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The Use of a Nursing Model to


Understand Diarrhea and the Role
of Probiotics in Patients With
Inflammatory Bowel Disease
Julie Savard, BN, RN
Jo-Ann Sawatzky, PhD, RN

Inflammatory bowel disease, an umbrella term used for Crohn disease and ulcerative colitis, is often
accompanied with the presenting symptom of diarrhea. This symptom can be a great nuisance and emotionally
distressing to the individual with inflammatory bowel disease. Although the exact etiology of inflammatory
bowel disease is still unknown, interactions between the host susceptibility, mucosal immunity, and intestinal
microflora are thought to be major factors. One intervention that is gaining increasing support by the research
and medical community is the use of probiotics, which work on the intestinal flora by altering the bacterial
composition and thereby rendering the environment unfavorable to pathogenic organisms. The human
response to illness model provides an ideal organizing framework to gain a comprehensive understanding of
the human response of diarrhea in the inflammatory bowel disease population. By examining the physiological,
pathophysiological, behavioral, and experiential perspectives as well as individual vulnerabilities, this model
establishes sound rationale to guide nursing interventions to help the individual better cope with the physical
and emotional effects of having diarrhea. This model also facilitates the provision of holistic and personalized
care, which may include the use of probiotics to help alleviate this distressing symptom.

I
nflammatory bowel disease (IBD) is an umbrella term 1996; Leshem, 2003; Pearson, 2004). A comprehensive
used for Crohn disease (CD) and ulcerative colitis (UC). understanding of the physiology, pathophysiology, behavioral,
These two disorders are grouped together because of and experiential perspectives of diarrhea would facilitate the
the similarities in their symptoms and medical treat- provision of holistic nursing care to IBD patients and their
ments (Pearson, 2004; Rayhorn, 2001). One characteristic families. The human response to illness (HRTI) model encom-
common to both is diarrhea. This symptom can be particu- passes all of these concepts, thereby enabling the development
larly distressing to an individual with IBD and is often man- of a quality care plan for these patients.
ifested by fear, anxiety, and embarrassment (Dudley-Brown, Medical interventions are often the focus of research with
individuals living with IBD, but recently, probiotics have been
discussed as a potential alternative or complimentary ther-
Received March 14, 2006; accepted May 30, 2007.
apy to the more commonly used pharmacological treatments.
About the authors: Julie Savard, BN, RN, is Public Health Nurse, This article uses the HRTI model as an organizing framework
Winnipeg, Manitoba, Canada. to provide nurses with insight into the human response of
Jo-Ann Sawatzky, PhD, RN, is Assistant Professor, Faculty of Nursing, diarrhea in IBD patients, to substantiate why probiotics may
Helen Glass Centre, University of Manitoba, Winnipeg, Manitoba, Canada.
be a viable alternative intervention for alleviating this dis-
Correspondence to: Julie Savard, BN, RN, Public Health Nurse, E 169
Horace Street, Winnipeg, Manitoba R2H 0W2, Canada (e-mail: tressing symptom in some of their patients, and to discuss the
juliesavard@shaw.ca). nursing implications of this alternative therapy.

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The HRTI Model Diarrhea in an Individual With


Heitkemper and Shaver (1989) originally described the HRTI
a Normal State of Function
In the GI tract, ionic balance, fluid absorption, and secretion
model as encompassing three main concepts used to describe
human function under different medical conditions. These are important factors in maintaining homeostasis. This bal-
concepts are (a) individual adaptations, (b) environmental fac- ance allows for adequate nutrient intake, normal gut motil-
tors, and (c) person factors. Individual adaptations are com- ity, protection against pathogens, and epithelial cell viability
prised of four interrelated perspectives of human responses: (Payne et al., 2006). This homeostasis is dependent on nor-
(a) physiological, (b) pathophysiological, (c) behavioral, and mal physiological function of the small intestinal and colonic
(d) experiential perspectives. Nurses can use this model as an cells. The major goal of the small intestine is to absorb nutri-
organizing framework to gain insight into the phenomenon ents, whereas the colon plays an important role in conserving
of diarrhea in patients with IBD. This model enables the fluid and electrolytes (Sellin, 2001). When regulatory mecha-
nurse to achieve a comprehensive understanding of all per- nisms are challenged, diarrhea may result. The mechanisms
spectives of this human response to illness, thus facilitat- of diarrhea in the individual with normal bowel function can
ing individualized, evidence-based management strategies. be classified as osmotic, secretory, and motile (McCance &
This holistic approach can be used to establish the ratio- Huether, 2006). Inflammatory changes are discussed within
nale for alternative or complimentary therapies, such as pro- the context of IBD.
