Introduction
GI motility refers to wall movement in the digestive
tract.
The enteric nervous system is the most important
regulator of physiological gut function including contraction, absorption and
secretion.
Other
regulatory systems in the gut include the CNS and humoral pathways.
Role of the ENS in GI motility
The ENS is an
autonomous collection of nerves within the wall of the GI tract.
It consists of:
The myenteric (Auerbach’s) plexus which is found
between the circular and longitudinal muscle layers
The submucosal (Meissner’s) plexus, found below
the epithelium.
Auerbach’s plexus is responsible for motor control,
while the Meissner’s plexus regulates secretion, fluid transport, and vascular
flow.
Overview of
motility disorders of the bowel
Decreased GI motility can affect one or more parts of
the GIT
Gastroparesis is the term used to describe delayed gastric
emptying.
Symptoms may range from postprandial bloating to nausea and vomiting.
Half of ingested
liquid should be emptied within 30 minutes and half of ingested solids should
be emptied within 2 hours.
Causes of decreased GIT
motility
Emptying time can be prolonged as a result of:
Autonomic neuropathy
which occurs in patients with long standing diabetes.
Pseudoobstruction due
to an idiopathic intestinal muscle disease or intestinal neuropathy
Electrolyte disorders and gastroenteritis.
Medications including anticholinergic medications,
tricyclic antidepressants, levodopa and β-adrenergic agonists.
GI motility disorders
GI motility disorders include:
Achalasia of the
esophagus (impaired relaxation of the lower esophageal sphincter associated
with defective esophageal peristalsis that results in dysphagia and
regurgitation),
Gastroparesis (delayed gastric emptying),
Myopathic forms of intestinal dysmotility
Neuropathic forms of intestinal dysmotility.
Prokinetic agents and other
stimulants of GI contractility
Drugs that enhance GI motility are termed prokinetic
agents.
They act either by enhancing the effect of
acetylcholine or by blocking the effect of an inhibitory neurotransmitter such
as dopamine.
Cholinergic agents:Choline
Derivatives
ACh itself is not used pharmacologically because it
affects all classes of cholinergic receptors (nicotinic and muscarinic) and is
degraded rapidly by Achase.
Modification of the ACh structure has yielded drugs
such as bethanechol that have increased receptor selectivity and that resist
enzymatic hydrolysis.
Bethanechol
Bethanechol has
low prokinetic efficacy
It also has significant side effects resulting from
its broad muscarinic effects on contractility and secretion in the GI tract and other organs, including
bradycardia, flushing, diarrhea and cramps, salivation, and blurred vision.
Acetylcholinesterase Inhibitors
These drugs inhibit the degradation of ACh by its
esterase, thereby allowing ACh to accumulate at sites of release.
Unlike muscarinic receptor agonists, these
parasympathomimetic drugs do not stimulate muscle directly,
However,they accelerate GI transit times by enhancing the
contractile effects of ACh released at synaptic and neuromuscular junctions.
Acetylcholinesterase
Inhibitors
Neostigmine methylsulfate is a cholinergic muscle
stimulant that has been used off-label
for some GI disorders
E.g. conditions
associated with acute colonic pseudo-obstruction .
Atropine should be
available in case of severe bradycardia.
Dopamine Receptor Antagonists
Dopamine is present in significant amounts in the GI
tract and has several inhibitory effects on motility, including reduction of
lower esophageal sphincter and intragastric pressures.
These effects, which result from suppression of ACh
release from myenteric motor neurons, are mediated by D2 dopamine receptors.
Dopamine Receptor Antagonists
They exert their prokinetic effects through
inhibition of dopamine on myenteric
motor neurons
They have the additional advantage of relieving
nausea and vomiting by antagonism of dopamine receptors in the CTZ .
Examples of such agents are metoclopramide and
domperidone.
