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8/13/2019 Diseases of the Lower Gastrointestinal Tract
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Winda, Agustus 2012
DISEASES OF THE LOWER
GASTROINTESTINAL TRACT
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Diarrhea
Definition
Diarrhea is defined as an increase in frequency of bowel movements
and/or an increase in water content of stools that affects either theconsistency or the volume of fecal output.
Other definitions describe abnormality in stool production as >200 g/day for
adults and >20 g/kg for children. (Donowitz,Kokke and Saidi 1995)
Etiology
Diarrhea can be classified in several different ways.
Diarrhea acute or chronic.
Diarrhea can also be classified as either osmotic or secretory.
Acute diarrhea is short-term (less than two weeks), whereas diarrhea lasting
longer than four weeks is considered chronic.Diarrhea can be associated with a number of health concerns, such as
electrolyte imbalances, malabsorption, dehydration, and malnutrition.
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Diarrhea Osmotic
Osmolality is a measurement of concentration of particles in solution.
Normal osmolality of the gastrointestinal tract is approximately 300
mOsm/L. When there is an increase in osmotically active particles in the
intestine, the body responds by pulling water into the lumen in an attempt
to normalize osmolality. When this occurs, increased water reflux results
in what we refer to as osmotic diarrhea.
Osmotic diarrhea can be caused by maldigestion of nutrients, excessive
sorbitol or fructose intake, enteral feeding, and some laxatives.
In general, when the causative agent is removed, osmotic diarrhea will
cease.
Secretory diarrhea
also results from excessive fluid and electrolyte secretions into the intestine.
The difference here is that the underlying disease is what causesexcessive secretions, not the hyperosmolality.
Furthermore, secretory diarrhea does not resolve when the patient is made
NPO.
Bacterial infections often produce enterotoxins that result in this type of
diarrhea. Protozoa, viruses, and other infections can also causesecretor diarrhea.
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Travelers diarrhea is a common health problem affecting those who travel
to other countries. The major infectious agents resulting in travelers
diarrhea are enterotoxigenic Escherichia coli, enteroaggregative E. coli,
and Shigella spp, Salmonella, Campylobacter, Yersinia, Aeromonas, and
Plesiomonas spp.
Other factors that could potentially cause secretory diarrhea include
medications, hormone-producing tumors, prostaglandins, and excessive
amounts of bile acids or unabsorbed fatty acids in the colon.
Antibiotics and other medications may cause diarrhea as a side effect.These medications generally cause diarrhea either by increasing GI
motility or by altering the normal flora of the colon.
Many gastrointestinal diseases have diarrhea as a common symptom.
Examples : Crohns disease, ulcerative colitis, and celiac disease.
These diagnoses can also result in malabsorption of lipids and othernutrients, which further contributes to the diarrhea.
AIDS enteropathy with HIV infection, thyroid disfunction, and some
malignancies.
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Clinical Manifestations
Diarrhea presents as a change from the normal bowel function. This is
generally a watery stool that is increased in frequency.
Other characteristics of stool output will vary depending on the etiology ofthe diarrhea.
For example, foul-smeeling, frothy stools are associated with steatorrhea,
which means fat in the stool. This would occur with fat malabsorption.
Frank blood is bright red blood on the surface of the stool, and represents
contamination with blood from the rectum or anus.
Occult blood is detected by testing the stool and usually results from
bleeding in the lower gastrointestinal tract.
Melena is a dark stool and is caused by contamination with blood within
the upper GI tract. Hemoglobin from blood contributes to the dark color.
Mucus in the stool may also be indicative of secretory diarrhea. High
amounts of electrolytes are also consistent with secretory diarrhea.
The presence of leukocytes in the stool indicates an inflammatory process
such as inflammatory bowel disease
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Other clinical manifestations that may occur with diarrhea are abdominal
pain and cramping.
When defecation relieves cramping, diarrhea is generally from the distal
colon. If abdominal pain and cramping continue after defecation, the originis generally from the small bowel.