biotics, and as the basis for delivering and evaluating quality In osmotic diarrhea, a nonabsorbable agent draws fluid
nursing care. into the intestinal lumen. Many agents can be metabolized by
bacteria and converted to substances with osmotic poten-
Physiological Perspective tial. Examples of agents that may produce osmotic diarrhea
Physiological regulatory mechanisms are what happen in a include laxatives, magnesium-based antacids, certain dietetic
normal or usual state of biological functioning (Mitchell, foods or candy containing sorbitol (Field, 2003) or mannitol,
Gallucci, & Fought, 1991). In the gastrointestinal (GI) tract, and certain medications when used on a chronic basis (Kroser
normal gut flora contains several hundred grams of bacteria & Metz, 1996).
that affect host homeostasis (Guarner & Malagelada, 2003). In secretory diarrhea, the movement of fluid into the
This homeostasis is kept in balance by a mix of beneficial intestinal lumen is caused by excessive mucosal secretion of
and pathogenic microorganisms (Mombelli & Gismondo, chloride or bicarbonate or by decreased sodium absorption.
2000). This balance is generally quite stable (Santosa, When transport into the lumen exceeds uptake, the result is
Farnworth, & Jones, 2006) and is responsible for specific net loss of fluid, which can result in secretory diarrhea. The
metabolic, trophic, and protective functions (Guarner & primary causes of secretory diarrhea are bacterial endo-
Malagelada, 2003). The following is a brief overview of the toxins (e.g., Escherichia coli) and neoplasms (McCance &
functions of the gut in a normal state. Huether, 2006).
Both increases and decreases in intestinal motility can lead
Metabolic Functions to diarrhea. Increases can be caused by hyperthyroidism and
A major metabolic function of the colonic microflora is the opiate withdrawal, whereas decreases can be caused by bac-
fermentation of nondigestible dietary residue such as carbo- terial overgrowth. Conditions causing bacterial overgrowth
hydrates. The outcome of this complex metabolic activity is include large diverticula, smooth muscle damage, or auto-
the generation of short-chain fatty acids, which in turn are a nomic neuropathy (Field, 2003).
supply of energy and nutritive products for bacterial growth There are many pathogens that induce diarrhea, all of
and proliferation (Guarner & Malagelada, 2003). which use different mechanisms to cause intestinal damage,
which include alteration in ion transport, disruption of tight
Trophic Functions junction complexes, and inflammatory responses (Field, 2003;
Arguably, the most important role of short-chain fatty acids Payne et al., 2006). Diarrhea in a person that is not afflicted
is their trophic effect on colonic epithelium (Limdi, O’Neill, with IBD or any other genetic illness predisposed to diar-
& McLaughlin, 2006). All three major short-chain fatty acids rhea will often be self-limiting and of short duration. The
(i.e., butyrate, acetate, and propionate) stimulate epithelial body will generally have the appropriate tools to self-
cell proliferation and differentiation in the large and small regulate and return to homeostasis.
bowel in vivo (Frankel et al., 1994).
Pathophysiological Perspective
Protective Functions A pathophysiological state results when normal bodily func-
Resident bacteria are an important line of resistance to colo- tions become disordered or decompensated (Mitchell et al.,
nization by exogenous microbes and are therefore highly sig- 1991). A person afflicted with IBD may not have the com-
nificant in preventing the intrusion of pathogenic microbes pensatory mechanisms needed to help return the body to a
(Guarner & Malagelada, 2003). Healthy epithelium, with its normal state of functioning.
