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9 Elimination (II)
Digestive observations
• Introduction
• Faeces
• The mechanism of defecation
• Disorders of faecal elimination
• The mechanism of vomiting
• Observations regarding vomiting
• Drugs affecting vomiting
• Key points
• Notes
• References
Introduction
The digestive system consists of the mouth, oesophagus, stomach, duodenum, jejunum,
ileum, colon (ascending, transverse and descending), caecum, rectum and anus (Figure
9.1). The function of the system, i.e. the digestion and absorption of food nutrients, is con-
trolled through enzymes from various glands and by the nervous system. The enzymes are
catabolic, i.e. they breakdown the food to the simplest forms for absorption into the blood
(Chapter 7). The nervous system causes the smooth muscles in the gut wall to contract in
waves (called peristalsis) in order to propel the contents forward.
The inside of the gut, i.e. the gut lumen, is technically part of the outside world. That
sounds strange, but for anything to get into the body it must rst be absorbed through the gut
wall. Swallowing food does not mean it is entering the body, it is simply entering the gut. So
the gut wall is the interface between the outside world (inside the lumen) and the body (the
blood and tissues). This is why the gut contents contain millions of bacterial and viral organ
-
isms (called the intestinal ora), whilst the internal body remains sterile. Also, the solid waste
eliminated from the anus has passed through the body without actually entering the body.
Abnormal elimination, such as diarrhoea and vomiting, indicates that important
changes have occurred within the digestive system. It is essential to establish if it is a pass-
ing phase or a symptom of something more persistent and potentially serious. The history
that led up to the event coupled with the observations made at the time are paramount.
DOI: 10.4324/9781003389118-9
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Elimination (II) 181
Oesophagus
Stomach
Pancreas
Liver
Diaphragm
Mouth with
tongue
Colon
(large intestines)
Ileum
(small
intestines)
Anus
Rectum
Figure 9.1 T he digestive system begins at the mouth. Food passes down the oesophagus to the stom-
ach. The ileum (small intestines) completes digestion, but food remnants are processed
through the colon before elimination at the anus. The intestines are drawn lower than
normal to expose the liver and pancreas which are subsidiary organs of digestion.
Faeces
Faeces is waste material obtained primarily from ingested food. It normally contains bre,
a term for several indigestible components of the diet that provides the bulk of the stool.
Fibre is derived mostly from the plant substances in the diet (i.e. fruit and vegetables), but
less is found in meats. The varieties of bre include cellulose, hemicellulose, pectins, gums
and lignins (Chapter 7, page 145). These are mostly large-molecular polysaccharides that
form the walls of plant cells. These particular polysaccharides are complex carbohydrate
molecules that are indigestible by any of the digestive enzymes in the small bowel (ileum),
but some can be broken down (catabolised) to a certain extent by digestive bacteria pre-
sent in the large bowel (colon). These bacteria, the intestinal ora, are commensals.
1
In
fact, human bowel commensals actually produce important vitamins from their activity on
bowel contents, e.g. niacin (or nicotinic acid), thiamine (vitamin B
1
) and vitamin K, which
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182 Elimination (II)
we can absorb and use (see Chapter 7, Table 7.3, page 142). Fibre has several properties;
i.e. it absorbs and holds water, electrolytes (see Chapter 6, page 130) and bile salts. Hold-
ing water makes it normally soft so that the stool is easy to pass. The action of the colon
in absorbing water from the bowel contents prevents the faeces from being too wet. The
absorption of electrolytes and bile salts into the bre itself aids the elimination of these
substances. Rened foods are those in which the bre is largely removed or cooked suf-
ciently to break it down to digestible carbohydrates and provide a greater degree of nutrient
efciency with less waste material. The rening of foods, which is becoming less common
in the Western diet, has resulted in an increase in bowel disorders such as colon cancers
and diverticular disease. The latter is a condition in which the mucous lining of the bowel
is pushed through the muscular wall into pouches that can become inamed. Clearly, bre
has a greater role to play in human digestion than was at rst thought, being vital for correct
bowel function, and as such it is protective against bowel disease.