Other symptoms such as dehydration, weight loss, and electrolyte and acid-
base imbalances are dependent on volumes of stool lost and represent
one of the most serious consequences of diarrhea.
DiagnosisConsiderations that will direct diagnostic procedures are the age of the
patient, hydration status, the presence of blood in the stool, and whether
the patient is immunocompromised. Other important symptoms to note
are any recurring characteristics of diarrheal episodes, including time of
day or any relationship to food intake.Treatment
Restoring normal fluid, electrolyte, and acid-base balance is crucial. This is
accomplished through either intravenous therapy or the use of rehydration
solutions (Bergogne-Berezin 2000;Guerrant et.al 2001)
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Prevention of diarrhea should be a major focus .
Recommendations for the prevention of diarrhea worldwide include
strategies such as ( Bateman and Mc Gahey 2001): Improving access to clean water and safe sanitation
Promoting hygiene education
Exclusive breast-feeding
Improving weaning practices Immunizing all children, especially against measles
Using latrines
Keeping food and water clean
Washing hands with soap (the babys as well) before touching food
Sanitary disposal of stools
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Nutrition Therapy
Nutritional implications of diarrhea are initially dependent on the volume of
gastrointestinal losses and then on the length of the disease course.
Large-volume losses can quickly lead to dehydration, and electrolyte andacid-base imbalances. Hyponatremia and hypokalemia are both
common with diarrhea.
Metabolic acidosis may occur due to excessive loss of bicarbonate ions in
stool output.
Infants and elderly are at particular risk because their systems are muchmore sensitive to rapid shifts in both fluids and electrolytes. Maintaining
homeostasis is much more difficult for both of these populations, in part
due to the inability of their renal systems to act quickly enough for
adequate compensation.
Chronic diarrhea can cause fluid and electrolyte complications and canresult in malnutrition and specific nutrient deficiencies.
Diarrhea can affect appetite and thus impair adequate ingestion.
Diarrhea also results in decreased transit time, which interferes with the
ability of the gastrointestinal tract to perform adequate digestion and
absorption.
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Nutrition Interventions
Current practice recognizes the importance of stimulating the
gastrointestinal tract by feeding the patient. This speeds recovery of
damaged cells. In addition, clear liquids are typically high in simplecarbohydrates, which increase osmolality of the gastrointestinal tract.
This actually can make diarrhea worse due to hyperosmolality.
Oral rehydration solutions are designed to both restore fluid and electrolyte
balance and enhance absorption in the intestinal tract.
Infant with diare are of special concern. Their risk of dehydration and
electrolyte imbalances are high.
It is recommended that infants who breast feed continue to do so. Formula-
fed infants can be fed half- strength formula.
Banana flakes, apple powder, or pectin sources can be added to formula in
an attempt to thicken the stool. If the infant has begun solid foods,
strained bananas, apple sauce, and rice cereal are the best initial food
choices.
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In adult and older children, introducing solid foods should begin with a low
residu diet. Beginning with starches, and then slowly adding foods as
they are tolerated. Use of products with pectin such banana flakes canalso assist increasing the consistency of the stool.
use of probiotics and prebiotics.(Barbut and Meynard 2002; broussard and
Surawics 2004; O Sullivan 2005).These foods and supplements
support growth of healthy flora and/or repopulate the intestinal tract with
healthy bacteriaProbiotics and prebiotics will increase the amount of short-chain fatty acids
(SCFA) produced. Recent research indicates SCFA promote water and
electrolyte absorption in the colon, which reduces the incidence of
diarrhea ( Cummings and Mc Farlane 2002)may play a significant
role in reducing diarrhea associated with enteral feeding (delzenne,cherbut, and nevrinck 2003).
Other research has studied the effect of using probiotics and prebiotics as
part of the treatment for radiation induced diarrhea, diarrhea secondary
to rotavirus, and travelers diarrhea ( De Ross and Katan 2000; Unger et
al 2001; Urbancsek et al 2001) .
