David E. Beck, Steven D. Wexner, Tracy L. Hull, Patricia L. Roberts, Theodore J. Saclarides, Anthony J. Senagore, Michael J. Stamos and Scott R. Steele (eds.)The ASCRS Manual of Colon and Rectal Surgery2nd ed. 201410.1007/978-1-4614-8450-9_2
© Springer Science+Business Media New York 2014
2. Colonic Physiology
(1)
Department of Colorectal Surgery, Cleveland Clinic Foundation, Cleveland, OH, USA
(2)
Department of Colorectal Surgery, Digestive Disease Institute, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Desk A 30, Cleveland, OH 44195, USA
Abstract
The colon plays a role in digestion by fermenting complex carbohydrates and proteins that prove resistant to digestion and absorption in the more proximal intestine.
Ten percent of ingested carbohydrates enter the cecum and are fermented by saccharolytic and proteolytic species of bacteria, the majority of which are obligate anaerobes.
The diverse end products of bacterial fermentation include complex carbohydrates (fiber) and the short-chain fatty acids: butyrate [15 %], propionate [25 %], and acetate [60 %].
Complex carbohydrates are fermented primarily in the ascending and proximal transverse colon, while proteins are fermented in the distal colon.
Colonic Function
Salvage, Metabolism, and Storage
The colon plays a role in digestion by fermenting complex carbohydrates and proteins that prove resistant to digestion and absorption in the more proximal intestine.
Ten percent of ingested carbohydrates enter the cecum and are fermented by saccharolytic and proteolytic species of bacteria, the majority of which are obligate anaerobes.
The diverse end products of bacterial fermentation include complex carbohydrates (fiber) and the short-chain fatty acids: butyrate [15 %], propionate [25 %], and acetate [60 %].
Complex carbohydrates are fermented primarily in the ascending and proximal transverse colon, while proteins are fermented in the distal colon.
Dietary prebiotics such as inulin result in saccharolytic fermentation.
Fermented proteins are converted into short-chain fatty acids, branched-chain fatty acids, amines, ammonia, phenols, indoles, and sulfurs. Some of these products are considered potential etiologic agents for colon cancer and ulcerative colitis.
Residual products of bacterial fermentation such as carbon dioxide, hydrogen, and methane are absorbed or passed with the feces.
Dietary fats are usually expelled with the stool.
An average of 400 mmol/day (range of 150–600 mmol/day) of short-chain fatty acids is produced in the colon. More than 95 % of short-chain fatty acids are immediately appropriated by the colon.
Reclamation of undigested matter in the colon provides 5–15 % of the total caloric needs of an individual.
Short-chain fatty acids are incorporated as the basic elements for mucin synthesis, lipogenesis, gluconeogenesis, and protein production.
Butyrate, the least abundant of the short-chain fatty acids, acts as the primary energy source for the colonocyte, supplying 70–90 % of its energy requirements. Colonocytes receive their nourishment solely from luminal substrates, not from the bloodstream.
Butyrate also advances colonic cell proliferation and differentiation, repair, and immune function as well as promotes the absorption of water, sodium, and chloride from the colon, acting as an antidiarrheal agent.
Fewer butyrate transporters are present in human colonic adenocarcinomas, resulting in a decrease in the utilization of the trophic butyrate by malignant cells. In vitro studies of cancer cell lines identified apoptosis, nonproliferation, and differentiation after the administration of butyrate.
Prebiotics, primarily nondigestable oligosaccharides, are slowly fermentable foods that selectively propagate microbial proliferation and/or activity.
In contrast, probiotics represent active bacterial cultures that benefit the host by replenishing the colonic microenvironment.
Synbiotics combine the action of pre- and probiotics.
The beneficial effect of these supplements is attributable to an increased production of butyrate, changes in mucin production, or interference in the binding of pathogenic bacteria to the colonic mucosa.
Currently, probiotics are prescribed in cases of disturbed microbial balance, such as antibiotic-associated diarrhea.
In the future, pre- and probiotics may become important supplements to promote health and to prevent illness.
The colon demonstrates regional differences but does exhibit adaptability.
The proximal colon is more saccular and serves as a reservoir.
The distal colon is more tubular and performs as a conduit.
The character of the luminal contents impacts transit times. Large volumes of liquid quickly pass through the ascending colon but remain within the transverse colon for as long as 20–40 h; in contrast, a solid meal is retained by the cecum and ascending colon for longer periods than a liquid diet.
Salvage of water and electrolytes occurs primarily in the proximal colon.
Transport of Water and Electrolytes
The colonic mucosal surface area is approximately 2,000 cm2. The colonic mucosa assists in fluid homeostasis.
The surface epithelial cells are primarily responsible for absorption, while the crypt cells are involved in fluid secretion.