The mechanism of defecation
The rectum is normally empty. Bowel wall movements push faecal matter into the rectum,
stretching the rectal wall. This triggers the defecation reex (Figure 9.2), an automatic
action involving afferent sensory pathways from stretch receptors in the rectal wall to the
spinal cord and efferent motor pathways from the cord to the rectal muscles.
Spinal cord
Parasympathetic
outflow
Posterior
sensory
root of
spinal nerve
Increased
intrathoracic and intra-
abdominal pressure
Rectum
Sensory
input
Faecal
movement
Internal
sphincter
External
sphincter
Anus
Anterior
motor root
of spinal
nerve
Internal
pressure
Figure 9.2 Ph ysiology of defecation. Internal pressure from descending stools into the rectum
stretches the rectal wall. Sensory input from stretch receptors triggers a parasympathetic
output from the spinal cord, which relaxes the internal sphincter and contracts smooth
muscle in the bowel wall. This puts pressure on the external sphincter to open, but
being voluntary skeletal muscle, this sphincter opens under conscious control. Increas-
ing intrathoracic and intra-abdominal pressure pushes the bowel contents forward.
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Elimination (II) 183
Activation of this pathway results in two actions: (1) the contraction of the muscular
walls of the sigmoid colon and rectum, pushing the contents further along and (2) the anal
sphincters to relax. Relaxation of sphincters causes them to open, and this means open-
ing the escape route for faeces. Whereas the internal anal sphincter is autonomic (smooth
muscle), the external requires voluntary control (skeletal muscle), thus allowing the time
needed for the sphincter to be opened appropriately. It is this last aspect that is important
in childhood, for control of the external sphincter is a skill that has to be learnt. Expulsion
of faeces is achieved by contraction of the rectal wall, depression of the diaphragm and
contraction of abdominal muscles, the last two causing an increase in the intra-abdom-
inal pressure. Although this is a spinal reex, achieved by the parasympathetic nervous
system from the sacral outow (Figure 9.1), the medulla is involved in coordinating the
various muscle activities. It is useful to think of the parasympathetic nervous system as
being the neurological control of all three normal emptying mechanisms of the body, i.e.
urination, defecation and – in males – ejaculation.
The age by which a child is ready for toilet training is between 18 and 36 months. The
average age for girls is 29 months, and for boys it is 31 months. The majority of children
will be toilet-trained by 36 months.
Disorders of faecal elimination
Diarrhoea
The term ‘rrhoea’ arises at the end of several words such as diarrhoea and steatorrhoea (see
page 184), and it means ‘ow’. Diarrhoea is a ow of faeces in uid form, since the water
content is excessive and the bre bulk is minimal. It often results in multiple bowel evacua-
tions throughout the day and night. Diarrhoea has numerous causes, and some basic obser-
vations are needed to establish a possible aetiology.
2
These observations are for quantity and
number of bowel evacuations that occur per day. This will give an estimate of the uid loss the
patient is experiencing, and uid balance records (Chapter 6) may be necessary. Identica-
tion of any obvious abnormal content (e.g. the presence of blood or mucus) is important, and
investigations may be required to establish if any infectious organisms are present.
Blood and fat in the stools
Blood in the stools may be fresh and red, indicating a bleed somewhere within the lower
bowel, i.e. the colon or rectum itself. Otherwise, it may be a darker red-brown or even
black, called melaena. The presence of melaena suggests that the blood has undergone
some degree of digestion and has mixed with the stools. In this case, it must come from
higher in the digestive system, i.e. a bleed within the stomach or ileum. Digestive bleeds
can arise from mucosal ulcerations, polyps or other growths that erode blood vessels,
inammatory bowel disease, ruptures of varicose veins within the oesophagus or rectum
or abdominal trauma. Being a liquid itself, blood can provide the necessary water to
prevent colonic contents from being converted to solid stool, and blood therefore can
become thoroughly integrated with the faecal matter. Of course, heavy digestive bleeds
are likely to be accompanied by other symptoms of blood loss, notably pallor, increased
and weakened pulse rate, low blood pressure and even shock.