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Constipation
The Rome Consensus Criteria define constipation as a condition where at
least two of the following symptoms have occurred in the previous year
for at least 12 nonconsecutive weeks (Locke,Pemberton,and Philips2000;Thompson et.al 2000)
Straining with > of defecations
Hard stools in > defecations
Sensation of incomplete evacuation or anorectal obstruction in >
defecations
Manual maneuvers to facilitate > defecations
Etiology
Constipation can be due to rectal outlet obstruction or other sources of
obstruction such as fecal impaction, adhesions, or even the presence ofa tumor.
Pelvic floor dysfunction ( university of southern california 2003) results not
only slowed colonic transit but also storage of fecal contents in the
rectum for long periods of time.
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Constipation can be secondary to other medical conditions, including
scleroderma, amyloidosis, and neurological diseases such as multiple
sclerosis (MS) or Parkinsons disease.
Constipation can be a side effect of many different classes of medications.
These include very common prescription drugs such as calcium channelblockers, antidepressants such as amitriptyline, pain medications such as
morphine, diuretics, and antihistamines.
Medications that often cause constipation include iron, calcium, and other
vitamin supplements, and, for some individuals, even nonsteroidal anti-
inflammatory drugs
Clinical Manifestations
Symptoms of constipation include decreased frequency of bowel
movements. Bowel movements are often hard and pellet like. Abdominal
pain, bloating, and gas are common accompanying symptoms.
Treatment
Treatment of the underlying etiology will direct medical care for constipation.
Common interventions include bowel retraining and use of enemas or
cathartic and laxative medications. Other medications involve bulking
agents and stool softeners. (Locke,Pemberton,and Philips 2000)
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Nutrition Therapy
Research regarding nutrition and constipation has concentrated on the role
of adequate fiber and fluid intake.
The National Health and Nutrition Examination Survey (NHANES)indicated most Americans consume an average 14 to 15 grams of fiber
each day (Alaimo et al 1998)
When compared to recommendations, most individuals are consuming only
40% to 50% of the recommended intake.
Adequate intake of whole grains, fruits, and vegetables has been one of theprimary focuses of both the Dietary Guidelines for Americans and the
Nutrition Recommendations for Canadians.(Departement of Health and
Human Services 2005; Health and Welfare Canada 2005).
Inadequate fiber intake has long been associated with many
gastrointestinal conditions, including constipation, diverticular disease,and haemorrhoids.
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Nutrition Interventions
Twenty to thirty-five grams of dietary fiber are recommended
For adults each day. Based on caloric intake, this would be approximately
10 to 13 g of dietary fiber per 1000 kcal.
For children over the age of 2 years, fiber intake is recommended to be the
amount equal to their age plus 5 grams/day (American Dietetic Association2000,2002).
More recent recommendation suggest adults under the age of 50 should
consume 38 grams of fiber per day(Food and Nutrition Board and Institute of
Medicine 2002).
Foods have a mixture of different kinds of fiber, but in general, the
recommendations are for a 3:1 ratio of insoluble to soluble fiber.
Adequate water intake, minimum of 2000 mL/day (approximately 8
cups/day).Use of probiotic and prebiotics has also been recommended for treatment
of constipation. For example, consumption of fructooligosaccharides has
been shown to soften feces and to assist in relieving constipation(Broussard and Surawicz 2004; Brown and Valiere 2004; Garleb et.al 2002; OSullivan
2005).
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Malabsorption
Definition
Malabsorption is a general term referring to malabsorption of fat,
carbohydrate, or protein as a result of maldigestion or from damage tothe anatomy and physiology of the small intestine.
Etiology
Damage to the anatomy and physiology of the small intestine due to
disease is the most common cause of malabsorption.
Conditions such as celiac disease, Crohns disease, and even protein-calorie malnutrition result in decreased villous height, decreased enzyme
production, and subsequen malabsorption and/or maldigestion.
Dysfunction of the accessory organs of digestion (liver, pancreas, and
gallbladder) may also serve as the origin of the maldigestion.
