Constipation: motility and the gut.
Worldwide, the prevalence of constipation varies between 2.5 and 79 per cent of adults. In Oceania, the reported rate is about 20 per cent. (1) Health-care professionals often define constipation as a reduction in, or difficulty with, bowel movements. People suffering from constipation describe this condition much more subjectively straining at stool, pain, cramping, and sensations of bloating, incomplete evacuation or anorectal blockage. (2)
Chronic constipation carries significant costs to the health-care system and to individuals. In 2004 in the United States (US), constipation was the primary reason for 6.3 million patient visits to health-care centres, and cost US$1.7 billion in both direct and indirect expenditure. (3)
Definitions of constipation do not rely on the absolute number of bowel movements, since the average "normal" number of bowel motions ranges from three times per week to three times per day. (4) Rather, constipation is determined by signs and symptoms identified as part of the Rome III diagnostic criteria for functional gastrointestinal disorders. (5) Under the Rome criteria, constipation is defined as persistently difficult, infrequent, or seemingly incomplete defecation that does not meet the criteria for irritable bowel syndrome.
After reading this article and completing the accompanying online learning activities you should be able to:
* Outline the normal mechanisms regulating motility in the small and large intestines.
* Discuss causes and consequences of constipation.
* Explain the actions of drugs and other therapies used to treat constipation.
* Discuss factors in the pathogenesis of bowel obstruction.
According to the Rome III criteria, a diagnosis of constipation can be reached when two or more of the following are present for at least 25 per cent of defecations in the last three months: (5)
* Lumpy or hard stools
* Sensation of incomplete evacuation
* Sensation of anorectal blockage or obstruction
* Manual manoeuvres used (digital evacuation or compression of pelvic floor)
* Fewer than three movements per week
Also, there must be no, or rare, loose stools (except with the use of laxatives) and insufficient criteria to meet the diagnosis of irritable bowel syndrome. Nurses should, however, be aware of the possibility of overflow diarrhoea in the presence of severe constipation and impaction.
Consistency of the stool is usually described using the Bristol Stool Chart (see Figure 2, p23), where Types 1 and 2 indicate constipation, 3 and 4 are normal stools and 5 to 7 are associated with diarrhoea and urgency. (6)
Constipation is usually due to slow or delayed transit of gut contents, normal transit but delayed defecation, or pelvic floor or anal sphincter dysfunction. (7) Knowledge of normal gut motility and the defecation reflex helps nurses understand the causes and treatment of constipation.
STRUCTURE OF THE INTESTINES
The walls of the small and large intestine are arranged in similar ways (see Figure 1, below). The innermost layer (the mucosa) is composed of epithelial cells lining the lumen of the gut, mucus and fluid-secreting cells, blood vessels and lymphatics. Outside this layer is the submucosa, consisting of connective tissue and containing the submucosal nerve plexus. Next comes a layer of smooth muscle, arranged in a circular fashion, covering the entire circumference of the gut. A second layer of smooth muscle lies lengthwise, and between these two layers is the myenteric nerve plexus. Finally, the gut is surrounded by the tough connective tissue of the serosa and peritoneum. (8)
The circular smooth muscle is responsible for segmentation in the gut--mixing contractions that churn intestinal contents without moving them along the tract. Longitudinal muscle is mainly concerned with peristalsis --the movement of the contents along the gut toward the anus. (8)
Apart from at the anus and oesophagus, the muscle layers of the gut are composed of smooth muscle cells. Smooth muscle contracts when an action potential causes the opening of calcium channels on the cell membrane. Action potentials travel from cell to cell via gap junctions that link adjacent smooth muscle cells. Action potentials that initiate contraction are generated by neurotransmitters released from nerve fibres in the region, or by pacemaker cells that spontaneously depolarise in a rhythmic pattern. Segmentation and peristalsis are regulated by the enteric nervous system.
THE ENTERIC NERVOUS SYSTEM
Sometimes referred to as the "second brain", the enteric nervous system is a highly complex network of neurons which controls motor functions, local blood flow, secretory activity, immune and hormonal functions along the gut. (9,10) It is found in two layers: the myenteric plexus is a layer of neurons that runs the length of the gut, from oesophagus to anus, in between the circular smooth muscle layer and the longitudinal smooth muscle layer. This layer of neurones controls movement along the gut. A second layer of neurons immediately beneath the mucosal layer of the gut controls secretion of fluid and electrolytes. (11)
The neuronal circuits involve sensory neurons that synapse locally onto interneurons and then to motor neurons that stimulate or inhibit smooth muscle contraction. (12) Interneurons carry signals up and down the length of the gut to ensure co-ordinated function. There is also sensory and motor communication with the central nervous system.
