According to the Rome IV criteria used to diagnose functional gastrointestinal disorders, constipation is present when the following symptoms are present for = 3 weeks [Wald, 2016]
1. At least 2 of the symptoms should be present:
- passing stools with a frequency of less than 3 times per week
- having difficulty in stools evacuation
- lumpy/hard stools > 25% of the time (i.e. at least one in four, on average, visits to the toilet result in lumpy or hard stools
- straining >25% of the time
- sensation of incomplete evacuation >25% of the time
- sensation of anorectal obstruction/blockage >25% of the time
- manual maneuvers required to ease defecation (digital evacuation, support of pelvic floor) >25% of the time
2. Loose stools are hardly present if laxatives are not used.
3. There are inadequate criteria for the diagnosis of irritable bowel syndrome
Movements of the small intestine and colon
Contractions of the small intestine may mixing and peristaltic. Mixing contractions are associated with segmentation of the bowel loops. Peristaltic contractions are sequential, and move the intestinal chyme at about 1 cm per minute: this means that it takes 3-5 hours for food to travel from the pylorus to the ileocecal valve [Hall, 2011].
Contractions of the colon are relatively sluggish. Circular constrictions similar to segmentation occur in the colon, while the propulsive movements normally result in a transit time of 8-15 hours between the ileocecal valve and the anus. This allows nearly all of the water to be absorbed. Normal stool volume is about 200 ml/day. [Hall, 2011]
Defecation is initiated by the presence of feces in the rectum. Autonomic afferents from the rectum initiate a sympathetic or parasympathetic response. The sympathetic response constricts the internal sphincter. The parasympathetic response relaxes it and allows defecation. The urge to defecate begins when rectal pressure crosses 18 mm Hg [Ganong, 1995]. The defecation reflex consists of the occurrence of strong peristaltic waves in the descending colon and rectum, associated with a closure of the glottis and contraction of the abdominal muscles [Hall, 2011].
The sensory innervation to the rectum is carried by autonomic afferents that travel along the pelvic splanchnic nerves to the S2-S4 spinal roots. The parasympathetic efferents, which allow defecation, travel back along the same paths. The sympathetic efferents, which prevent defecation, travel to the rectum from the lumbar splanchnic nerves and the superior and inferior hypogastric plexuses [Ferzandi, 2016].
The muscles mainly controlling defecation are the internal sphincter [Hall, 2011], the external sphincter, and the (important) levator ani.
The internal sphincter is a thickening of the terminal end of the inner circular component of the muscular layer of the large intestine [Ferzandi, 2016]. Sympathetic stimulation constricts it, while parasympathetic stimulation relaxes it.
The external sphincter is a voluntary muscle complex that surrounds the anal canal, and is usually described as a composite of three muscles [Ferzandi, 2016]. It is supplied by a branch from S4 [Gray, 1918].
The levator ani forms the pelvic diaphragm. It is supplied by the fourth sacral nerve, and may receive branches from the pudendal nerve. It includes the puborectalis muscle [Gray, 1918], which is probably of great importance to continence. [Fraga and Luis, 2005]
Conditions such as anatomical obstruction, slow transit constipation, pelvic floor disorders, irritable bowel syndrome, medications, metabolic, neurological and psychiatric disorders may contribute to the development of constipation.
In normal transit constipation which is a functional gastrointestinal disorder, patient complains of constipation despite no mechanical obstruction is present. In slow transit constipation, there is a decreased in number of high amplitude propagated contractions (HAPCs) post prandially, causing slow colonic transit and reduced mass movements. This causes an increase in water absorption which produces a harder and more concentrated stool which is more difficult to evacuate. Abnormally strong rectal contractions, injury to the colonic pacemaker cells and the interstitial cells of Cajal may all lead to constipation. Uncommon smooth muscle disorders such as scleroderma, amyloidosis and hollow visceral myopathy cause a myopathic process and a loss of colonic contraction.