Decreased transit time, as seen in diarrhea or from surgical changes in the
anatomy, also can result in either maldigestion or malabsorption.
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Pathophysiology
Nutrient digestion and absorption are dependent on normal anatomy;
normal physiology with adequate production of enzymes, hormones, and
other secretions such as bile; and appropriate motility.FAT MALABSORPTION
The digestion and absorption process for lipid or fat is the most complex,
and therefore the easiest to disrupt.
Fat malabsorption is called steatorrhealiterally meaning fat in the stool.
Digestion and absorption of fat requires adequate colipase and pancreatic
lipase, adequate emulsifierbilefrom the liver and gallbladder, and
adequate secretion through the common bile duct and pancreatic ducts.
Motility needs to be normal due to the lengthy process lipid has to undergo
from micelle to chylomicron for absorption. When any of these processes
is disrupted, fat remains in the stool and travels undigested and
unabsorbed to the large intestine.
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Fat-soluble vitamins are malabsorbed as well. An additional concern for fatmalabsorption is the potential presence of excess oxalate.
Excessive amounts of oxalate have been linked to development of urothiasis orkidney stones.
Hyperoxaluria (excessive oxalate in the urine) is responsible for about 30% ofkidney stones and is considered to be the most common cause.
Persons with fat malabsorption will experience abdominal pain, cramping, anddiarrhea. Stools produced will be frothy, foul-smelling, and greasy inappearance.
CARBOHYDRATE MALABSORPTION
The most common example of carbohydrate malabsorption is lactosemalabsorption,commonly referred to as lactose intolerance.
When there is inadequate lactase available for digestion, or if anatomy ormotility does not allow adequate exposure to lactase, lactose will travel to thelarge intestine undigested and unabsorbed.
Bacteria in the large intestine will cause the lactose to undergo fermentation,which creates increased gas and abdominal cramping. Undigested lactose
also pulls additional water into the large intestine, contributing to abdominalcramping and resulting diarrhea.
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PROTEIN MALABSORPTION
Protein malabsorption is most commonly referred to as protein-
losingenteropathy.
Excessive protein is lost in the stool, and the patient will experiencereduced serum levels of proteins and an increasing amount of peripheral
edema due to the reduced oncotic pressure.
Treatment
Appropriate treatment for malabsorption will depend on the nutrient that is
malabsorbed and the underlying disease causing malabsorption.
NUTRITION THERAPY FOR FAT MALABSORPTION
Restriction of fat to 25 to 50 grams per day is a standard first step in
reducing the symptoms of fat malabsorption.
Medium-chain triglyceride (MCT) supplements can be used to increase
caloric intake.
MCT is absorbed directly into the circulatory system from the small intestine
and does not require the normal lipid digestion and absorption processes
that long-chain fatty acids require.
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NUTRITION THERAPY FOR LACTOSE MALABSORPTION
Lactose is the simple carbohydrate found in milk and dairy products.
Lactose is also found as an ingredient in many other food products inwhich it is often used as a filler.
Milk provides approximately 11 grams of lactose per cup.
Other dairy products have varying amounts, with ice cream havingapproximately 9 grams per cup and cheese having 1 to 2 grams perounce.
Restriction of all milk and dairy products is the major step to treat lactose
malabsorption - individuals do vary on amounts of lactose they cantolerate.
Celiac Disease
Definition
Celiac disease (CD) , previously referred to as gluten- sensitiveenteropathy, gluten intolerance, or non-tropical sprue, is a complexdisease whose etiology originates from both genetic and autoimmunefactors.
In this disease, exposure gluten results in damage to the intestinal mucosa.
Other diseases or conditions associated with CD are type 1 diabetesmellitus and thyroid dysfunction as well as dermatitis and muscle and
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Etiology
The damage to the intestinal mucosa observed in CD, occurs when the
small intestine is exposed to the prolamin fraction-gliadin and other
protein components of gluten. Gluten is found in wheat, rye, malt, barley,
and, in smaller amounts, in oats.