Water is passively absorbed along an osmotic gradient, enabled by a luminal sodium concentration lower than that of the epithelial cells.
Normally, the colon is presented with 1.5–2 L of water daily.
Approximately 90 % of this water is reclaimed by the colon, leaving 100–150 mL in the feces. Approximately 200 g of solid feces per day is produced following fluid and electrolyte absorption and secretion as well as bacterial activity.
The ascending colon demonstrates the greatest absorptive capability.
As a consequence, diarrhea more consistently ensues after a right as opposed to a left hemicolectomy.
Fluid retention is promoted by the antidiuretic hormone.
When challenged, the colon, with the additional contribution of the sigmoid colon and rectosigmoid, is able to save a further 5–6 L of intestinal water daily.
This facility for fluid salvage is contingent upon the composition, rate of flow (less than 1–2 mL/min), and amount of the effluent.
Fluid secretion in the colon only transpires in the presence of diverse secretagogues, such as laxatives, bacterial endotoxins, hormones (e.g., VIP), and endogenous substances (e.g., bile acids).
Under normal conditions, the colon principally absorbs sodium and chloride but secretes bicarbonate and potassium.
If required, the colon is able to increase its salvage of sodium to 800 mmol/L/day.
The transport mechanisms for sodium absorption, located on the luminal surface of the epithelial cells, vary throughout the colon: a Na+/H+ exchange channel in the proximal colon and an electrogenic sodium-specific channel (ENaC) in the distal colon and rectum.
The Na+/H+ exchange channels (NHE 2 and 3) are coupled to the Cl−-HCO3 − exchange channels. The activity of the electrogenic sodium-specific channel in the distal colon and rectum is requisite for the desiccation of stool.
These two types of transport channel allow for the passive diffusion of sodium into the colonic epithelial cells along an electrochemical gradient, consisting of a low intracellular sodium concentration (<15 mM) and a negative intracellular electrical potential difference as compared to the lumen.
This favorable electrochemical gradient is created by the active extrusion of sodium via the Na+/K+ ATPase pump on the basolateral membrane of the epithelial cell: three sodium ions are expelled in exchange for two potassium ions.
Aldosterone, a mineralocorticoid secreted by the adrenal gland in response to sodium depletion and dehydration, enhances fluid and sodium absorption in the colon.
The absorption of sodium is further promoted by somatostatin, α2-adrenergic agents (e.g., clonidine), and the short-chain fatty acids.
In the proximal colon, chloride is traded for bicarbonate via the Cl−-HCO3 − exchange channel found on the luminal surface of the epithelial cells; the activity of this channel is linked to the Na+/H+ exchange protein.
However, chloride also is absorbed through a Cl−-HCO3 − exchange channel that is not associated with sodium.
Chloride absorption is supported by an acidic luminal milieu. The transport mechanism for bicarbonate secretion is poorly understood.
Potassium transport is primarily a passive process, following the movement of sodium across cell membranes.
The H+/K+ ATPase actively conveys potassium into the epithelial cells of the distal colon and rectum.
Potassium secretion, combined with potassium derived from bacteria and colonic mucous, may explain the relatively high concentration of this electrolyte—50–90 mmol/L—in stool.
Approximately 0.4–1 g of urea enters the colon daily and is converted by colonic microorganisms into ammonia, which is then passively absorbed by the surface epithelial cells.
Ammonia is also derived from dietary nitrogen, the sloughed mucosal lining, and bacterial waste.
The majority of the ammonia that reaches the colon is returned via the enterohepatic circulation to the liver, where it is refashioned into urea.
Colonic Motility
Methods to Measure Colonic Transit
Altered motility plays a role in various gastrointestinal disorders, but it is poorly understood due to the inaccessibility of the colon for direct study.
Bowel questionnaires assess stool frequency and colorectal transit time (75 % of total intestinal transit time).
Techniques to determine colonic motility begin with the calculation of colonic transit time via markers, scintigraphy, and wireless capsules.
Radiopaque Markers
Total and regional colonic transit times are reflected by the number and the location of the markers on sequential abdominal radiographs.
For men, the average total colonic transit is 30.7 h (SD 3.0) and for women, 38.3 h (SD 2.9).
Various protocols for this type of examination exist, all of which suggest the cessation of all laxatives 48 h prior to swallowing the markers:
In one approach that focuses on total colonic transit, an abdominal radiograph is obtained 5 days after taking a capsule containing 20 markers. A normal study demonstrates evacuation of 80 % (14) of the markers. The retention of more than 20 % of the markers suggests slow transit constipation.
Currently commercial available markers (SitzmarkersTM, Konsyl Pharmaceuticals) contain 24 markers in the capsule.