Besides, megarectum may reduce the rectal contractile forces and impair the rectal sensation which affects the initiation of a normal rectal reflex. Patients with an impaired rectal sensation require larger volumes of rectal distention to stimulate the normal urge of defecation. A large rectocele or sigmoidocele, intussuception and rectal prolapse can impede the normal stool evacuation process. Descending perineum syndrome in which the perineum descends >3cm below the ischial tuberosity during straining and a diminished rectal contraction function may also cause constipation. This syndrome can be caused by injury to the pudendal nerves which lead to prolapse of the anal canal by the anterior rectal mucosa hence affecting rectal emptying. In pelvic floor dyssnergia which is most common in women, the internal anal sphincter fails to relax properly or the external anal sphincter inappropriately contracts during defecation [Lacy and Cole, 2004].
- Normal-transit constipation (NTC). NTC is the commonest subtype of primary constipation [Basson MD, 2017]. Stools pass through the colon at a normal rate and stool frequency is normal. However, patients believe that they experience constipation due to the perception of difficult evacuation and the passage of hard stools. The patient may also experience abdominal pain and bloating [Kumar and Clark, 2017].
- Slow-transit constipation (STC). This condition normally occurs in young women who have bowel movements of <1 per week. It starts during puberty at patients may experience symptoms such as abdominal pain, bloating, discomfort and a decreased urge to defecate [Kumar and Clark, 2017]. This condition may also occur following an abdominal or pelvic surgery [Bailey and Love’s, 2013].
- Pelvic floor dysfunction. In normal defecation, puborectalis and the external anal sphincter relax. A paradoxical contraction, also known as pelvic floor dyssynergia or anismus, due to dysfunction of anal sphincter and pelvic floor can prevent evacuation [Basson MD, 2017; Kumar and Clark, 2017].
- Negligence of the defecation impulse. This causes dry and large piles of feces to accumulate, leading to distension of the rectum. This constant distension causes patient to become less aware of the fullness of the rectum, which eventually leads to chronic constipation [Talley and O’Connor, 2014].
- Drugs. The following drugs are known to be associated with constipation[Talley and O’Connor, 2014; Basson MD, 2017]:
- Antidepressants (cyclic antidepressants, Monoamine oxidase inhibitors: MAOIs)
- Anticholinergics (benztropine, trihexyphenidyl)
- aluminium/calcium antacids
- calcium channel blockers
- metals (iron, bismuth)
- NSAIDs (ibuprofen, diclofenac)
- opiods (codeine and morphine): common in patients who have chronic pain/cancer-related pain [Rao, 2017]
- cholestyramine, long – term use of stimulant laxatives: This causes development of a dilated atonic laxative colon, which requires more laxatives being used due to its reduced efficacy.
- Psychotropic drugs
- Insufficient supplementation of thyroid hormone
- Metabolic or endocrine diseases. Metabolic and endocrine disorders associated with constipation include hypothyroidism, hypokalemia, hyperparathyroidism, hypercalcemia, diabetes mellitus, phaeochromocytoma, porphyria [Talley and O’Connor, 2014; Basson, 2017].
- Neurological disorders. Constipation may occur in Hirschsprung’s disease, diabetic autonomic neuropathy, spinal cord injury, multiple sclerosis, stroke, Parkinson disease, head injury, cerebral vascular accident, Chagas disease, and familial dysautonomia [Talley and O’Connor, 2014; Basson MD, 2017].
- Structural causes. Diseases causing narrowing of the bowel lumen alter the bowel habit, causing constipation, diarrhea, or alternating diarrhea and constipation [Basson MD, 2017; BMJ Best Practice, 2016] [Talley and O’Connor, 2014] [Luniss and Nugent, 2013]. Some examples include the following:
- Carcinoma causing colonic obstruction, hence it is crucial to take note of any altered bowel habits as this can indicate malignancy
- Idiopathic megarectum
- Anal fissure and thrombosed hemorrhoids may be caused by constipation, but the pain associated with defecation may also worsen constipation.
- Pregnancy. Hormonal changes during pregnancy may affect the motility of small and large bowels [Bianco, 2016; Talley and O’Connor, 2014]. The activity of colonic smooth muscle is mostly affected by the increased concentration of progesterone, leading to the prolongation in gastrointestinal transit time. Progesterone also inhibits the release of motilin (gastrointestinal stimulatory hormone) causing low concentration of motilin in the plasma which again prolongs the gastrointestinal transit time. Besides, during the late gestational stage, the gravid uterus may mechanically obstruct the small bowel transit.
