To critically review the literature addressing the definition, epidemiology, aetiology and pathophysiology of acute colonic pseudo-obstruction (ACPO).

A systematic search was performed to identify articles investigating the aetiology and pathophysiology of ACPO. A narrative synthesis of the evidence was undertaken.

No consistent approach to the definition or reporting of ACPO has been developed, which has led to overlapping investigation with other conditions. A vast array of risk factors has been identified, supporting a multifactorial aetiology. The pathophysiological mechanisms remain unclear, but are likely related to altered autonomic regulation of colonic motility, in the setting of other predisposing factors.

Future research should aim to establish a clear and consistent definition of ACPO, and elucidate the pathophysiological mechanisms leading to altered colonic function. An improved understanding of the aetiology of ACPO may facilitate the development of targeted strategies for its prevention and treatment.

The characterisation and management of chronic severe gastrointestinal (GI) dysmotility are challenging. It may cause intestinal failure requiring home parenteral nutrition (HPN).

To review the presentation, aetiology, characterisation, management and outcome of chronic severe GI dysmotility, and to suggest a pragmatic management algorithm.

PubMed search was performed up to December 2012 using appropriate search terms, restricted to human articles and reviewed for relevance. Segmental dysmotility, acute ileus, functional syndromes and non-English articles were excluded. Evidence and recommendations were evaluated using the GRADE system.

In total, 721 relevant articles were reviewed. A coherent and definitive picture is hampered by overlapping classification systems using multi-modal characterisation methods, subject to pitfalls and some requiring further validation. The literature is confined to case series with no randomised trials. Fewer than 20% undergo full thickness jejunal biopsy, which are otherwise labelled idiopathic. However, in studies with up to 80% biopsy rates, neuromuscular abnormalities may be found in 90%. Between 14% and 50% will require HPN, comprising 8-14% of all HPN patients, of which 2/3 are primary/idiopathic and 1/3 secondary, with scleroderma being the leading secondary cause. Ten-year  mortality ranges from 13% to 35% and is worst in elderly scleroderma patients. Management includes limited treatments for secondary causes, prokinetics, symptom palliation, psychological support, nutrition, hydration and judicious surgery.

Severe dysmotility often remains idiopathic. It is rarely possible to alter disease trajectory; consequently, prognosis may be poor. Multi-disciplinary teams in a specialist setting can improve outcomes. Graded recommendations are enumerated and a pragmatic algorithm is suggested.

Although uncommon, medication-induced colonotoxicity is important to recognize because medication cessation generally leads to prompt clinical improvement, while medication continuation results in disease exacerbation. This review categorizes the association between medications and colonotoxicity as "well-established" or "probable," according to the following criteria: total number of reported cases, number of different research groups reporting an association, experimental and pharmacologic evidence of an association, and validity of an association in each reported case. Cocaine, ergotamine, estrogen, sodium polystyrene, alosetron, amphetamines, pseudoephedrine, and vasopressin are associated with colonic ischemia. The mechanisms include vasospasm, thrombogenesis, and shunting of blood from mesenteric vessels. Narcotics, phenothiazines, vincristine, atropine, nifedipine, and tricyclic antidepressants are associated with colonic pseudo-obstruction. The mechanisms include antagonizing prokinetic neurotransmitters, stimulating antikinetic neurotransmitters, promoting dysmotility, relaxing smooth muscle, and injuring enteric neurons. Numerous antibiotics are associated with pseudomembranous colitis; ampicillin is associated with hemorrhagic colitis; chemotherapy is associated with neutropenic colitis; and deferoxamine is associated with Yersinia enterocolitis. Mechanisms of these toxicities include altering normal bowel flora, weakening immunologic defenses, promoting microorganism virulence, and mucosal injury. Gold compounds, nonsteroidal antiinflammatory drugs, alpha-methyldopa, salicylates, and sulfasalazine are associated with an inflammatory or cytotoxic colitis. The mechanisms include direct mucosal cytotoxicity, antimetabolite effects, or drug allergy. Nonsteroidal antiinflammatory drugs, cyclo 3 fort, flutamide, lansoprazole, and ticlopidine are associated with lymphocytic colitis. The mechanisms include immunologic activation or attenuated immunologic defenses. Chronic cathartic use leads to colonic hypomotility and abdominal distention. Intrarectally administered corrosive compounds can produce a toxic colitis.

Acute colonic pseudo-obstruction (Ogilvie's syndrome) in the immunosuppressed patient is associated with increased morbidity and mortality. Renal transplant recipients possess several comorbidities that increase the risk of acute pseudo-obstruction of the colon. The aims of this study were to present our experience with this syndrome and to evaluate the potentiating factors in these patients. A review of the literature for pseudo-obstruction following renal transplantation is presented.

Seven patients who developed Ogilvie's syndrome were identified in a retrospective review of 550 kidney-only transplants. Pretransplant data, potential risk factors, presentation, management, and outcome details were retrieved. The medical literature was reviewed using Medline.

Seventy-eight patients with Ogilvie's syndrome in the early posttransplant period have been reported. The associated morbidity and mortality was heightened in this immunocompromised population. Obese transplant recipients (body mass index >30 kg/m2) were at significantly increased risk for developing this syndrome.