Pathophysiology
When the small intestine is exposed to certain sequences of amino acids
found in the prolamin fraction of wheat (gliadin), rye (secalin), and barley
(hordein), there appears to be both a toxic and inflammatoryresponse.(Thompson 2003).
This response damages villi; height is reduced, and they are flattened in
appearance. Lack of surface area and reduction of enzyme production
cause both malabsorption and maldigestion. Celiac disease is often
accompanied by other systemic autoimmune disorders, including type 1diabetes mellitus, thyroid disease, systemic lupus erythematous, primary
biliary cirrhosis, rheumatoid arthritis, Sjgrens syndrome.
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Clinical Manifestations
Classic clinical symptoms of CD include diarrhea, abdominal pain and
cramping, bloating, and gas production. Other symptoms that can occur
in the absence of GI problems include bone and joint pain, muscle
cramping, fatigue, peripheral neuropathy, seizures, skin rash, and mouth
ulcerations.
Prognosis and Treatment
The only current treatment for CD is nutrition therapy consisting of a gluten-
free diet.After avoidance of all gluten, villous height generally returns to normal. As
the anatomy returns to normal, maldigestion and malabsorption resolve.
The most common reasons for nonresponsive CD were unknown gluten
contamination and the presence of coexisting diseases such as
pancreatic insufficiency, irritable bowel syndrome as well as the presenceof malignancies.
Nutrition Therapy
Nutritional consequences of CD are dependent on the extent of
malabsorption present. Severe malabsorption will results in significant
weight loss, vitami and mineral deficiencies, and, ultimately, protein-
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Nutrition therapy will be consistent with the level of damage to the intestinal
mucosa and the degree of malabsorption.
Most often, the individual diagnosed with CD will need to initially begin onnutrition therapy using a low- residu, low- fat, lactose free, gluten- free
diet.
A low- fat diet of approximtely 45 to 50 grams/day can assist in minimizing
symtoms of steatorrhea. Lactase deficiency will be common in this
disorder due to damaged villi and enzyme secretion.As villi are regenerated and absorptive capability returns, these nutrients
(fiber, lactose and fat) can be added back to the diet slowly and usually
does not require a lifelong restriction.
On the other hand, gluten does require a lifelong restriction. The patient will
need to avoid all foods and other products that contain wheat, rye, barley,and malt. Restriction of oats is still controversial, but most recent
research has indicated individuals may tolerate oats, as long as the oats
are from a pure, uncontaminated source.( Thompson 2003)
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The major controversy regarding use of oats is contamination within oat
products by wheat, barley, or rye. Thompson recommended that oats
should be limited to cup per day, and that step should be taken reduce
the chance of contamination. This would include, in part, contacting
manufacturers regarding the methods of production and avoiding
products sold in bulk bis (Thompson 2003).
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Irritable Bowel Syndrome
Definition
Throughout the last century, varying names such as spastic colon, irritable
colon syndrome, and neurogenic mucous colitis have been given to thissyndrome. Currently, irritable bowel syndrome (IBS) is defined using the
rome II criteria, that for at least 12 weeks (they need not be consecutive
weeks) and in the past 12 months, the individual has experienced
abdominal pain that has at least two of the following three criteria ;
(1) pain relieved defecation,(2) onset associated with change in frequency of stool
(3) onset associated with change in form of stool.
Subtypes of IBS include conditions that primarily involve diarrhea,
conditions that primarily involve constipation alternate
(Adeniji,Barnett and DiPalma 2004;Thompson et.al 2000; Holten,Wetherington, and Bankston
2003).
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Certain red-flag symtomps should be eliminated prior to diagnosis of IBS.
These symptoms may actually signal other conditions. They include age
at onset over 50, progresively severe symptoms, symptoms at night that
wake the patient, persistent diarrhea, bleeding, anemia, weight loss,
vomiting, fever, or a family history of colon cancer.
Etiology
IBS historically has been designated as a functional disorder.