tight junction complexes, normally provides an effective bar-
rier against antigens and pathogenic microbes. These intes- Pathogenesis of IBD
tinal epithelial cells have developed control mechanisms that The pathogenic origin of IBD involves interactions between
limit inappropriate activation of immune responses (Hanauer, host susceptibility, mucosal immunity, and intestinal micro-
2006). A mucus gel also covers the intestinal epithelium, act- flora. Although many studies have investigated the possibility
ing as a protective barrier against pathogens. Any change in of a single infectious agent causing IBD, none have yet been
mucus content or structure may compromise barrier function isolated (Ewaschuk & Dieleman, 2006). The most widely
(Limdi et al., 2006). accepted theory is that the chronic intestinal inflammation in

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IBD is the consequence of an overly aggressive immune sodium (and thus of chloride and water) is the critical ion
response to the commensal (i.e., normal endogenous) intes- transport abnormality in UC. The inflamed mucosa is very
tinal microflora in a genetically susceptible individual. This leaky to all monovalent ions, leading to decreased epithelial
hypothesis is supported by the facts that most inflammation resistance (Sandle, 2005). This lack of resistance reflects a
occurs in areas with the highest luminal bacterial concen- generalized impairment of tight junction integrity, thereby
tration (i.e., distal ileum and colon), that broad spectrum increasing intercellular permeability (Payne et. al., 2006).
antibiotics reduce intestinal inflammation, and that surgical The overall effect of these changes impairs the capacity of the
diversion of the fecal stream can prevent recurrences of CD inflamed intestinal mucosa to absorb sodium, chloride, and
(Sartor, 2003). water, thereby contributing significantly to the pathogenesis
A healthy gut is typically comprised of significant num- of diarrhea in this population (Sandle, 2005).
bers of bifidobacteria and lactobacilli, which do not con-
tain any known pathogens and are considered primarily as Experiential Perspective
carbohydrate-fermenting bacteria. The products of carbo- Experiential perspectives are assessed through patient reports
hydrate fermentation are principally short-chain fatty and verbalizations of the meaning of the event on the basis
acids, which are known to be beneficial to host health of introspection, personal experience, sociocultural factors,
(Macfarlane, Macfarlane, & Cummings, 2006). Con- knowledge, and coping mechanisms (Mitchell et al., 1991).
versely, increased numbers of mucosa-associated bacteria, Patients with IBD who experience diarrhea commonly report
such as the Bacteroides species and members of the Enter- several different emotions related to this symptom. Fear and
obacteriaceae group, and decreased numbers of bifidobac- embarrassment are often described as they relate to the poten-
teria and lactobacilli have been found in the IBD popula- tial for incontinence or to the actual experience of inconti-
tion (Rioux, Madsen, & Fedorak, 2005). It is believed that nence. This often inhibits social activities and thus prevents
this imbalance may perpetuate the inflammatory response the individual from leading a “normal” life (Dudley-Brown,
seen in IBD (Santosa et al., 2006). 1996; Pearson, 2004). One participant in Daniel’s (2001)
Individuals with IBD also have increased intestinal study described how humiliating it was to be with somebody
mucosal secretion of IgG-type antibodies against commensal and then have to suddenly run to the bathroom or else “. . .
bacteria. Immuno-inflammatory responses mediated by these go in your pants . . .” (p. 86). Many studies have reported
IgG antibodies can damage the intestinal mucosa (Macpher- that individuals with IBD have feelings of uncertainty, related,
son, Khoo, Forgacs, Philpott-Howard, & Bjarnason, 1996), in part, to the fact that this illness is characterized by remis-
thus resulting in disruption of the tight junction complexes. sions and exacerbations (Daniel, 2001; Dudley-Brown, 1996;
Pathogenic bacteria are then able to invade the lymph system Rayhorn, 2001). Most individuals in these studies were not
and subsequently cause an inflammatory immune response able to predict the next exacerbation and therefore worried
(Santosa et al., 2006). considerably about the uncertainty of the disease. This uncer-
It is believed that enhanced mucosal permeability, which is tainty revolved primarily around the symptoms experienced
due to either a genetic predisposition or to direct contact with each occurrence, as voiced by one of the participants
of bacteria with the mucosa, may play a pivotal role in main- in Dudley-Brown’s (1996) study: “The hard part is that
taining a chronic inflammatory state (Bergonzelli, Blum, there is always a chance of a flare-up . . . You just never,
Brussow, & Corthésy-Theulaz, 2005). The increased perme- ever know” (p. 86).