Dopamine Receptor Antagonists:
Metoclopramide
Metoclopramide stimulates upper GI motility where it
increases lower oesophageal sphincter tone and stimulates antral and small
intestinal contractions.
It has both
central and peripheral actions.
Centrally, it is a
dopamine antagonist, an action that is important for its antiemetic effects and
some of its undesirable effects.
Peripherally it
stimulates the release of intrinsic postganglionic stores of Ach and sensitizes
gastric smooth muscle to muscarinic stimulation.
Dopamine Receptor Antagonists: Metoclopramide
Metoclopramide has no clinically significant effects
on large-bowel motility.
The ability of metoclopramide to antagonize the
inhibitory neurotransmitter effect of dopamine on the GI tract results in increased
gastric contraction and enhanced gastric emptying and small bowel transit.
Therapeutic Use and
Pharmacokinetics
Metoclopramide is used to alleviate symptoms in
patients with gastroparesis in whom it may modestly improve gastric emptying.
Since metoclopramide can decrease the acid reflux into
the oesophagus that results from slowed
gastric emptying or lower oesophageal
sphincter pressure , it is used as an adjunct in treatment of reflux
oesophagitis.
It is also used to
ameliorate the nausea and vomiting that often accompany GI dysmotility
syndromes.
Adverse Effects
The major side effects of metoclopramide include
extrapyramidal effects.
Dystonias, usually
occurring acutely after IV use and parkinsonian-like symptoms that may occur
several weeks after initiation of therapy generally respond to treatment with
anticholinergic or antihistaminic drugs and are reversible upon metoclopramide
discontinuation.
Tardive dyskinesia
also can occur with chronic treatment (months to years) and may be
irreversible.
Metoclopramide can elevate prolactin levels by
blocking the inhibitory effect of dopamine on pituitary lactotropes.
This can cause
galactorrhoea and menstrual disorders.
D2 Receptor
Antagonists:Domperidone
Unlike metoclopramide, domperidone predominantly
antagonizes the dopamine D2 receptor without major involvement of other
receptors.
It has modest
prokinetic activity in doses of 10–20 mg three times a day.
Although it does not readily cross the BBB to cause
extrapyramidal side effects, domperidone exerts effects in the parts of the CNS
that lack this barrier, such as those regulating emesis, temperature, and
prolactin release.
5-HT Receptor Modulators
5-HT plays an important role in the normal motor and
secretory function of the gut .
Most of the total (
>90%) l 5-HT in the body exists in the GI tract.
The enterochromaffin
cell, a specialized cell lining the mucosa of the gut, produces most of this
5-HT and rapidly releases 5-HT in response to chemical and mechanical
stimulation
e.g., food boluses; noxious agents such as
cisplatin; certain microbial toxins; adrenergic, cholinergic, and purinergic
receptor agonists.
5-HT triggers the peristaltic reflex by stimulating intrinsic sensory neurons in
the myenteric plexus via variant 5-HT receptors, 5-HT1p, and via 5-HT4
receptors, as well as extrinsic vagal and spinal sensory neurons via 5-HT3
receptors.
5-HT Receptor Modulators
In addition, stimulation of submucosal intrinsic
afferent neurons activates secretomotor reflexes resulting in epithelial
secretion.
5-HT receptors
also are found on other neurons in the ENS, where they can be either
stimulatory (5-HT3 and 5-HT4) or inhibitory (5-HT1a).
5-HT Receptor Modulators
Serotonin also stimulates the release of other
neurotransmitters, depending upon the receptor subtype.
Thus, 5-HT1 stimulation of the gastric fundus
results in release of nitric oxide and reduces smooth muscle tone.
5-HT4 stimulation of
excitatory motor neurons enhances ACh release at the neuromuscular junction,
Both 5-HT3 and 5-HT4 receptors facilitate
interneuronal signaling.
5-HT Receptor Modulators
Reuptake of
serotonin by enteric neurons and epithelium is mediated by the same mechanism
as 5-HT reuptake by serotonergic neurons in the CNS.