It is not a psychosomatic disorder, although its symptoms can be
aggravated by stress, anxiety, depression, or emotional trauma.The spesific cause of IBS is unknown , but etiological factors may include
increased levels serotonin, an elevated inflammatory response to
infection, and an increased sensitivity of the enteric nervous system that
cause abnormal motility and pain.
There are often conditions associated with IBS, which include anxiety,panic, mood, and somatization disorders.
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Pathophysiology
The pathophysiology of IBS is complex and, as previously stated, not
completely understood.
In IBS, abnormal motility is considered to be one of the major factorsinvolved in symptoms of abdominal pain and altered bowel habits (lyfordet.al 2002).
Individuals with IBS have been found to have an increased sensitivity to
stimulation of the gastrointestinal tract. This means the same stimuli in
normal patients do not result in symptoms that patients with IBS
experience: abdominal pain, urgency, diarrhea, or constipation. When
IBS patients were evaluated using balloon-distention, they experienced
abdominal pain and gastrointestinal symptoms at much lower levels of
distention than controls
(American College of Gastroenterology Functional Gastrointestinal Disorders Task Force
2002; Cash 2004).
Other studies have observed development of IBS after infectious enteritis.
Specific organisms that have been documented include Blastocystis
hominis, Campylobacter, Salmonella, and parasites such as Trichinella
spiralis.
( Gomez-Escuder2003)
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Clinical Manifestations
Abdominal pain, alteration in bowel habits or motility, gas, and flatulence as
well as some upper GI symptoms (reflux and noncardiac chest pain) aremajor symptoms for IBS. Abdominal pain can be acute and relieved by
defecation. At the same time, some patients with IBS experience
constant, chronic abdominal pain.
Alterations in bowel habits are seen in both major types of IBS
constipation and diarrhea. In some patients, both constipation anddiarrhea are experienced.
In people with IBS, there appears to be an increased sensitivity to certain
foods such as lactose, wheat, or high- fiber foods, which results in an
exaggreated response to these nutrients.
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Treatment
For those patients with IBS-D, antidiarrheal agents can be used. These
medications assist by decreasing motility and increasing consistency of
the stool.
Other treatment for IBS include behavioral therapies (hypnosis, relaxation
techniques, guided imagery), antibiotics, probiotics and nutrition therapy(Beradi 2004;Crowell 2004) (American Dietetic Association 1996, 1997).
Nutrition Therapy
Symptoms of IBS can lead to changes in oral intake that lead to nutrient
deficiencies, potential underweight, and malnutrition.
Once a baseline nutritional history has been established, the RD and patient
can begin to identify any needed changes in diet. Overall nutritional
adequacy should be addressed first. Many patients with IBS tend to eaterratically due to their gastrointestinal symptoms, and often eating is
associated with a high level of anxiety and stress. Establishing a regular
eating pattern that does not exacerbate symptoms is a crucial initial step.
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The next goal is to focus on increasing fiber intke to approximately 25
grams/day. Higher fiber intakes may not be initially tolerated
adequate fluid is also necessary as fiber intake is increased.(Nobak et.al 2000).
Both prebiotics and probiotics have received attention for their potential use
in IBS. adding these foods and supplements may be beneficial in the
overall MNT plan
Due to problems with gas and flatulence, providing recommendations to
relieve these symptoms will also be beneficial.Avoiding foods that produce gas and taking steps to decrease swallowed air
will decrease gas production
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Inflammatory Bowel Disease
Definition
Inflammatory bowel disease (IBD) is characterized as an autoimmune,
chronic inflammatory condition of the gastrointestinal tract. IBD isactually the general term for either of two diagnoses: ulcerative colitis
(UC) and Crohns disease.
These diagnoses are very similar but have very distinct differences.
Etiology
The complete etiology for both Crohns disease and UC is unknown at thistime. it is understood that multiple factors play a role in these
conditions.(Thompson Chagoyan 2005).