Myenteric reflex arcs in the gut generate peristalsis and mixing movements, designed to aid digestion and absorption, and to propel the gut contents toward the anus for expulsion. The reflex arc is stimulated by changes in the chemical composition of gut contents, or stretching of the cells lining the gut wall. (13) This reflex ensures that smooth muscle behind a food bolus contracts at the same time muscle ahead of the bolus is inhibited and relaxes. Simultaneously, intrinsic pacemaker activity in the smooth muscle of the gut wall triggers regular slow propulsive waves.
Dysfunction in the enteric system can occur through congenital or acquired disorders, or secondary to other disease processes. Hirschsprung's disease is a developmental disorder where absence of part of the enteric nervous system leads to bowel obstruction. It is life-threatening unless the affected area is removed. Irritable bowel syndrome is an acquired disorder of enteric nervous function, while diabetic neuropathy is an example of a condition that has secondary effects on the enteric nervous system. (13)
The complexity of the enteric nervous system is reflected in its vast number of neurotransmitter or hormone receptors--more than 30 have been identified to date. (10) These include serotonin receptors (95 per cent of the body's serotonin is found in the gut), muscarinic, dopamine and opioid receptors, as well as receptors for locally released and systemic hormones such as cholecystokinin, corticotrophin, ghrelin and somatostatin. (13) It is not surprising, then, that many conditions and drug therapies have adverse effects on gut function. In addition, the autonomic nervous system modifies enteric nervous function, allowing central nervous input to gut function.
The sympathetic nervous system acts to inhibit gut motility and secretion, following the release of noradrenaline and adrenaline. This is mainly through inhibition of enteric neurons and vasoconstriction of blood vessels supplying the small and large intestine. Strong sympathetic stimulation can be associated with sensations of nausea, as blood supply to the gut is diminished and gastric plus intestinal stasis ensues.
The parasympathetic system exerts its effects on intestinal motility indirectly through its action in stimulating the enteric neurons that cause contraction of smooth muscle.
Chyme (the thick fluid bolus of partially digested food) entering the colon from the small intestine is propelled toward the rectum. Motor activity in the colon is strongly stimulated following ingestion of a meal via the gastrocolic reflex. This movement peaks 10 to 50 minutes after eating and again at 70 to 90 minutes. This reflex is most strongly stimulated by fatty meals but more rapidly by carbohydrate-rich meals. It is inhibited by protein-rich meals and alcohol, and may be reduced in chronic constipation. (4)
As chyme moves through the colon, it is mixed and exposed to gut bacteria that trigger fermentation of undigested carbohydrates. At the same time, water and electrolytes are absorbed across the gut wall. The slower the transit time along the large intestine, the more water is absorbed and the harder the faecal mass becomes. Normal colonic transit time ranges from less than 57 hours (in children) to around 72 hours in adults. (4)
Box 1. Opioids good for chronic pain but bring on constipation UP TO 45 per cent of patients taking opioids for chronic pain (or recreationally, or as drugs of abuse) will experience constipation, affecting quality of life, activities of daily living and ability to attain adequate analgesia. (20) Opioid drugs act on receptors throughout the GI tract to cause: * decreased contraction * increased muscle tone (inhibits relaxation) * decreased intestinal secretion of water and electrolytes * decreased mucus secretion * increased anal sphincter tone * decreased defaecation reflex Combined, these effects lead to a slow transit time through the colon with a hard stool and difficulty with initiating defecation. (11) These effects, unlike many of the adverse effects of opioids, do not reduce over time. Opioid-receptor agonists are active ingredients in anti-diarrhoeal medicine, eg loperamide. Lifestyle interventions (increased fibre, fluid and exercise) are rarely sufficient to address opioid-induced constipation. Management with oral laxatives should begin with the initial doses of opioids and be escalated at need. A combination of softener and stimulant laxatives will probably be needed. These do not address the underlying cause of the constipation and may not be successful, particularly as the dose of opioid increases. Opioid antagonist drugs successfully manage constipation, but also reduce the analgesic effects. Naloxone, given orally in low doses combined with oxycodone (a strong opioid), has had some success. Naloxone is largely inactivated by the liver once absorbed from the gut, so does not readily access the central nervous system. Newly developed antagonist drugs, such as methylnatrexone, have been formulated so they can't cross the blood-brain barrier. This ensures the central analgesic effects of opioids are not affected while constipation is largely alleviated.