This reuptake
therefore also is blocked by selective serotonin reuptake inhibitors which explains the common side effect of
diarrhea that accompanies the use of these agents.
5-HT Receptor Modulators:
Tegaserod Maleate
Tegaserod is
structurally related to serotonin and is a partial 5-HT4 agonist with
negligible affinity for other receptor subtypes.
Tegaserod
stimulates motility and accelerates transit in the esophagus, stomach,
small bowel, and ascending colon.
Stimulation
of 5-HT4 also activates cAMP-dependent
chloride secretion from the colon leading to increased stool liquidity.
Tegaserod is used in
treatment of patients with chronic constipation.
5-HT Receptor Modulators: Tegaserod Maleate
Diarrhea and headache are the most common side effects
of tegaserod, occurring in ~10% of patients.
Tegaserod has not been
found to have any clinically relevant drug-drug interactions.
No dosage adjustment
is required in elderly patients or those with mild-to-moderate hepatic or renal
impairment,
However,tegaserod
should not be used in patients with severe hepatic or renal impairment.
Motilin agonists: Macrolides
and erythromycin
Motilin, a 22–amino acid peptide hormone found in the
GI M cells and some enterochromaffin cells of the upper small bowel, is a
potent contractile agent of the upper GI tract.
The effects of motilin can be mimicked by erythromycin
and by other macrolide antibiotics , including oleandomycin, azithromycin, and
clarithromycin.
Erythromycin :Therapeutic uses
The best-established use of erythromycin as a
prokinetic agent is in patients with diabetic gastroparesis, where erythromycin
can improve gastric emptying in the short term.
Erythromycin stimulated gastric contractions can be
intense and result in “dumping” of relatively undigested food into the small
bowel.
This potential
disadvantage is exploited clinically to clear the stomach of undigestible
residue such as plastic tubes or bezoars.
Erythromycin: Therapeutic uses
Use of erythromycin as a prokinetic agent has been
limited by:
Rapid development of
tolerance to erythromycin due to down-regulation of the motilin receptor,
Undesirable antibiotic effects
Miscellaneous agents for
stimulating motility
The GI hormone cholecystokinin (CCK) is released from
the intestine in response to meals and delays gastric emptying.
Dexloxiglumide is a
CCK1 (or CCK-A)–receptor antagonist that can improve gastric emptying and is
being investigated as a treatment for gastroparesis and constipation-dominant
irritable bowel syndrome.
Clonidine (an α2-adrenergic receptor agonist)
also may be of benefit in patients with gastroparesis.
Agents that suppress motility: Smooth
Muscle Relaxants
Smooth muscle relaxants e.g. organic nitrates and Ca2+
channel antagonists often produce temporary relief of symptoms in motility
disorders such as achalasia, in which the lower esophageal sphincter fails to
relax, resulting in a functional obstruction to the passage of food and severe
difficulty in swallowing.
Agents that suppress motility: Botulinum Toxin
Botulinum toxin
can be injected in doses of 80–200 units directly into the lower esophageal
sphincter via an endoscope.
This agent inhibits ACh release from nerve
endings and can produce partial
paralysis of the sphincter muscle, with significant improvements in symptoms
and esophageal clearance.
LAXATIVES,
CATHARTICS, AND THERAPY FOR CONSTIPATION
Overview of GI water and electrolyte flux
Fluid content
is the principal determinant of stool volume and consistency.
Water normally
accounts for 70–85% of total stool weight.
Net stool fluid
content reflects a balance between luminal input (ingestion and secretion of
water and electrolytes) and output (absorption) along the length of the GI
tract.
Overview of gi water and electrolyte flux
Normally ~8–9 L of fluid enter the small intestine
daily from exogenous and endogenous sources .