A second variation involves ingesting the capsule on Sunday evening and obtaining abdominal x-rays on days 1, 3, and 5. The film on the first day provides evidence that gastric and small motility are grossly normal if all the markers are in the colon. A normal study shows the passage of 80 % of the markers by day 5.
In another alternative, patients ingest single capsules (containing 24 markers) on 3 successive days, with only one abdominal radiograph done on day 4 of the study. The number of markers present equals the colonic transit time in hours.
An accumulation of the markers in the rectosigmoid indicates a dyssynergic defecation pattern (outlet obstruction).
The reliability of the technique is affected by patient compliance as well as by differences in the interpretation of the results.
Scintigraphy
Colonic scintigraphy measures colonic transit by following the passage of a radioactive isotope that is ingested as a delayed release capsule or placed directly in the cecum by orocecal intubation. The delayed release capsule, coated with the pH-sensitive polymer methacrylate, is comprised of activated charcoal or polystyrene pellets labeled with either 111In or 99mTc. The coating dissolves at the pH of 7.2–7.4 found in the distal ileum, after which the radioactive material is delivered into the colon.
Images are taken with a gamma camera at specified intervals, usually at 4, 24, and 48 h after consumption of the isotope, although this can be performed as frequently as twice daily.
Segmental transit is usually determined for the ascending, transverse, descending, and rectosigmoid regions of the colon. The proportion of the counts is calculated in each section and then multiplied by a weighing factor: 0 for the cecum, 1 for the ascending colon, 2 for the transverse colon, 3 for the descending colon, 4 for the rectosigmoid colon, and 5 for stool.
The results are expressed as the geometric center of the isotope mass at any given time point, with a low count indicating that the isotope is close to the cecum and a higher count that it has progressed more distally.
For clinical use, the total percentage of retained isotope as compared to normal data appears to be the most convenient reporting system.
Scintigraphy correlates well with the radiopaque marker technique in assessing colonic transit, with a similar sensitivity in diagnosing patients with slow transit constipation.
The total exposure to radiation is also equivalent. Due to its greater costs, in most cases scintigraphy serves as a research instrument.
Wireless Motility Capsule
The wireless motility capsule (SmartPill®) uses a capsule containing miniature intraluminal pressure, temperature, and pH measurement devices.
The capsule is ingested, after which continuous recordings are obtained in an ambulatory setting, with the data captured over 5 days via a wireless instrument.
A drop in pH and a change in motility delineate the transition from the distal ileum into the cecum. From these data, whole gut transit and colonic transit can be separated and calculated.
In one trial, the results from the capsule approach correlated well with those acquired from the radiopaque markers, with a similar sensitivity and specificity in detecting abnormal transit in those patients with constipation.
The capsule is able to gauge phasic colonic contractions but not colonic motor patterns.
This costly procedure is not widely employed but is attractive in that radiation exposure is avoided and patient compliance is facilitated.
Techniques to Record Colonic Motility
Colonic motility is gauged by the monitoring of electrical activity using surface electrodes or of intraluminal pressure via a manometry or barostat apparatus.
Indirect assessment of colonic motility has been hindered by the instruments available, colonic anatomy, the need for prolonged readings, and the absence of standardization.
Placement of the intraluminal devices is difficult, requiring either oral or nasal intubation or colonoscopy; furthermore, application of the surface electrodes demands surgery.
Additionally, the necessity to purge the colon of stool may impact the results, producing an increase in the number of high-amplitude propagated contractions, although these findings are conflicting.
Determinations of colonic pressure are further influenced by artifact from extrinsic forces such as cough, straining, and sneezing.
Recordings are usually obtained over 6 h in the laboratory and over 24 h in an ambulatory setting.
Most of these approaches are in the researcher’s domain.
Manometry
Colonic manometry uses a flexible catheter (solid-state or a water-perfused catheter system) that is inserted into the colon. The water-perfused system increases the amount of fluid in the colon, which may alter results, while solid-state catheters are fragile, expensive, and sensitive to corrosive damage from colonic irritants.
The validity of the readings depends upon the proper placement of the catheter. As noted, the introduction of the catheter occurs via an oral or nasal route, confirmed with fluoroscopy, or by colonoscopy.
To adhere to more physiologic conditions, unprepared colons are currently advocated, despite the impediment presented by the retained stool to the retrograde placement of the catheters; in some cases, enemas are instead used.
The patients are often asked to maintain a diary to mark events such as bowel movements, flatus, and meals.
Manometry is well able to detect the changes in intraluminal pressure after eating or the administration of a colonic stimulant (e.g., bisacodyl).
However, these variations in pressure do not consistently correspond to contractions, and contractions are not reliably identified. Measurements obtained from manometry are also affected by the luminal diameter at the location of the catheter tip.
Manometry also recognizes patterns of motor activity due to the multiple recording sites along the catheter.
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