Normal defecation requires the co-ordinated function of the central, autonomic and enteric nervous systems. The anal canal has two sphincters-an internal sphincter that is composed of smooth muscle and is under the control of the parasympathetic system, and an external sphincter, which is made up of skeletal muscle and is under conscious control. Faecal continence is maintained when pressure in the anus (due to the action of the sphincters) is higher than pressure in the rectum. Movement of the faecal mass from the sigmoid colon into the rectum causes stretching of the rectal wall and stimulates the defecation reflex. Relaxation of the internal anal sphincter occurs. This triggers a message to the central nervous system and the urge to defecate is experienced. At this point, the urge can be suppressed by voluntary contraction of the external anal sphincter and muscles in the pelvic floor. The rectal wall gradually relaxes, retrograde contraction of the rectal wall pushes the faecal mass back up out of the rectum and the urge to defecate passes. (14)
Distension of the rectum will increase as further faecal material arrives from the sigmoid colon. Once maximal pressure or stretch is reached, the urge to defecate may become intense. (4) Repeatedly postponing the "call to stool" may impair a person's perception of rectal distension and this contributes significantly to "busy-lifestyle" constipation. Ongoing rectal hyposensitivity may lead to faecal impaction, secondary dilation and the development of a megacolon.
If it is convenient to pass a stool, the person assumes a posture that involves flexion of the hips (sitting on the toilet or squatting), which opens up the anorectal angle, facilitating movement of the faecal mass into the rectum. (4) The muscles of the pelvic floor normally maintain the anorectal angle. An inability to relax these muscles (pelvic floor dyssynergia) will obstruct defecation. Pelvic floor relaxation is mediated by reflexes from the spinal cord and higher centres. These are normally triggered by increased rectal pressure and by an increase in abdominal pressure generated when straining at stool. Reflex relaxation of the pelvic floor is suppressed with pain from anal fissures or inflamed haemorrhoids, causing the external anal sphincter to become hypertonic. (4)
Passing of faeces occurs when intrarectal pressure is raised above anal pressure. This pressure is generated by contractions in the sigmoid colon and rectum, and by raised intra-abdominal pressure due to the valsalva manoeuvre. Pressure in the anal canal is reduced by relaxation of the external sphincter and the pelvic floor and shortening of the anal canal by contraction of longitudinal muscles in the wall. Rectal contents are expelled and as the sensation of emptying occurs, reflex closure of the external sphincter terminates defecation. (4)
CAUSES OF CONSTIPATION
Prevalence of constipation varies considerably across the world. (1) This may reflect differences in cultural, dietary, genetic or economic conditions, but may also be related to cultural definitions of constipation and normal bowel habit. Differences in study and reporting methods make generalisation of risk difficult, but increasing age, female gender and low socio-economic or educational status appear to increase risk. (1)
Figure 2. Bristol Stool Chart Type 1 Separate hard lumps, like nuts Type 2 Sausage-like but lumpy Type 3 Like a sausage but with cracks in the surface Type 4 Like a sausage or snake, smooth and soft Type 5 Soft blobs with clear-cut edges Type 6 Fluffy pieces with ragged edges, a mushy stool Type 7 Water, no solid pieces
Constipation is a symptom of an underlying condition affecting gut motility. Primary causes include impaired enteric nervous activity and sphincter or pelvic floor dysfunction. Constipation can occur secondary to an obstruction of the gut (due to colonic strictures, volvulus or tumours), neurological disorders that affect neural regulation of motility (eg spinal cord lesions, Parkinson's disease, diabetic neuropathy) or metabolic disturbances.
Smooth muscle contraction requires tight regulation of the ions involved in action potential generation and contractility. Hypercalcaemia or hypokalaemia may both cause constipation by interfering with normal muscle function. In pregnancy, hormones inhibit contraction of smooth muscle to prevent uterine contractility until term, but this also affects intestinal motility.