Net absorption of the water occurs in the small
intestine in response to osmotic gradients that result from the uptake and
secretion of ions and the absorption of nutrients (mainly sugars and amino
acids), with only ~1–1.5 L crossing the ileocecal valve.
The colon then extracts most of the remaining fluid,
leaving ~100 mL of fecal water daily.
Overview of GI water and electrolyte flux
Under normal circumstances, these quantities are well
within the range of the total absorptive capacity of the small bowel (~16 L)
and colon (4–5 L).
Neurohumoral
mechanisms, pathogens, and drugs can alter these processes, resulting in
changes in either secretion or absorption of fluid by the intestinal
epithelium.
Altered motility also contributes to this process, as
the extent of absorption parallels transit time.
With decreased motility and excess fluid
removal, feces can become inspissated
(thickening through dehydration) and impacted (accumulation of
hardened(inspissated stool), leading to constipation.
When the capacity of
the colon to absorb fluid is exceeded, diarrhea will occur.
Constipation: general principles of pathophysiology
and treatment
Constipation is defined as infrequent passage of
stool.
This term is also used
by patients to describe not only
decreased stool frequency, but also for difficulty in initiation or passage,
passage of firm or small-volume feces, or a feeling of incomplete evacuation.
Causes of constipation
Constipation has many reversible or secondary causes,
including:
Lack of dietary fiber,
Drugs,
Hormonal disturbances,
Neurogenic disorders,
Systemic illnesses.
In most cases of chronic constipation, no specific
cause is found.
Colonic motility and constipation
Colonic motility is responsible for mixing luminal
contents to promote absorption of water and moving them from proximal to distal
segments by means of propulsive contractions.
In any given patient, the predominant factor
underlying constipation (propulsive vs. nonpropulsive colonic motility) often
is not obvious.
Consequently, the pharmacological approach to
constipation remains empirical and nonspecific.
Non-pharmacological measures
Constipation can be corrected by:
adherence to a fiber-rich (20–30 g daily)
diet,
adequate fluid intake
Constipation related
to medications can be corrected by use of alternative drugs where possible, or
adjustment of dosage.
Pharmacological treatment of
constipation
If nonpharmacological measures alone are inadequate,
they may be supplemented with bulk-forming agents or osmotic laxatives.
When stimulant laxatives are used, they should be
administered at the lowest effective dosage and for the shortest period of time
to avoid abuse.
Use of laxatives: General considerations
Habitual use of laxatives may lead to excessive loss
of water and electrolytes;
Secondary aldosteronism may occur if volume depletion
is prominent.
Steatorrhea, protein-losing enteropathy with
hypoalbuminemia, and osteomalacia due to excessive loss of calcium in the stool
have been reported.
Laxatives are employed before surgical, radiological,
and endoscopic procedures where an empty colon is desirable.
Laxatives, cathartics and purgatives
The terms laxatives, cathartics and purgatives are often used interchangeably. However:
Laxation refers to the evacuation of formed fecal
material from the rectum while
Catharsis or purgation is the evacuation of unformed,
usually watery fecal material from the entire colon.
Most of the commonly used agents promote laxation but some are cathartics that act as laxatives
at low doses.
Effects of Laxatives
Laxatives act by:
Enhancing retention of intraluminal fluid by
hydrophilic or osmotic mechanisms,
Decreasing net absorption of fluid by effects on small-
and large-bowel fluid and electrolyte transport,
Altering motility by either inhibiting segmenting
(nonpropulsive) contractions or stimulating propulsive contractions.
Laxatives: Classification
Laxatives: Mechanism of action
A variety of laxatives, both osmotic agents and
stimulants, increase the activity of NO synthase and the biosynthesis of
platelet-activating factor in the gut.
Platelet-activating factor is a phospholipid
proinflammatory mediator that stimulates colonic secretion and GI motility.
NO also may stimulate intestinal secretion and inhibit
segmenting contractions in the colon, thereby promoting laxation.