ability of the gut lining results in continuous stimulation of
the mucosal immune system (Hanauer, 2006). What distin- Behavioral Perspective
guishes IBD from inflammatory responses seen in the normal Behavioral perspectives are observable and measurable verbal
gut is an inability to down regulate immune responses. In a and motor behaviors (Mitchell et al., 1991). Behavioral man-
healthy gut, the intestine returns to a state of tolerance once ifestations of diarrhea are directly measurable by the quality
the pathogen is eradicated. In individuals with IBD, inflam- and quantity of the bowel movements. There are several instru-
mation is not down regulated, and consequently the mucosal ments, which measure disease activity indices in patients
immune system remains chronically activated and the intes- with either CD or UC that can be used to objectively eval-
tine is chronically inflamed (Hanauer, 2006). uate diarrhea. These instruments include questions directed
specifically at measuring how often an individual has daily
Pathogenesis of Diarrhea in IBD bowel movements. Instruments that measure quality of life,
In CD, damage to the distal ileum can lead to bile acid mal- such as the Inflammatory Bowel Disease Questionnaire
absorption, which can lead to diarrhea. Conjugated bile acids (Guyatt et al., 1989), address the specific bowel, systemic,
are normally reabsorbed in the distal ileum. When the distal emotional, and social function of IBD patients.
ileum is affected, unabsorbed bile acids become amphophiles, Indirect, objective measures of diarrhea include some diag-
which in turn have a secretory effect leading to diarrhea nostic markers, such as physical examination, stool studies,
(Field, 2003). Fistulas may also develop in CD, resulting laboratory testing, and radiologic studies (Kroser & Metz,
in bacterial overgrowth in the small bowel. Bacterial over- 1996). Weight, nutritional status, and orthostatic changes in
growth causes mucosal injury, which consequently leads to an individual’s vital signs could indicate severe volume losses.
diarrhea (Elphick, Elphick, & Sanders, 2006). Bacteria in the Stool studies could rule out other causes of diarrhea such
small bowel also deconjugate bile acids, thereby reducing the as bacterial infections, toxins, fat malabsorption, or laxative
capacity for fat absorption and further potentiating the symp- abuse. Laboratory tests can help determine any electrolyte
tom of diarrhea (Field, 2003). abnormalities that are due to diarrhea, and radiologic studies
Diarrhea is said to be the most common and debilitat- can be helpful in showing anatomic abnormalities that could
ing symptom of UC (Sandle, 2005). Impaired absorption of be the cause of diarrhea (Kroser & Metz, 1996). Knowledge

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of these diagnostic markers enables the nurse to assess the alternative form of this intervention, which has been gaining
effectiveness of the individual’s response to any given thera- more and more interest not only in the scientific community,
peutic intervention. but also in the market place among consumers, is probiotics
(Walker, Goulet, Morelli, & Antoine, 2006).
Person and Environmental Factors
The HRTI model also encompasses individual vulnerabilities, What Are Probiotics?
or person and environmental risk factors, which must be con- An expert panel for The Food Agricultural Organization/
sidered in the planning of patient-centered interventions World Health Organization (2001) has described probiotics
(Heitkemper, Levy, Jarrett, & Bond, 1995). These factors are as “live microorganisms which when administered in ade-
interwoven throughout the physiological, pathophysiologi- quate amounts confer a health benefit on the host” (p. 5).
cal, experiential, and behavioral perspectives of the model. Thus, a microorganism is not considered a probiotic unless it
has demonstrated to be viable at time of use and in sufficient
Person Factors quantity to produce a physiologic health benefit (Reid &
These factors can be divided into either modifiable or non- Hammond, 2005). Most probiotics belong to a group of
modifiable vulnerabilities (Heitkemper & Shaver, 1989). Non- lactic-acid producing bacteria (i.e., lactobacilli, streptococci,
modifiable factors associated with IBD have included acquired and bifidobacteria), which are part of the normal intestinal
or inherited immune function, genetics, age, race, and ethnic- microflora and exist as harmless organisms (Gionchetti,
ity (Listrom & Holt, 2004; Rayhorn, 2001). Although no spe- Rizzello, Venturi, & Campieri, 2000).