Identification of secondary causes of constipation can help manage it, especially conditions that are amenable to correction. Often, however, constipation is associated with dietary and lifestyle factors. In older adults especially, constipation may be an adverse effect of drug therapy. Table 1 (see p24) lists drugs most commonly associated with constipation. Most act by inhibiting smooth muscle activity in the gut. Opioid-induced constipation is particularly problematic for those with chronic pain or in terminal care (see Box 1, left).
Key risk factors associated with constipation are:
* Sedentary lifestyle, including institutionalisation.
* Poor hydration (causing increased absorption of water from the colon and hardening of the stool).
* Low residue diet (reducing faecal volume).
* Reduced mental status.
* Lack of privacy and time.
MANAGEMENT OF CONSTIPATION
New onset constipation, or worsening of symptoms, should always be assessed. Physical assessment should include listening for bowel sounds and palpating for tenderness or abdominal mass. Absent, reduced, excessive, or tinkling bowel sounds and/or abdominal tenderness may indicate obstruction. The patient should be further assessed before administering laxatives (especially stimulant laxatives).
Exercise, high-fibre diet and hydration are primary interventions in preventing and treating constipation. The effect of exercise on colonic motility is not well understood, but subjective improvements in constipation are well-documented. (15) A risk with increased exercise is dehydration, which can worsen constipation. For people with average mobility, 20 to 30 minutes' walking per day is recommended, but even short distances twice per day, or leg exercises for the immobile, may help. (15)
Dehydration is not normally a factor in constipation for well adults. In older adults, especially those taking multiple medications, dehydration may be a factor. A daily fluid intake of at least 1.5 litres is recommended to avoid constipation and this should be increased in strenuous exercise or when additional fibre is added to the diet. (15)
Increasing fibre in the diet will help manage constipation for some, but not all, patients. Fibre consists of indigestible plant material, which adds bulk to the faecal mass and also draws water into the lumen of the gut through osmotic action. These two activities soften the stool and allow it to transit more rapidly. High-fibre diets for children should be used with caution as they can lead to decreased absorption of essential nutrients. (4) Natural sources of fibre include prunes, kiwifruit and bran products.
Fibre supplements such as psyllium (eg Metamucil) are often the first-line treatment for constipation. These are generally safe, although they may cause bloating, flatulence and abdominal pain. They should not be administered in suspected bowel obstruction. Evidence to support their use in constipation is poor and, because they also reduce mild diarrhoea, fibre supplements are more appropriately used to regulate bowel function rather than as a treatment solely for constipation. (16) Psyllium must always be taken with a full glass of water, as it swells on contact with water and needs to be properly ingested to avoid choking. It takes several days to achieve peak effect.
Laxatives help manage constipation by softening the stool, increasing the stool bulk or increasing gut motility.
Bulk laxatives: This class of laxative includes natural fibres (psyllium) and semisynthetic fibres such as methylcellulose. As described above, they are mild and slow to act but have few adverse effects. Osmotic laxatives: Lactulose is an insoluble sugar which draws water into the lumen of the colon, softening the stool and increasing its bulk, which may stimulate peristalsis through distension of the gut wall. Fermentation of lactulose by colonic bacteria can lead to bloating and abdominal distension. (17) Sorbitol, used as an artificial sweetener, is of the same class. Polyethylene glycol (PEG, Movicol) is a more recently developed osmotic laxative that has been shown in clinical trials to be well-tolerated and more effective than lactulose. (18) It is recommended as a first-line treatment for many forms of constipation but is only available under special authority in New Zealand. Osmotic laxatives take one to three days for effect (depending largely on dose). Glycerol suppositories and Fleet enema both have osmotic action, taking from 15 to 60 minutes to act.
Faecal softeners/lubricants: Sodium docusate and poloxamer act as a surface detergent on the stool, allowing fat and water to enter. This softens the stool and may have a slight peristaltic effect due to increased bulk. These laxatives take two to three days to work. Stimulant laxatives: Bisacodyl, senna and dantron all act by stimulating the myenteric nerve plexus of the gut, and possibly by direct action on the smooth muscle. They increase peristalsis and may also increase secretion of water electrolytes and mucus through stimulation of the submucosal plexus. (17) They are often formulated with a faecal softener. Orally administered stimulant laxatives take about six hours to work; by suppository, they take about 20 minutes. Stimulant laxatives can cause abdominal cramping and diarrhoea, and long-term use may lead to decreased bowel function. Fleet enemas, which also have a softening action, trigger peristalsis, as do bisacodyl enemas and suppositories. New laxative therapies: Lubiprostone is a chloride channel stimulator that increases the secretion of water into the intestine (secretogogue). This softens the stool and increases bulk, to stimulate peristalsis. The main adverse effects are nausea and headaches. This drug is approved for use in the US but not yet in New Zealand. Another secretogogue under trials is linclotide. (17)
Serotonin agonist drugs are being developed as laxatives. Serotonin is known to be a key mediator of gut motility and secretion. (16) Drugs that act as opioid antagonists in the gut but not in the central nervous system have also become available recently (see Box 1).