- Psychological. Depression, anorexia nervosa may result in constipation [[Kumar and Clark, 2017].
The following section describes how to take a history of constipation.
- Frequency of bowel movement
- Abdominal features
- Systemic features
- Past medical history
- Family history
- Personal history
- Psychosocial issues
Infrequent bowel movements define constipation, therefore this question should be asked first.
This can help to differentiate a congenital or acquired cause in adolescents and young children. It is less likely for young patients and elderly patients (> 50 years old) having symptoms for at least 2 years and have had done a recent screening colonoscopy to develop neoplastic obstruction [Basson, 2017].
The nature of onset provides etiological information. Intestinal obstruction, ileus due to other medical illness and Ogilvie syndrome may present as acute constipation [Basson, 2017]
Color. Black stools occur due to upper GI bleed, ingestion of large doses of iron or bismuth [Das, 2013b]. Blood mixed with feces occurs if it originates from bowel higher than sigmoid colon, where stools is still soft [Das 2013c]. Whitish/ clay colored stool indicates biliary obstruction [Das , 2013b].
Character. Hard, dry stools occur when defecation is delayed. The colon absorbs all the water, leaving behind stools that are difficult to pass. The presence of hard stools is a defining factor in constipation. Most causes of constipation can cause hard stool. Importantly, difficult-to-pass hard stool is a risk factor for anal disorders like fissures and hemorrhoids [Lunniss and Nugent, 2013]. A growth in the lower part of rectum and anal canal may change the shape of the stools causing it to be pipestem or tape-like [Das, 2013c].
Blood or mucus. Both cancer and hemorrhoids can cause bright red rectal bleeding. Patients with hemorrhoids may also present with rectosigmoid cancer. Patients who age more than 50 and have a family history of colorectal disease should be screened for colorectal cancer. [Basson, 2017b] Children who have intestinal obstruction symptoms with passage of blood and mucus per anum may have acute intussuception [Das, 2013a].
Change in bowel habit. This may indicate development of a malignancy as colonic obstruction due to carcinoma can cause constipation [Talley and O’Connor, 2014]. Patients with colorectal carcinoma may present with increasing constipation, or alternating diarrhea and constipation, according to the site of the lesion. [Das, 2013b] In ulcerative rectal carcinoma, there is an overnight accumulation of blood, mucus, pus and feces causing patient to have an urgent call to pass stools upon waking. This condition is also known as ‘spurious morning diarrhoea’ [Das, 2013c].
Abdominal pain. An annular lesion high in the rectum can obstruct the bowel lumen and cause lower abdominal colic [Das, 2013c] .
Pain during defecation. This suggests the presence of fissure or tenesmus due to a rectal tumor. If there is no pain but patient could not pass out soft stools, this means that there is obstruction of the rectal outlet [Basson, 2017] .
Flatus. Absolute constipation (inability to pass feces and flatus) is usually associated with intestinal obstruction and peritonitis [Das, 2013a] .
Straining on passing stool. Disorders of the pelvic floor muscles, nerves or anorectal disease can cause difficulty in evacuation [[Talley and O’Connor, 2014] .
Tenesmus. Tenesmus is the painful straining to empty the bowel without any result. It can be due to a proliferative growth at the ampulla of the rectum. [Das 2013c] Patients with pelvic abscess or pelvic appendicitis may present with ‘tenesmus’ with the passage of blood and mucus due to irritation of the rectum [Das, 2013a] .
Sensation of rectal fullness. This may be caused by a proliferative growth in the ampulla of rectum causing patient to feel that he has not completely emptied his bowel after defecation [Das, 2013c]. Patients who feel there may be a blockage at the anus area when they try to pass stool may have disorders of the pelvic floor muscles, nerves or anorectal disease [Talley and O’Connor, 2014].
Use of pharmacologic or physical method to help stools pass. Ask the patient if he or she needs the help of a finger to press around the anus or vaginal region to facilitate the passage of stools? [Talley and O’Connor, 2014] This can indicate chronic laxative abuse or colonic obstruction. [Basson, 2017]
Weight loss.Ask about weight loss [Das, 2013b]. Gastrointestinal tract malignancies present with marked and progressive weight loss.