cific factors that increase the risk for diarrhea in those with Probiotics work by rendering the luminal environment
IBD have been verified, gender has been identified in the unfavorable for more aggressive bacteria by secreting anti-
research literature as a possible person factor. For example, microbial substances such as hydrogen peroxide, organic
researchers have studied women with IBD and how the men- acids, and bacteriocins. They occupy the limited physical
strual cycle can affect gastrointestinal symptoms (Kane, Sable, space in the mucus layer, thereby excluding pathogenic micro-
& Hanauer, 1998; Parlak et al., 2003). Results reveal that organisms (Ewaschuk & Dieleman, 2006). Probiotics have
women with IBD often report worsening of their diarrhea dur- also been shown to induce intestinal production of anti-
ing their menstrual cycle. inflammatory cytokines, all the while reducing the produc-
Potentially modifiable person factors include dietary intake tion of pro-inflammatory cytokines (i.e., tumor necrosis
and smoking (Listrom & Holt, 2004). Although studies factor) (Fedorak & Madsen, 2004).
linking diet as an etiological factor have been inconclusive Probiotics have to be safe for human consumption and
(Hanauer, 2006), carbohydrate consumption and dairy need to be able to survive stomach and bile acids (Ewaschuk
products may contribute to diarrhea (Mishkin, 1997; Vernia, & Dieleman, 2006). Probiotics have been used for centuries
Gnaedinger, Hauck, & Breuer, 1988). Smokers are twice as in the form of dairy-based fermented products. For example,
likely to develop CD, have more frequent relapses, and tend in 1905, Elie Metchnikoff suggested that Bulgarian peasants
to have a more active disease (Listrom & Holt, 2004). live longer because of their consumption of yogurt. In the
1930s, Minoru Shirota, a Japanese physician, suggested that
Environmental Factors the right mix of bacteria in the gut could prevent illness
Environmental factors, described as either physical or social, (Brown & Valiere, 2004). Nowadays, probiotics can be sold
could place the person at risk for not responding positively to in capsules and powders as dietary supplements, used in the
the intervention or not complying with the therapeutic regi- production of various fermented products such as yogurt, or
men (Heitkemper et al., 1995). An example of an environ- found in infant formula (Santosa et al., 2006; Broekaert &
mental factor that has been shown to increase diarrhea in Walker, 2006). Unfortunately, most probiotics that have
patients with IBD is stress (Pearson, 2004). Although its role proven to be effective are unavailable in the author’s country
as an etiological factor remains to be determined, it is clear (Canada); however, patients and healthcare providers are able
that stress definitely plays a role in their lives and not only is to access products from other countries such as the United
a consequence of their illness, but also is a trigger for a flare- States (Reid & Hammond, 2005).
up. For example, Daniel (2001) found that all of the partici-
pants in his study mentioned stress as a major factor in their Probiotics and IBD
lives. Most felt the stress affected flare-ups and increased the Research has suggested a significant role for bacteria in the
severity of their symptoms. pathogenesis of IBD. By altering the intestinal microflora,
probiotics may exert beneficial effects in the management of
Alternative Intervention for Diarrhea diarrhea related to IBD (Limdi et al., 2006). Several random-
ized control trials (RCTs) have been conducted with pro-
Related to IBD: The Use of Probiotics
biotics in various IBD-related conditions (Marteau, Seksik, &
Within the HRTI framework, interventions for diarrhea Jian, 2002; Rioux et al., 2005; Walker et al., 2006). The evi-
related to IBD should focus on the knowledge gleaned from dence suggests that three specific probiotics have demon-
the four perspectives as well as the person and environmen- strated promising results in patients with pouchitis, CD, and
tal factors. By using this knowledge, appropriate manage- UC. VSL #3, which contains a mixture of eight different
ment therapies can be developed and then subsequently eval- strains of bacteria, has been shown to maintain remission
uated within the context of the experiential and behavioral and prevent clinical recurrence in individuals with pouchitis.
perspectives. The focus of much of the literature on IBD is E. coli Nissle 1971, a nonpathogenic E. coli, has been shown
based on altering the pathophysiologic response to diarrhea to maintain remission in individuals with UC, and S. boulardii
with pharmacological interventions, such as steroids. An has been shown to be effective in the prevention of relapse in

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CD (Bergonzelli et al., 2005; Limdi et al., 2006; Marteau ficial adjunctive therapy in IBD management (Broekaert &
et al., 2002; Rioux et al., 2005; Santosa et al., 2006). Walker, 2006).