All laxative therapies are enhanced by increased fluid intake--many rely on adequate hydration to have full effect. Also essential is privacy and time for complete evacuation of the bowel. The timing of defecation is also important to success--being able to answer the "call to stool" that naturally occurs after meals may greatly help prevention and management of incipient constipation--particularly for older adults in care.
Adhesions, hernia, volvulus or tumours may physically obstruct the movement of chyme or faecal mass through the gut. Ischaemia may also be a cause. Intestinal ischaemia can occur as a result of impaired arterial or venous flow to the gut. This can be due to generalised hypotension (eg in shock) or thrombosis in vessels supplying the gut. Regions that are particularly vulnerable are the so-called watershed areas, where the arterial supply terminates: the sigmoid colon, rectum and splenic flexure of the colon. (19)
Paralytic (adynamic) ileus is a usually temporary failure of smooth muscle contractility. It is commonly associated with abdominal surgery where the guts have been displaced. Contributing factors include anaesthetic agents, local inflammation, opioid analgesia, and sympathetic stimulation. Paralytic ileus also arises with peritonitis, hypokalaemia, ischaemic bowel, sepsis and neuropathy. (14)
Onset of obstruction may be rapid or gradual (often related to tumour growth) and the obstruction can be partial or complete. The sequence of events occurring in bowel obstruction is due to a combination of increased pressure in the bowel, and loss of water and electrolytes through accumulation behind the obstruction and vomiting.
Distension of the bowel causes colicky abdominal pain, which can be very severe. The prolonged stretching of the gut wall interrupts blood flow in the region, leading to ischaemia and increasing risk of perforation. Ischaemia also causes oedema, with loss of fluid into the peritoneum and disruption of the epithelial barrier. Toxins and bacteria are able to enter the peritoneal cavity and peritonitis ensues.
Loss of fluid into the peritoneum, through vomiting and accumulation in the obstructed bowel, may cause alkalosis (high obstruction) or acidosis (low/late obstruction), dehydration, hypokalaemia (contributing to decreased motility), hypovolaemia and shock. (14) Accompanying signs and symptoms depend on the location and extent of the obstruction. Management relies on early identification, replacement of fluids and alleviation of the pressure within the gut lumen. Complete obstruction or that caused by strangulation of the bowel require immediate surgery. (14)
Constipation is a symptom of underlying defects in either transit of faecal mass through the gut or defecation. While chronic constipation is rarely life-threatening, prolonged or severe constipation may increase the risk of bowel obstruction or perforation. Acute constipation may indicate an evolving obstruction.
Nurses are the key professionals responsible for monitoring and supporting bowel function in clients in all care settings. Constipation has a high prevalence in older adults and the risk is increased with institutionalisation and immobility. Best practice dictates that prevention of constipation be a priority in these care settings. Knowledge of the underlying events in gut motility and normal defecation allows understanding of the rationale for selection and use of interventions designed to prevent and treat constipation.
* References for this article can be found at www.cpd4nurses.co.nz.
Georgina Casey, RN, BSc, PGDipSci, MPhil (nursing), is the director of CPD4nurses.co.nz. She has an extensive background in nursing education and clinical experience in a wide variety of practice settings.
Table 1. Medications that may cause constipation * Antidepressants * Iron supplements * Opioids * Antacids containing aluminium * Calcium channel blockers * NSAIDs * Antipsychotics * Diuretics * Calcium supplements * Antiarrhythmics * Antidiarrhoeal agents * Serotonin antagonists (ondansetron) * Antiparkinson's drugs * Long-term use of stimulant laxatives
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|Title Annotation:||CPD + Nurses|
|Publication:||Kai Tiaki: Nursing New Zealand|
|Date:||Dec 1, 2013|
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