687-711, x. [Medline].

  6. De Giorgio R, Cogliandro RF, Barbara G, Corinaldesi R, Stanghellini V. Chronic intestinal pseudo-obstruction: clinical features, diagnosis, and therapy. Gastroenterol Clin North Am. 2011 Dec. 40(4):787-807. [Medline].

  7. Rudolph CD, Hyman PE, Altschuler SM, Christensen J, Colletti RB, Cucchiara S, et al. Diagnosis and treatment of chronic intestinal pseudo-obstruction in children: report of consensus workshop. J Pediatr Gastroenterol Nutr. 1997 Jan. 24(1):102-12. [Medline].

  8. Wouters MM, Vicario M, Santos J. The role of mast cells in functional GI disorders. Gut. 2016 Jan. 65 (1):155-68. [Medline].

  9. Knowles CH, Martin JE. Slow transit constipation: a model of human gut dysmotility. Review of possible aetiologies. Neurogastroenterol Motil. 2000 Apr. 12(2):181-96. [Medline].

  10. Amiot A, Tchikviladze M, Joly F, et al. Frequency of mitochondrial defects in patients with chronic intestinal pseudo-obstruction. Gastroenterology. 2009 Jul. 137(1):101-9. [Medline].

  11. Li B, Wang JR, Ma YL. Bowel sounds and monitoring gastrointestinal motility in critically ill patients. Clin Nurse Spec. 2012 Jan. 26(1):29-34. [Medline].

  12. Remes-Troche JM, Rao SS. Diagnostic testing in patients with chronic constipation. Curr Gastroenterol Rep. 2006 Oct. 8(5):416-24. [Medline].

  13. Maqbool S, Parkman HP, Friedenberg FK. Wireless capsule motility: comparison of the SmartPill GI monitoring system with scintigraphy for measuring whole gut transit. Dig Dis Sci. 2009 Oct. 54(10):2167-74. [Medline].

  14. [Guideline] American College of Radiology (ACR), the Society of Nuclear Medicine (SNM), and the Society for Pediatric Radiology (SPR). ACR–SNM–SPR Practice parameter for the performance of gastrointestinal scintigraphy. Res. 29 – 2010, Amended 2014 (Res. 39). ACR American College of Radiology. Available at http://www.acr.org/Quality-Safety/Standards-Guidelines/Practice-Guidelines-by-Modality/Nuclear-Medicine. Accessed: October 29, 2014.

  15. Alyami J, Spiller RC, Marciani L. Magnetic resonance imaging to evaluate gastrointestinal function. Neurogastroenterol Motil. 2015 Dec. 27 (12):1687-92. [Medline].

  16. Burns AJ. Disorders of interstitial cells of Cajal. J Pediatr Gastroenterol Nutr. 2007 Dec. 45 Suppl 2:S103-6. [Medline].

  17. He CL, Burgart L, Wang L, Pemberton J, Young-Fadok T, Szurszewski J, et al. Decreased interstitial cell of cajal volume in patients with slow-transit constipation. Gastroenterology. 2000 Jan. 118(1):14-21. [Medline].

  18. Pardi DS, Miller SM, Miller DL, Burgart LJ, Szurszewski JH, Lennon VA, et al. Paraneoplastic dysmotility: loss of interstitial cells of Cajal. Am J Gastroenterol. 2002 Jul. 97(7):1828-33. [Medline].

  19. Sanders KM. Interstitial cells of Cajal at the clinical and scientific interface. J Physiol. 2006 Nov 1. 576(Pt 3):683-7. [Medline].

  20. Vanuytsel T, Tack JF, Boeckxstaens GE. Treatment of abdominal pain in irritable bowel syndrome. J Gastroenterol. 2014 Aug. 49 (8):1193-205. [Medline].

  21. Hotta R, Stamp LA, Foong JP, McConnell SN, Bergner AJ, Anderson RB, et al. Transplanted progenitors generate functional enteric neurons in the postnatal colon. J Clin Invest. 2013 Mar 1. 123(3):1182-91. [Medline]. [Full Text].

  22. Cleveland Clinical Foundation, Center for Gastrointestinal Motility Disorders. Intestinal motility disorders. Available at: http://www.ccf.org/gastro/motility/default.htm. Cleveland, Ohio: Cleveland Clinic;. 1999. [Full Text].

  23. Fu A. Neostigmine: an alternative treatment for constipation. Dynamics. 2005. 16(1):13-5. [Medline].

  24. Karamanolis G, Tack J. Promotility medications--now and in the future. Dig Dis. 2006. 24(3-4):297-307. [Medline].

  25. Sarna SK. Molecular, functional, and pharmacological targets for the development of gut promotility drugs. Am J Physiol Gastrointest Liver Physiol. 2006 Oct. 291(4):G545-55. [Medline].

  26. Quigley EM. Prucalopride: safety, efficacy and potential applications. Therap Adv Gastroenterol. 2012 Jan. 5(1):23-30. [Medline]. [Full Text].

  27. Bassotti G, Gambaccini D, Bellini M. Prucalopride succinate for the treatment of chronic constipation: an update and future directions. Expert Rev Gastroenterol Hepatol. 2015 Dec 8. [Medline].

  28. Mellgren A, Matzel KE, Pollack J, et al.; for the Nasha Dx Study Group. Long-term efficacy of NASHA Dx injection therapy for treatment of fecal incontinence. Neurogastroenterol Motil. 2014 Aug. 26 (8):1087-94. [Medline].

  29. Mazzone A, Farrugia G. Evolving concepts in the cellular control of gastrointestinal motility: neurogastroenterology and enteric sciences. Gastroenterol Clin North Am. 2007 Sep. 36(3):499-513, vii. [Medline].

  30. Sigurdsson L, Reyes J, Kocoshis SA, et al. Intestinal transplantation in children with chronic intestinal pseudo- obstruction. Gut. 1999 Oct. 45(4):570-4. [Medline].

  31. Millar AJ, Gupte G, Sharif K. Intestinal transplantation for motility disorders. Semin Pediatr Surg. 2009 Nov. 18(4):258-62. [Medline].

  32. Parthasarathy G, Ravi K, Camilleri M, Andrews C, et al. Effect of neostigmine on gastroduodenal motility in patients with suspected gastrointestinal motility disorders. Neurogastroenterol Motil. 2015 Dec. 27 (12):1736-46. [Medline].

  33. Menys A, Butt S, Emmanuel A, et al. Comparative quantitative assessment of global small bowel motility using magnetic resonance imaging in chronic intestinal pseudo-obstruction and healthy controls. Neurogastroenterol Motil. 2015 Dec 10. [Medline].

 
Previous
Next
 
Dilated cecum (16 cm) and colon in patient with pseudocolonic obstruction.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.