The link between gut microflora and IBD has been estab-
lished, and altering the composition of microflora by using
Implications for Nursing
probiotics holds promise as a therapeutic strategy for intes-
The HRTI model provides an appropriate framework for tinal inflammation. Further understanding of the relationship
nurses practicing in the area of gastroenterology to gain between bacteria and the GI tract will help identify which
insight related to the human response of diarrhea in the IBD probiotic strains may be effective in the management of
population. The following discussion illustrates how the IBD (Ewaschuk & Dieleman, 2006). Although the results of
evidence-based knowledge of the physiological, patho- studies on the effects of probiotics in IBD are encouraging,
physiological, experiential, and behavioral perspectives pro- there continues to be the need for large, well-designed, double-
vides guidance for nursing practice, education, and research, blind placebo-controlled clinical trials in individuals with IBD
particularly in relation to the alternative treatment of IBD (Goossens et al., 2003; Marteau et al., 2002; Rioux et al.,
with probiotics. 2005). Research related to the human response of diarrhea
It is essential for nurses involved in the care of patients should be guided by the insight gleaned from the four per-
with diarrhea related to IBD to fully understand what these spectives and the person and environmental factors, whereas
patients experience and what their goals are for optimal outcome evaluation should be based on the behavioral and
health. By using the HRTI model as a framework for under- experiential perspectives. Thus, the HRTI model would be an
standing the phenomenon of diarrhea, nurses are able to appropriate framework to guide future research in this area.
complete an accurate and thorough assessment that estab-
lishes sound rationale for interventions and outcome evalua- Conclusion
tions. This assessment must encompass the behavioral and
experiential perspectives. As well, person and environmental Nurses play an important role in the management of IBD.
influencing factors must be considered. Given the knowledge The HRTI model provides a comprehensive framework to
that fear, embarrassment, and uncertainty are emotions gain an understanding of the physiological, pathophysiologi-
often described by patients experiencing diarrhea, nurses cal, behavioral, and experiential perspectives and the influ-
can address these emotions and help these individuals find enced person and environmental factors related to diarrhea in
adaptive strategies that will enable them to regain a sense of the IBD population. The use of this model facilitates the pro-
vision of holistic and quality nursing care. In addition, it
control in their lives and to cope effectively. In addition, the
enables nurses working with IBD patients who have diarrhea
knowledge that stress can play a part in the exacerbation of
to participate effectively in practice, education, and research
diarrhea, thereby contributing to these feelings, uniquely
related to new, alternative therapies such as probiotics.
positions nurses to help these patients develop effective stress
management techniques.
On the basis of the complexity of the pathophysiology of References
diarrhea related to IBD, several treatment modalities may Bergonzelli, G., Blum, S., Brussow, H., & Corthésy-Theulaz,
be needed to ensure a comprehensive plan of care. With the I. (2005). Probiotics as a treatment strategy for gastro-
emerging research evidence, and a growing interest in alter- intestinal diseases? Digestion, 72, 57–68.
native medicine by the consumer market, probiotics provide Broekaert, I., & Walker, A. (2006). Probiotics and chronic dis-
a promising complementary or alternative treatment modal- ease. Journal of Clinical Gastroenterology, 40, 270–274.
ity. If probiotics can in fact decrease the symptom of diarrhea Brown, A., & Valiere, A. (2004). Probiotics and medical
in these individuals, and thus improve their overall quality of nutrition therapy. Nutrition in Clinical Care, 7, 56–68.