Fissures and internal piles are associated with habitual constipation. [Talley and O Connor, 2014]. Patients having hemorrhoids may deny that they were previously treated for constipation or are currently being treated for constipation [Basson, 2017b]. Hypothyroid patients can present with slow transit time and reduced motility. Diabetes is associated with chronic dysmotility. Besides, panhypopituitarism, pheochromocytoma, or multiple endocrine neoplasia 2B increase the risk of having constipation. Central nervous disorders (Parkinson’s, multiple sclerosis, spinal injury or tumors, stroke, CNS syphilis) can also cause constipation [Basson, 2017b].
Polyposis is a hereditary disease. Patients who have piles, fissures, prolapse and rectal carcinoma may have a positive family history [Das, 2013c] .
Ask if patients take the following drugs as they can cause constipation. Codeine, antidepressants, antacids: reduce bowel motility [Basson, 2017]. Chronic laxative abuse contributes to constipation [Basson, 2017b]
Ask about the following:
Change in diet. Too little fibre or water may cause an acute onset of constipation [Basson, 2017b].
Amount and types of fluid consumed daily. Milk causes constipation in certain individuals. The diuretic effects of coffee, tea and alcohol reduce the amount of water available in the colon, leading to constipation [Basson, 2017]
Exercise. Exercise stimulates bowel motility [Basson, 2017].
In some situations, there may be a need to ask about social isolation, dependency, poor nutrition, reduced mobility may cause constipation [Rao, 2017]. Patients who have chronic constipation, especially when associated with anismus (failure of normal relaxation of pelvic floor muscles during defecation), may have a history of being sexually abused [Basson, 2017b].
- Abdominal examination
- Rectal examination
- Pelvic examination
- Neurological examination
- Endocrine system examination
Inspect for any scars of previous surgery which might have affected the nerves supplying the colonic and pelvic floor function such as the autonomic nervous system and pudendal nerve. Inspect for distension. [Lacy and Cole, 2004]
Palpate for masses, and to determine if there is a significant amount of stool in the colon: Examine for abdominal distention or masses, which may indicate the presence of colonic stools or tumors. Large abdominal wall hernias such as ventral hernias interrupts the generation of intra-abdominal pressure needed to initiate defecation.[Lacy and Cole, 2004]
Auscult for bowel sounds. Complete absence of sounds for 4 minutes indicates paralytic ileus [Talley and O’Connor, 2014b]. Loud, high-pitched, tinkling quality (due to presence of air and liquid) indicates obstructed bowel [Talley and O’Connor, 2014b]
Inspect for fissures, haemorrhoids, masses, evidence of previous surgery can cause difficult defecation [Lacy and Cole, 2004]. Excoriation of perianal skin indicates fecal soiling which may occur in elderly patient with fecal impaction and overflow incontinence [Lacy and Cole, 2004]. Inspect to check for the presence of internal rectal prolapse. Distinguish a true full-thickness rectal prolapse from a mucosal prolapse, which is unlikely to cause constipation (instruct the patient to bear down as if to have a bowel movement) [Basson MD, 2017]. During straining, patients with descending perineum syndrome show abnormal perineal descent of > 3cm (Normal: 1-3 cm). Check presence of rectocele: this is usually at the anterior rectal wall [Basson MD, 2017].
Palpate for neurological defects: stroke the perianal skin: there is a neurological defect if the reflex contraction of the external anal sphincter is absent [Lacy and Cole, 2004]. Ask patient to voluntarily contract external anal sphincter to assess the strength of external anal sphincter and puborectalis muscle [Lacy and Cole, 2004]. Assess the tone of internal anal sphincter. Patients who have pelvic floor dyssynergia may present with elevated tone and incomplete relaxation of the anal sphincter. [Lacy and Cole, 2004]. A rectal prolapse can be identified during straining when a fold of tissue strikes the examiner’s finger or when tissue is pushed out through the anus [Lacy and Cole, 2004]
An internal prolapse or rectocele may be present hence it is important to palpate the woman’s posterior vaginal wall while patient is resting or straining to defecate. [Basson MD, 2017]
Parkinson’s disease, brain or spinal cord injury, peripheral neuropathy and multiple sclerosis can cause constipation [Basson MD, 2017].
Constipation is also associated with hypothyroidism, hypopituitarism, and diabetes mellitus [Basson MD, 2017]
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