Blood is not always visible in the stool, and in very small quantities it may only be
detected by chemical test. This is referred to as occult blood
3
and occurs when the bleed
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184 Elimination (II)
into the bowel is very small, sometimes microscopic. It is most likely to have arisen from a
bleed higher in the bowel before the stools are fully formed, so the blood gets mixed into
the stool. The cause needs to be investigated because it could be from the early stages of
a bowel tumour.
Fat present in the stool is called steatorrhoea. It is caused by poor fat digestion and a
low level of absorption (a fat malabsorption), so most of the fat in the diet passes through
the digestive tract unchanged. Poor digestion of fat may be due to problems with bile
production in the liver or lack of bile drainage through the biliary ducts, since bile is
required for fat absorption. It may also be due to failure of the pancreas to produce lipase,
the enzyme responsible for the breakdown of fat. Lipase may be obstructed from reaching
the intestines if the pancreatic duct is obstructed. A high level of fat in the stools has the
effect of softening the stool to a pulp and making it lighter in colour. Fat-laden faeces also
oat on water, making them difcult to ush.
Mucus in diarrhoea
Mucus is the natural secretion of the mucous membrane and acts as a lubricant in the
bowel for the passage of food and faecal content and dissolves some nutrients before it is
itself reabsorbed. Mucus in diarrhoea is an indication of excessive inammatory changes
within the mucous membrane that result in overproduction of mucus. Inammatory
bowel disease (IBD) is a term that encompasses at least two bowel disorders, ulcerative
colitis and Crohn’s disease (inammation of mainly the small bowel but sometimes seen
in the colon). Both diseases are characterised by inammation of the mucous lining of the
bowel with blood and mucus present in the diarrhoea.
Other causes of diarrhoea
Diarrhoea can also be caused by overstimulation of bowel movements by the parasym-
pathetic nervous system, which promotes digestive activity. Normally, bowel contents are
propelled along by waves of muscle contraction (called peristalsis) at a speed that allows
water to be absorbed and therefore faeces to be well formed. If this rate of propulsion
is sped up (known as increased bowel motility), the contents reach the rectum before
all the water is absorbed, and liquid faeces results. This speeding up of peristalsis also
causes the other symptom associated with diarrhoea, i.e. very frequent bowel evacua
-
tions and abdominal pain that occurs during peristalsis, known as colic. A patient suffer-
ing from a severe form of IBD e.g. 40 or more diarrhoea bowel evacuations in 24 hours,
may often incur sleep loss and restriction of activities. Other symptoms include dehydra-
tion and electrolyte imbalance (Chapter 6), with distressing pain and tenderness around
the anal sphincter. Infections such as Shigella – an organism that causes dysentery – or
food-poisoning organisms such as Staphylococcus or Salmonella can have similar effects.
Non-infectious causes include the overuse of purgatives (or laxatives; see page 186),
malabsorption syndromes, certain foods in the diet that increase bowel propulsion, treat-
ments such as radiation therapy involving the digestive tract and even anxiety (‘nervous
diarrhoea’).
Drug-induced diarrhoea is an important cause of the problem, especially in elderly
people because this group often requires more medication than younger people, and
therefore they suffer more side effects (Ratnaike and Jones 1998). Antibiotic drugs can
cause diarrhoea as a side effect because their activity against living organisms may also
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Elimination (II) 185
involve killing the natural colonic commensals (see Note 1), i.e. bacteria we need for
normal bowel function, known as the intestinal ora. This becomes particularly important
with oral antibiotics (see Chapter 15).
Diarrhoea normally settles down once the cause has been corrected and the bowel is
empty. However, there are occasions when medical intervention is required and it can
be relieved with drug therapy. Loperamide hydrochloride (Imodium) reduces the bowel
motility (i.e. it reduces peristalsis) and therefore calms the bowel propulsive actions.
Opium and morphine mixed with kaolin (an adsorbent clay) are sometimes used to help
control persistent acute diarrhoea when other treatments fail. Opium (which contains
mostly morphine) requires specialist supervision. Co-phenotrope is used to help manage
faecal consistency as part of stoma management.