life, they should be considered when planning a care man- Daniel, J. M. (2001). Young adults’ perceptions of living
agement strategy. Probiotics have demonstrated the ability to with chronic inflammatory bowel disease. Gastroenterol-
alter the physiological response by enhancing the intestinal ogy Nursing, 25, 83–64.
microflora and the pathophysiological response, decreasing Dudley-Brown, S. (1996). Living with ulcerative colitis.
the symptom of diarrhea and thereby improving one’s over- Gastroenterology Nursing, 19, 60–64.
all quality of life. Elphick, H., Elphick, D., & Sanders, D. (2006). Small bowel
Patient education regarding pharmacological and alterna- bacterial overgrowth. An underrecognized cause of mal-
tive or complementary interventions facilitates positive and nutrition in older adults. Geriatrics, 61, 21–26.
beneficial responses to illness. This intervention also aims to Ewaschuk, J., & Dieleman, L. (2006). Probiotics and pre-
empower patients, to facilitate self-management, and to pro- biotics in chronic inflammatory bowel diseases. World
mote compliance with the medical regime. Although patients Journal of Gastroenterology, 12, 5941–5950.
may not be aware that probiotics are available, nurses can Fedorak, R., & Madsen, K. (2004). Probiotics and the man-
advocate on the behalf of their patients by discussing and sug- agement of inflammatory bowel disease. Inflammatory
gesting them either as an alternative or as a complementary Bowel Disease, 10, 286–299.
form of therapy. A sound understanding of how probiotics Field, M. (2003). Intestinal ion transport and the pathophys-
work and how they can benefit those who have IBD also iology of diarrhea. Journal of Clinical Investigation, 111,
enables nurses to share this knowledge through the education 931–943.
of their peers and other healthcare professionals. Probi- Food and Agriculture Organization of the United Nations and
otics are not and should not be considered a cure; however, World Health Organization. (2001). Health and nutri-
when used appropriately, probiotics can represent a bene- tional properties of probiotics in food including powder

422 GASTROENTEROLOGY NURSING


10904-05a_GN3006-Savard.qxd 11/30/07 1:17 PM Page 423

milk with live lactic acid bacteria. Retrieved September 23, McCance, K., & Huether, S. (2002). Pathophysiology: The
2007 from, ftp://ftp.fao.org/docrep/fao/meeting/009/ biologic basis for disease in adults and children (4th ed.).
y6398e.pdf Toronto, Ontario, Canada: Mosby.
Frankel, W., Zhang, W., Singh, A., Klurfeld, D., Don, S., Mishkin, S. (1997). Dairy sensitivity, lactose malabsorption,
Sakata, T., et al. (1994). Mediation of the trophic effects and elimination diets in inflammatory bowel disease.
of short-chain fatty acids on the rat jejunum and colon. American Journal of Clinical Nutrition, 65, 564–567.
Gastroenterology, 106, 375–380. Mitchell, P., Gallucci, B., & Fought, S. (1991). Perspectives
Gionchetti, P., Rizzello, F., Venturi, A., & Campieri, M. on human responses to health and illness. Nursing Out-
(2000). Probiotics in infective diarrhea and inflammatory look, 39, 154–157.
bowel diseases. Journal of Gastroenterology & Hepatol- Mombelli, B., & Gismondo, M. (2000). The use of probi-
ogy, 15, 489–493. otics in medical practice. International Journal of Anti-
Goossens, D., Jonkers, D., Stobberingh, E., van den Bogaard, microbial Agents, 16, 531–536.
A., Russel, M., & Stockbrugger, R. (2003). Probiotics in Parlak, E., Dagli, U., Alkim, C., Disibeyaz, S., Tunc, B.,
gastroenterology: Indications and future perspectives. Ulker, A., & Sahin, B. (2003). Pattern of gastrointestinal
Scandinavian Journal of Gastroenterology, 38(Suppl. 239), and psychosomatic symptoms across the menstrual cycle
15–23. in women with inflammatory bowel disease. Turkish Jour-
Guarner, F., & Malagelada, J.-R. (2003). Gut flora in health nal of Gastroenterology, 14, 250–256.
and disease. Lancet, 360, 512–519. Payne, C., Fass, R., Bernstein, H., Giron, J., Bernstein, C.,
Guyatt, G., Mitchell, A., Irvine, E., Singer, J., Williams, N., Dvorak, K., & Garewal, H. (2006). Pathogenesis of diar-
Goodacre, R., & Tompkins, C. (1989). A new measure of rhea in the adult: diagnostic challenges and life-threatening
health status for clinical trials in inflammatory bowel dis- conditions. Journal of Gastroenterology & Hepatology,
ease. Gastroenterology, 96, 804–810.