A broad armamentarium of treatment options is available, but the key to successful resolution lies in early recognition.

Acute pseudo-obstruction is a rare complication in burns patients. An awareness of the factors implicated in its pathogenesis such as prolonged bed rest, narcotic medications, hypokalaemia, sepsis and surgery (all commonly associated with burns patients) is essential if this condition is to be avoided. Early diagnosis, prokinetic and cathartic agents, and aggressive endoscopic intervention are essential to halt the progression of caecal dilatation. Excisional surgery and stoma formation are necessary for salvage of complicated colonic pseudo-obstruction.

Acute colonic pseudo-obstruction as a syndrome was first described by Ogilvie in 1948 (Br. Med J. 2, 671). It is characterized by colonic dilatation with no mechanical cause which affects critically ill patients. As a result of this complication the prognosis worsens. Initially there are few clinical symptoms, but subsequently colonic obstruction develops which, if not treated, can cause perforation of the caecum resulting in a high mortality rate. The treatment includes decompression via rectal and nasogastric probes, colonoscopy and caecostomy.

Colonic pseudo-obstruction may have many possible causes. Some of these are well described and pose no diagnostic problems. Drug-related colonic pseudo-obstruction remains underreported, but is of importance in modern society where drugs are endemically abused. This case highlights the importance of drugs in altering colonic motility and emphasizes the nonsurgical management of this condition.

Gastrointestinal motility is the function of gastrointestinal smooth muscle. It is controlled by both the intrinsic and extrinsic nerves of the gastrointestinal tract and, to a lesser degree, the gastrointestinal hormones. Therefore, any abnormality of the above factors, theoretically, can cause gastrointestinal dysmotility. In a clinical situation, commonly seen is gastrointestinal dysmotility caused by either smooth muscle or intrinsic and extrinsic nerves dysfunction. Diseases that cause smooth muscle dysfunction include familial visceral myopathies, nonfamilial visceral myopathies, collagen disease, muscular dystrophies, amyloidosis, thyroid disease, and so on. Diseases that cause enteric nerve dysfunction include familial visceral neuropathies, nonfamilial visceral neuropathies, diabetes mellitus, Chagas' disease, ganglioneuromatosis of the intestine, visceral neuropathy of carcinomatosis, Parkinson's disease, and so on. The patients with neuromuscular disease of the gastrointestinal tract have a wide range of clinical manifestations regardless of the underlying cause. At one end of the spectrum, the patients may be asymptomatic, and at the other end of the spectrum, the patients may have functional obstruction of the gastrointestinal tract. Plain abdominal x-rays, upper gastrointestinal (UGI) and small bowel x-rays, enteroclysis, barium enema, and manometric studies are useful for the work-up of these patients. Enteroclysis is especially helpful in ruling out mechanical obstruction of the small intestine in patients with chronic intestinal pseudo-obstruction. Treatment is mainly symptomatic and supportive. There is no effective drug to improve gastrointestinal motility. Surgery may be helpful in selected cases of severe gastrointestinal dysmotility.

Pseudo-obstruction of the colon is characterized by an adynamic unobstructed colon which rapidly progresses to marked dilatation of the cecum and transverse colon. Disagreements exist regarding the etiology or pathogenesis of this syndrome; it has been associated with metabolic, traumatic, postoperative, and idiopathic causes. In reviewing the literature we have concluded that in pseudo-obstruction of the colon after cesarean section, the mean age of occurrence is 35 years. The symptoms occur in the first 72 hours after operation. Straight x-ray examination of the abdomen is the most useful diagnostic measure. All cecal perforations occurred by the fifth postoperative day. For this reason, we recommend early diagnosis and prompt surgical intervention before that time. In cases when the cecal distention is 12 cm or more, decompression is urgent.

Pseudo-obstruction of the colon, or Ogilvie's syndrome, is characterized by an adynamic, dilated, unobstructed colon, the exact cause of which remains obscure. Although several precipitating factors have been described in the literature, we have observed three patients whose pseudo-obstruction of the colon occurred during interstitial and intracavitary pelvic irradiation. Such a cause has not been noted previously. Pseudo-obstruction of the colon can have serious consequences if it is not recognized early and treated vigorously.

Pseudoobstruction of the colon is a specific variety of adynamic ileus. Its characteristic clinical presentation is severe cramping lower abdominal pain, a massively distended abdomen, and a characteristic x-ray picture. Thirty-five patients with this disease complex have been reviewed, and their surgical and medical therapy is discussed. Guidelines for continued medical versus surgical intervention are suggested. Two patients underwent decompression with the colonoscope. Its use and a possible hazard of the procedure are discussed. For those patients who develop pseudoobstruction after trauma or surgery, a pathophysiologic explanation is offered. The possible role of prostaglandin abnormality in the genesis of pseudoobstruction is also discussed.

The gastrointestinal tract is a common target for adverse drug reactions. The resultant changes are often nonspecific (e.g., mucosal ulceration, intestinal infarction, motility disturbance) and in many cases no radiographically detectable lesion may occur. A comprehensive review of the reported drug-induced disorders of the digestive organs is herein presented and their radiographic manifestations are described.