Constipation
Constipation is the failure to evacuate the bowel adequately, often totally, leading to an
increasing collection of faeces in the colon. Possibly as much as 10% of the Western
world population suffers from some degree of retained bowel content. Unlike diarrhoea,
constipation provides few external clues to its presence, and a history of bowel activ-
ity over the previous few days is necessary to identify the problem. There may be some
abdominal pain or discomfort. It is important to recognise the patient who is at risk of
constipation: notably, the patient with reduced mobility, altered levels of consciousness,
inadequate uid or dietary bre intake, taking medication which has constipation as a
side effect, ignoring regular toiletry habits, suffering from a bowel disease or any combi-
nation of these. The elderly are most likely to suffer constipation as they may possess more
risk factors than the young (Nazarko 2017).
Constipation is preventable, not just curable, by the identication of the patient’s risk
status, by the monitoring of bowel movements with intervention if necessary and by the
correction of dehydration. In some patients, improvements in their mobility also contrib-
utes to the prevention of constipation, as well as the many other complications of immo-
bility (see Chapter 14).
One bowel evacuation each 24 hours is the average, but considerable variation does
occur, with some individuals claiming that bowel evacuations of only once or twice
per week is normal for them. Others may pass faeces more than once a day. What is
abnormal is a total absence of any bowel evacuation, and what may be abnormal is a
signicant change in a person’s bowel habit, especially if this change is persistent. If
once a day is normal for an individual, then three days without evacuation is a poten-
tial for constipation, and the reason should be identied if possible. Additional signs
to aid the diagnosis of constipation include the presence or absence of anorexia (loss
of appetite), abdominal pain (especially colic) and distension, nausea and confusion.
The presence of confusion is particularly important in elderly people, when the brain
becomes especially susceptible to the toxic effects of constipation (i.e. waste products
in faeces that are normally excreted are reabsorbed into the blood). Confusion as a
result of constipation must be identied as families can think that their elderly relative
is becoming demented when all that is required is treatment for constipation. Diet is
also important to note, since a lack of oral uid or bre in the diet is an important fac-
tor leading to constipation. Lack of exercise, especially complete immobility, reduces
bowel movement, which, in turn, causes the contents to remain longer in the colon.
During this longer stay in the colon, more water is absorbed from the contents, which
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186 Elimination (II)
then get drier and harder to propel and evacuate. Total obstruction of the bowel with
hard, solid faeces can follow on from this in some extreme cases, made worse by any
condition that narrows the bowel lumen (e.g. new growths). High dosage of some
drugs that have a constipating side effect, including morphine, as in the management
of some terminal disorders, may cause constipation, which then requires additional
management. Assessing the risk of constipation requires keen observation of diet and
uid input, mobility, attempts at defecation, abdominal pain and mental alertness, and
these are sometimes put together in risk assessment scales, which may be useful in
some clinical areas (Duffy and Zernike 1997). Elderly people are always said to be at
highest risk because of reduced mobility and a decline in the health status of the bowel
with age (Bouras and Tangalos 2009).
Management of constipation may include the use of laxative drugs, enemas or sup-
positories. Laxative drugs fall into four main groups: (1) Bulk-forming agents, (2) Bowel
stimulants, (3) Faecal softeners and lubricants and (4) Osmotic laxatives (Table 9.1).
Table 9.1 Laxative medications
Group Drug Notes
1 (1) Ispaghula husk (Isogel) Bulk-forming agents. These improve the
(2) Sterculia (with or without bre and water content within the bowel
frangula) (bulk forming) and provide something
for the muscle wall to work on. They
increase the bowel transit times and
soften the stool so it can be passed easier
and with more comfort.
2 (1) Senna (Senokot; with or
Bowel stimulants. They act on the bowel
without ispaghula husk)
wall and its nerve supply, which then
(2) Bisacodyl
increases peristalsis to propel the stools
(3) Co-danthramer
forward. These must not be used regularly
(4) Co-danthrusate
on a daily basis since the bowel can
(5) Glycerol
become dependent on them to function
(6) Sodium acid phosphate with
in the long term and will not function
sodium bicarbonate
without them. So, they are best used as
(7) Sodium picosulfate
a one-off treatment. They may also cause
bowel cramping pain.