Agents that reduce the expression of NO synthase or
its activity can prevent the laxative effects of castor oil, cascara, and
bisacodyl (but not senna), as well as magnesium sulfate.
Dietary Fiber and Supplements
Bulk, softness, and hydration of feces depend on the
fiber content of the diet.
Fiber resists enzymatic digestion and reaches the
colon largely unchanged.
Colonic bacteria ferment fiber to varying degrees,
depending on its chemical nature and water solubility.
Fermentation of fiber
produces short-chain fatty acids that are trophic for colonic epithelium and
increases bacterial mass.
Dietary Fiber and Supplements
Although fermentation of fiber generally decreases
stool water, short-chain fatty acids also may have a prokinetic effect, and
increased bacterial mass may contribute to increased stool volume.
Fiber that is not fermented can attract water and
increase stool bulk.
The net effect on bowel movement therefore varies with
different compositions of dietary fiber .
Dietary Fiber and Supplements
In general, insoluble, poorly fermentable fibers, such
as lignin, are most effective in increasing stool bulk and transit.
Bran, the residue left when flour is made from
cereals, contains >40% dietary fiber.
Wheat bran, with its
high lignin content, is most effective at increasing stool weight.
Fruits and vegetables
contain more pectins and hemicelluloses, which are more readily fermentable and
have less effect on stool transit.
Dietary Fiber and Supplements
Psyllium husk, derived from the seed of the plantago
herb, is a component of many commercial products for constipation.
Psyllium husk contains
a hydrophilic mucilloid that undergoes significant fermentation in the colon,
leading to an increase in colonic bacterial mass.
The usual dose is
2.5–4 g (1–3 teaspoonfuls in 250 mL of fruit juice), titrated upwards until the
desired goal is reached.
A variety of semisynthetic
celluloses—e.g., methylcellulose and the hydrophilic resin calcium
polycarbophil, a polymer of acrylic acid resin—also are available. These poorly
fermentable compounds absorb water and increase fecal bulk.
Osmotically Active Agents:
Saline Laxatives
Saline Laxatives
Laxatives
containing magnesium cations or phosphate anions are commonly
called saline laxatives.
These include
magnesium sulfate, magnesium hydroxide, magnesium citrate, sodium
phosphate.
Their cathartic action results from osmotically
mediated water retention, which then stimulates peristalsis.
Osmotically Active Agents:
Saline Laxatives
Saline Laxatives
Magnesium-containing laxatives may stimulate the
release of cholecystokinin, which leads to intraluminal fluid and electrolyte
accumulation and to increased intestinal motility.
For every additional
mEq of Mg2+ in the intestinal lumen, fecal weight increases by ~7 g.
The usual dose of
magnesium salts contains 40–120 mEq of Mg2+ and produces 300–600 mL of stool
within 6 hours.
Osmotically Active Agents:
Saline Laxatives
Saline Laxatives
Phosphate salts are better absorbed than
magnesium-based agents and therefore need to be given in larger doses to induce
catharsis.
The most frequently employed preparation of sodium
phosphate is an oral solution which
contains 1.8 g of dibasic sodium phosphate and 4.8 g of monobasic sodium
phosphate in 10 mL.
The usual adult dose is 20–30 mL taken with ample
water.
Osmotically Active Agents:
Saline Laxatives
Saline Laxatives
For colonic
preparation before a procedure, larger doses of sodium phosphate are used, typically in the form of two doses
of 45 mL each, a few hours apart, the evening before the procedure.
A newer preparation of
phosphate salts is available in tablet
form, containing 1.5 g total sodium phosphate per tablet.
For colon preparation,
two doses of 20 tablets each (30 g sodium phosphate) are recommended.
Osmotically Active Agents:
Saline Laxatives
Saline Laxatives
Adequate fluid intake (1–3 L) is essential for any
oral sodium phosphate regimen used for colonic preparation.