18, 1047–1051.
Heitkemper, M., Levy, R., Jarrett, M., & Bond, E. (1995),
Pearson, C. (2004). Inflammatory bowel disease. Nursing
Interventions for irritable bowel syndrome: A nursing
Times, 100, 86–90.
model. Gastroenterology Nursing, 18, 224–230.
Rayhorn, N. (2001). Treatment of inflammatory bowel dis-
Heitkemper, M., & Shaver, J. (1989). Nursing research
ease in the adolescent. Journal of Infusion Nursing, 24,
opportunities in enteral nutrition. Nursing Clinics of
255–262.
North America, 24, 415–425.
Reid, G., & Hammond, J. (2005). Probiotics. Some evidence
Hanauer, S. (2006). Inflammatory bowel disease: Epidemiol-
of their effectiveness. Canadian Family Physician, 51,
ogy, pathogenesis, and therapeutic opportunities. Inflam-
1487–1493.
matory Bowel Disease, 12(Suppl. 1), S3–S9.
Kane, S., Sable, K., & Hanauer, S. (1998). The menstrual Rioux, K., Madsen, K., & Fedorak, R. (2005). The role of
cycle and its effect on inflammatory bowel disease and enteric microflora in inflammatory bowel diseases: Human
irritable bowel syndrome: A prevalence study. American and animal studies with probiotics and prebiotics. Gastro-
Journal of Gastroenterology, 93, 1867–1872. enterology Clinics of North America, 34, 465–482.
Kroser, J., & Metz, D. (1996). Evaluation of the adult patient Sandle, G. (2005). Pathogenesis of diarrhea in ulcerative coli-
with diarrhea. Primary Care: Clinics in Office Practice, tis. New views on an old problem. Journal of Clinical
23, 629–647. Gastroenterology, 39(Suppl. 2), S49–S52.
Limdi, J., O’Neill, C., & McLaughlin, J. (2006). Do probi- Santosa, S., Farnworth, E., & Jones, P. (2006). Probiotics
otics have a therapeutic role in gastroenterology? World and their potential health claims. Nutrition Reviews, 64,
Journal of Gastroenterology, 12, 5447–5457. 265–274.
Listrom, C., & Holt, K. (2004). Inflammatory bowel disease. Sartor, R. (2003). Targeting enteric bacteria in treatment of
Emergency Medicine, 36(8), 24–28. inflammatory bowel diseases: Why, how, and when. Cur-
Macfarlane, S., Macfarlane, G., & Cummings, J. (2006). rent Opinion in Gastroenterology, 19, 358–365.
Review article: Prebiotics in the gastrointestinal tract. Ali- Sellin, J. (2001). The pathophysiology of diarrhea. Clinical
mentary Pharmacology & Therapeutics, 24, 701–714. Transplantation, 15(Suppl. 4), 2–10.
Macpherson, A., Khoo, U., Forgacs, I, Philpott-Howard, J., Vernia, P., Gnaedinger, A., Hauck, W., & Breuer, R. (1988).
& Bjarnason, I. (1996). Mucosal antibodies in inflamma- Organic anions and the diarrhea of inflammatory bowel
tory bowel disease are directed against intestinal bacteria. disease. Digestive Diseases & Sciences, 33, 1353–1358.
Gut, 38, 365–375. Walker, W., Goulet, O., Morelli, L., & Antoine, J.-M. (2006).
Marteau, P., Seksik, P., & Jian, R. (2002). Probiotics and Progress in the science of probiotics: From cellular micro-
intestinal health effects: a clinical perspective. British Jour- biology and applied immunology to clinical nutrition.
nal of Nutrition, 88(Suppl. 1), S51–S57. European Journal of Nutrition, 45, 1–18.

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