3 (1) Arachis oil Faecal softeners. These line the bowel and
(2) Docusate sodium prevent water absorption so the stools
(3) Liquid parafn will not dry out. This softens the stools
to make them easier to eliminate by
lubricating the passage. They should be
used only as a short-term, temporary
measure since there is evidence that
they may prevent the absorption of some
important nutrients.
4 (1) Lactulose
Osmotic laxatives. These attract more water
(2) Macrogol 3350 (with or
into the bowel to soften and lubricate the
without KCl, NaCl and
stools.
NaHCO
)
4
3
(3) Magnesium hydroxide
(4) Sodium acid phosphate with
sodium phosphate
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Elimination (II) 187
Table 9.2 Red and amber ag warnings of deteriorating condition
O Red Flag = serious situation which needs urgent medical attention.
O Amber Flag = Important to get a medical assessment as soon as possible.
Flag Details
warning
O Red Flag
Vomiting and/or abdominal swelling with an ongoing history of
constipation (possible bowel obstruction).
Diarrhoea and/or vomiting associated with dehydration.
Melaena stool or blood in the vomit, a symptom of gastrointestinal
bleeding.
O Amber Flag Possibility of serious bowel disease if there is blood in the stools, unusual
alteration of bowel habit, weight loss, abdominal pain and a history of
bowel disease.
High frequency of diarrhoea, especially associated with blood.
(After Hill-Smith and Johnson 2021, with permission)
Stomas
A stoma is an articial surgical opening into the bowel to allow the excretion of bowel
contents into a collection bag worn on the abdominal wall. This is done when normal def-
ecation is not possible due to bowel disease. Stomas are made into the ileum (ileostomy)
or colon (colostomy), depending on the nature of the problem. Stomas are sometimes
used in the management of bowel cancers, ulcerative colitis, diverticular disease or after
permanent bowel resection (removal of part of the bowel). A colostomy opening made
into the proximal half of the colon, on the right side of abdomen, will initially result in a
more liquid stool than an opening into the distal half of the colon, on the left side of the
abdomen (Figure 9.3).
This is due to the water extraction function of the colon. The proximal half contains
liquid stools from the small intestine, whereas the distal half contains stools that have trav-
elled nearly the entire length of the bowel and are therefore much drier. Stoma bags require
changing, which the patient can often do themselves after being taught about their stoma.
The stoma should be observed for the normal red colour of healthy mucous membrane with
no bleeding. Pallor or cyanosis (blue coloration) may indicate reduced blood supply which
can cause complications and must be reported. The skin around the stoma is inspected for
soreness, inammation, infection and any broken areas. Some collection devices stick to
the skin and this could cause skin problems. The bag contents are observed for the same
constituents as faeces, i.e. for diarrhoea, blood, bile or mucus and also colour and quantity.
Some drugs may affect the function of stomas or change the colour of the contents. These
drugs include laxatives and antacids, both of which are best avoided for most stoma patients
unless prescribed and monitored carefully. Narrow-spectrum antibiotics are preferable to
broad-spectrum antibiotics when such drugs are necessary, since narrow spectrum means
they will have less effect on the normal bowel commensals with less risk of diarrhoea. Diar-
rhoea in a stoma patient is very difcult to manage since it requires numerous and frequent
bag changes which disrupts normal daily activities and could cause complications of the
skin at the stoma site. Skin irritation and breakdown around the stoma should be avoided.
Antibiotics can change the faeces to a grey-green colour and irritate the skin. Other colour
changes caused by drugs include iron (black), tetracycline (red), heparin (pink or red),
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188 Elimination (II)
1
2
3
4
Figure 9.3 Colonic stoma sites. (1) Within the ascending colon. (2) Within the transverse colon. (3)
Within the descending colon. (4) Within the sigmoid colon.
indometacin (green) and aspirin (pink or red). Aspirin is acidic and may cause mucosal and
skin irritation at the stoma site. It also contributes to anticoagulation of blood, i.e. helps to
stop blood clotting and promotes bleeding, and is therefore best avoided. Stoma patients
will be referred to the care of a stoma specialist nurse who should be consulted on all mat-
ters concerning these patients.