These may include environmental factors such as smoking, infectious
agents, intestinal flora, and physiological changes in the small intestine
from which an abnormal inflammatory response is triggered. There is astrong genetic association for IBD. There is a positive family history in
approximately 5% to 15% of patients with IBD. In identical twins, the
incidence of IBD is 44% versus only 3.8% in fraternal twins.
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Clinical Manifestations
Patients with UC present with signs and symptoms including abdominal
pain, bloody diarrhea, and tenesmus (urgency for defecation). Patients
with severe disease often are febrile, are tachycardic, and have diarrhea
that contains pus and mucus. Disease activity is rated using the Truelove
and Witts Criteria (Truelove and witts 1995).
Treatment
Treatments for both UC and Crohns disease include antibiotics,
immunosuppressive medications, immunomodulators, and biologictherapies as well as surgical intervention.(Hanuver and Sandborn 2001)
Medical treatment for ulcerative colitis historically has used combinations of
both antibacterial coverage with sulfapyridine and anti-inflammatory 5
aminosalicylic acid
Immunomodulators work to inhibit inflammatory cell proliferation byinterrupting cellular RNA and by inhibiting the overall immune response.
These medications include azathioprine (AZA) and 6-mercaptopurine (6-
MP).
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Corticosteroids work to inhibit the overall inflammatory response and are
commonly used to treat UC. Antibiotics are used in UC only when there is
an acute infection.
Surgical intervention is required in both UC and Crohns disease in over
60% of patients. The most common procedure in UC is a total colectomy,
and in Crohns disease, the ileostomy. Surgery is performed due to
nonresponsive disease and due to acute complications such as
perforation, obstruction, or abscess. These surgical procedures will be
described in greater detail later in this chapter in the section Common
Surgical Interventions for the Lower GI Tract.
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Nutrition Therapy
Nutrition implications. Patients with IBD are at significant nutritional risk. It is
estimated that from 60% to 75% of patients with Crohns disease
experienc malnutrition. (Krok and Lichenstein 2003).Both Crohns disease and UC have dramatic effects on nutritional status
and often require nutritional support during periods of
exacerbation.These diagnoses affect normal digestion and absorption;
may increase caloric, protein, and micronutrient requirements; can result
in protein-energy malnutrition; and additionally may require nutritiontherapy to minimize symptoms. Nutrition therapy may also be implicated
in treatment of the disease process.
When infection is present or when the patient is febrile, energy needs are
increased.
Protein needs are increased, in some cases up to 150% of normalrequirements.This is due, in part, to increased protein losses in
inflammatory exudate.
Micronutrients, especially iron, zinc, magnesium, and electrolytes, are at
risk for deficiencies due to their losses in blood and diarrhea.
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IBD is common in both children and young adults. Meeting nutritional
needs of the growing child or adolescent poses its own challenge. It is
crucial for nutrition therapy to be designed to ensure adequate nutrients
to support growth and development.
Since the mainstay of treatment for IBD involves multiple medications and
often surgery, these nutritional risks compound those of the disease
process.
use of corticosteroids can result in hyperglycemia, nitrogen wasting, and
increased risk of osteoporosis.
use of sulfasalazine, which interferes with folate metabolism .
Surgery increases calorie and protein requirements and additional nutrients
are needed to support wound healing.
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NUTRITION THERAPY DURING EXACERBATION OF DISEASE
During acute exacerbations of both UC and Crohns disease, the extent of
diarrhe output, and bleeding will the level of direct the level of nutrition
intervention. For fulminant disease, parenteral nutrition support or enteral
nutrition with a chemically defined formula will probably be necessary.
Most research indicates parenteral nutrition is not necessarily
advantageous, and the gastrointestinal tract can benefit from exposure to
enteral nutrition (Dominioni 2003).
Glutamine and arginine supplementation may assist with modifyinginflammatory response in the disease process (Akisu et.al 2003; Kanauchi et al2003; Panigrahi et al 1997; Van der Hulst et al 1993).