Sodium phosphate also can be given as an enema for
laxative purposes.
Osmotically Active Agents:
Saline Laxatives
Saline Laxatives
Magnesium- and phosphate-containing preparations are
tolerated reasonably well by most patients.
However, they must be
used with caution or avoided in patients with renal insufficiency or
preexisting electrolyte abnormalities, and in patients on diuretic therapy.
Patients taking >45
mL of oral sodium phosphate as a prescribed bowel preparation may experience
electrolyte shifts that pose a risk for the development of symptomatic
dehydration, renal failure, metabolic acidosis, hypocalcemic tetany, and even
death in medically vulnerable populations.
Osmotically Active Agents: Nondigestible Sugars and
Alcohols
Lactulose is a
synthetic disaccharide of galactose and fructose that resists intestinal
disaccharidase activity.
This and other nonabsorbable sugars such as sorbitol
and mannitol are hydrolyzed in the colon to short-chain fatty acids, which
stimulate colonic propulsive motility by osmotically drawing water into the
lumen.
Sorbitol and lactulose
are equally efficacious in the treatment of constipation caused by opioids and
vincristine, of constipation in the elderly, and of idiopathic chronic
constipation.
They are available as
70% solutions, which are given in doses of 15–30 mL at night, with increases as
needed up to 60 mL/day in divided doses. Effects may not be seen for 24–48
hours after dosing is begun.
Osmotically Active Agents: Nondigestible Sugars and
Alcohols
Abdominal discomfort or distention and flatulence are
relatively common in the first few days of treatment but usually subside with
continued administration.
Role of lactulose in hepatic encephalopathy
Lactulose also is used to treat hepatic
encephalopathy.
Patients with severe
liver disease have an impaired capacity to detoxify ammonia produced by
bacterial metabolism of urea in the colon.
The drop in luminal pH
that accompanies hydrolysis to short-chain fatty acids in the colon results in
“trapping” of the ammonia by its conversion to the polar ammonium ion.
Combined with the
increases in colonic transit, this therapy significantly lowers circulating
ammonia levels. The therapeutic goal is to give sufficient lactulose (usually
20–30 g, 3–4 times/day) to produce two to three soft stools a day with a pH of
5–5.5.
Osmotically Active Agents: Polyethylene
Glycol–electrolyte Solutions
Long-chain
polyethylene glycols (PEGs; molecular weight ~3350) are poorly absorbed, and
PEG solutions are retained in the lumen by virtue of their high osmotic nature.
When used in high volume, aqueous solutions of
PEGs produce an effective catharsis and
are used widely for colonic cleansing for radiological, surgical, and
endoscopic procedures (4 L of this solution taken over 3 hours, beginning at
least 4 hours before the procedure).
Stool-Wetting Agents and Emollients:Docusate
Docusate salts are anionic surfactants that lower the
surface tension of the stool to allow mixing of aqueous and fatty substances,
softening the stool, and permitting easier defecation.
However, these agents also stimulate intestinal fluid
and electrolyte secretion and alter intestinal mucosal permeability.
Docusate sodium and docusate calcium are available in
several dosage forms.
Despite their widespread use, these agents have
marginal, if any, efficacy in most cases of constipation.
Stool-Wetting Agents and Emollients: Mineral Oil
Mineral oil is a mixture of aliphatic hydrocarbons
obtained from petrolatum.
The oil is indigestible and absorbed only to a limited
extent.
When mineral oil is taken orally for 2–3 days, it
penetrates and softens the stool and may interfere with water resorption.
Stool-Wetting Agents and Emollients: Mineral Oil
The side effects of mineral oil preclude its regular
use and include:
interference with
absorption of fat-soluble vitamins,
elicitation of foreign
body reactions in the intestinal mucosa and other tissues,
leakage of oil past
the anal sphincter.
Rare complications such as lipid pneumonitis due to
aspiration also can occur,
Therefore “heavy” mineral oil should not be taken at
bedtime and “light” (topical) mineral oil should never be administered orally.