The mechanism of vomiting
Vomiting (or emesis) can be regarded generally as a normal physiological response to an
abnormal condition affecting either the digestive system or its neurological control. It is
protective because it removes from the body any ingested substance that is unwanted and
may be potentially dangerous. Stomach and sometimes bowel contents are driven the
wrong way up the oesophagus back into the mouth. Accurate observations of the patient
and the contents of the vomited matter, plus a history of events leading up to the episode
of vomiting, can provide important clues about the nature of the cause.
The brainstem medullary vomit reex centres coordinate what is a relatively complex
process involving a range of different stimuli. Also, closely associated with the vomit cen-
tres are the chemoreceptor trigger zones (CTZ; Figure 9.4).
These are a bilateral pair of centres under the oor of the fourth ventricle, within an
area called the area postrema, and this receives impulses from adverse chemical stimuli
in the blood. Chemicals of this type include various drugs (e.g. cytotoxic agents) and other
toxins from perhaps food or infectious organisms. Such stimulation of the CTZ causes
stimulation of the vomit reex centres, which then coordinates and controls vomiting.
The vomit centres themselves receive nerve impulses directly from:
1 The cerebellum, part of the brain that coordinates muscle activity and balance. The
cerebellum obtains sensory information on balance (vestibular information) from the
semicircular canals in both ears via the vestibular branch of the eighth cranial nerve,
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Elimination (II) 189
the vestibulocochlear nerve. These canals register changes in balance and head move-
ment as nerve impulses that are transmitted rst to the vestibular nuclei in the medulla,
then to the cerebellum (Figure 9.5).
Any disturbing movements or upsets in balance, as in motion sickness, can produce
adverse nerve impulses that pass through the vestibular nuclei, the cerebellum and on
to the vomit reex centre, and vomiting occurs. A disease that causes dizziness and
vomiting via this route is Ménière’s disease, a chronic disorder of the inner ear where
the amount of the uid called endolymph becomes excessive. This causes sudden
attacks of vertigo (dizziness), nausea and vomiting, progressive deafness and tinnitus
(continuous internal sounds in the ear). The word vertigo is usually linked to dizziness
caused by heights. The word actually means dizziness linked to a ‘whirling round’ sen-
sation, i.e. the environment is spinning around. It is not especially related to heights,
and people can suffer from vertigo at any height, often at ground level (see also Chap-
ter 15, page 324).
2 The gag reex, a feeling of retching when the back of the tongue or throat is touched
with a nger or tongue depressor.
3 Bad sights or odours, fear, brain injury and high pressure within the skull (raised inter-
cranial pressure) can all stimulate the vomit reex centre via the cerebral cortex, our
conscious part of the brain.
4 Stimuli from the digestive tract itself, especially from the stomach, such as over-disten-
sion from eating too much or inammatory irritation from extra spicy or acidic food.
Some drugs or excessive alcohol can cause vomiting. Such stimuli arrive at the vomit
centre via the vagus nerve (the tenth cranial nerve; Figure 9.6).
Drugs, (e.g. morphine,
anaesthetics,
cytotoxics)
Gag reflex
Sensory stimuli,
(e.g. bad sight,
smell, pain)
Gut stimuli, (e.g
.
overdistension,
irritation)
Motion sic
kness or
Ménière's disease
Cerebellum
Vomiting
Respiratory
centre
Control
of saliva
VMC
Vomit centre
Chemoreceptor
trigger zone
Vagus nerve
Figure 9.4 Stimulation of the vomit centre is often via the chemoreceptor trigger zone, which itself
is stimulated by motion or drugs. Sometimes the vomit centre is affected directly by bad
sensory stimuli (e.g. an unpleasant smell or sight) or by vagal stimuli from the gut. The
vomit centre output is via the vasomotor centre (VMC) – which inuences the blood
pressure during the event – and via the respiratory centre which regulates breathing
throughout vomiting. The vomit centre also controls saliva production.
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