Stimulant (Irritant) Laxatives
Stimulant laxatives have direct effects on
enterocytes, enteric neurons, and GI smooth muscle
They also
induce a limited low-grade inflammation in the small and large bowel to
promote accumulation of water and electrolytes and stimulate intestinal
motility.
Included in this group
are diphenylmethane derivatives, anthraquinones, and ricinoleic acid.
Diphenylmethane derivatives: Sodium Picosulphate
Sodium picosulfate
is hydrolyzed by colonic bacteria to its active form, and hence acts
locally only in the colon.
Effective doses vary as much as four- to eightfold in
individual patients.
Consequently, recommended doses may be ineffective in
some patients but may produce cramps and excessive fluid secretion in others.
Diphenylmethane derivatives: Bisacodyl
Bisacodyl is the only diphenylmethane derivative
available as an enteric coated preparation and as a suppository for rectal
administration.
The usual oral daily dose of bisacodyl is 10–15 mg for
adults and 5–10 mg for children 6–12 years old.
Diphenylmethane derivatives: Bisacodyl
The drug requires hydrolysis by endogenous esterases
in the bowel for activation,
Therefore the
laxative effects after an oral dose usually are not produced in <6 hours;
i.e. taken at bedtime, it will produce its effect
the next morning.
Suppositories work
within 30–60 minutes.
Due to the possibility of developing an atonic
nonfunctioning colon, bisacodyl should not be used for more than 10 consecutive
days.
Anthraquinone laxatives
These derivatives of plants such as aloe, cascara, and
senna share a tricyclic anthracene nucleus modified with hydroxyl, methyl, or
carboxyl groups to form monoanthrones.
For use, monoanthrones are converted to dimeric
(dianthrones) or glycoside forms.
This process is reversed by bacterial action in the
colon to generate the active forms.
Senna is obtained from the dried leaflets on pods
of Cassia acutifolia or Cassia angustifolia.
Cascara sagrada is obtained from the bark of the buckthorn
tree.
Castor oil
Castor oil is derived from the bean of the castor
plant, Ricinus communis, which contains two well-known noxious ingredients: an
extremely toxic protein, ricin, and an oil composed chiefly of the triglyceride
of ricinoleic acid.
The triglyceride is hydrolyzed in the small bowel by
the action of lipases into glycerol and the active agent, ricinoleic acid,
Ricinoleic acid
acts primarily in the small intestine to stimulate secretion of fluid
and electrolytes and speed intestinal transit.
Castor oil
When taken on an empty stomach, as little as 4 mL of
castor oil may produce a laxative effect within 1–3 hours;
However, the usual dose for a cathartic effect is
15–60 mL for adults.
Enemas and Suppositories
Enemas commonly are employed, either by themselves or
as adjuncts to bowel preparation regimens, to empty the distal colon or rectum
of retained solid material.
Bowel distention by any means will produce an
evacuation reflex in most people, and almost any form of enema, including
normal saline solution, can achieve this.
Enemas and Suppositories
Specialized enemas contain additional substances that
either are osmotically active or irritant.
Repeated enemas with tap water or other hypotonic
solutions can cause hyponatremia;
Repeated enemas
with sodium phosphate–containing solution can cause hypocalcemia.
Enemas and Suppositories: Glycerin
Glycerin is a trihydroxy alcohol that acts as a
hygroscopic agent and lubricant when given rectally.
The resultant water retention stimulates peristalsis
and usually produces a bowel movement in less than an hour.
Glycerin is for rectal
use only and is given in a single daily dose as a 2- or 3-g rectal suppository
or as 5–15 mL of an 80% solution in enema form.
Rectal glycerin may
cause local discomfort, burning, or hyperemia and (minimal) bleeding.
Some glycerin
suppositories contain sodium stearate, which can cause local irritation.
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