Energy needs for adults can be estimated using the Harris- Benedict or Miffl
in-St. Jeor ,equation with appropriate stress factor (1.31.5). The amount
of prior weight loss and the presence of infection will support the need for
higher energy provision. To meet growth needs of infants, children, and
adolescents, specific attention to their unique requirements is important.
As much as 120 kcal/kg for infants and 80 kcal/kg for adolescents may
be required (see Chapter 5). If available, indirect calorimetry provides the
most reliable indicator of energy needs in the hospitalized patient.
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Energy needs for adults can be estimated using the Harris- Benedict or
Miffl in-St. Jeor equation with appropriate stress factor (1.31.5).
The amount of prior weight loss and the presence of infection will support
the need for higher energy provision.
To meet growth needs of infants, children, and adolescents, specific
attention to their unique requirements is important.
As much as 120 kcal/kg for infants and 80 kcal/kg for adolescents may be
required If available, indirect calorimetry provides the most reliableindicator of energy needs in the hospitalized patient.
Estimation of protein requirements will be based on the presence of any
lean body mass wasting and biochemical parameters measuring protein
status such as prealbumin and albumin.
Protein needs may be as high as 1.5 to 1.75 g protein/kg for adults and 2.0to 2.5 g/kg for infants, children, and adolescents.
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If oral intake can be initiated, a low-residue, lactose-free diet with small,
frequent meals is best tolerated.
If steatorrhea is present, then fat should be reduced with added MCT or anMCT-containing supplement to assist with meeting energy requirements.
As the patient responds to medical therapy, adding small amounts of fiber
and then lactose as the patient can tolerate will advance the diet.
Other foods that may need to be initially restricted may be gas-producing
foods, spicy or fried foods, caffeinated beverages, or any other food theindividual patient identifies as problematic.
The addition and advancement of an oral diet will need to be highly
individualized.
Some research has indicated that there is no improvement in complication
rates when comparing a low- residue diet to a reguler diet in patients withCrohns (Levenstein et.al 1985).
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All patients should receive a multivitamin that meets the RDA or AI for all
nutrients. Patients with IBD are at higher risk for deficiencies of vitamin
B12 and iron. In a normal small intestine, the ileum has specific receptorsites that allow for B12 absorption. Therefore, disease affecting the ileum
specifically can potentially result in B12 deficiency. Supplementation of
B12 to prevent pernicious anemia can be accomplished using nasal gel
or oral tablets, or by intramuscular injection.( little 1999; Eiden 2003).
Micronutrient requirements are additionally increased during exacerbationsof disease.
It is recommended that additional supplementation should include zinc (12
to 15 mg/liter of stool output); calcium (10 to 25 mEq/day); magnesium
(15 to 30 mEq/day); and copper (0.5 to 1.5 mg/day).( Eiden 2003;Jeejeehboy 2002)
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Research has shown patients with Crohns disease have lower serum
levels of antioxidants (vitamin E, vitamin C, and betacarotene). (Krok
and lichenstein 2003) . It is thought that this might contribute to higher
levels of oxidative stress in this disease. Higher levels of antioxidants
may be warranted, but specific levels have not been established at this
time; nor is it clear that supplement forms produce the same effect as
foods.
The most convincing evidence for the relationship between antioxidants
and disease prevention has been in epidemiologic studies where strong
associations have been demonstrated between dietary sources of fruits
and vegetables and disease risk (Mc Dermott 2000).
Patients with IBD may avoid fruits and vegetables due to their disease
symptoms and perceived intolerance to these foods.
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NUTRITION THERAPY FOR REHABILITATION DURING PERIODS OF
REMISSION
Maximizing energy and protein intake to facilitate rehabilitation should be the
primary goal. Weight gain within a normal healthy range combined with
physical activity will ensure rebuilding of protein stores and muscle mass.
Depending on the extent of disease and the response to treatment, specific
dietary modifications will need to be individualized. It is always a goal to
normalize dietary patterns and encourage a variety of all foods as the patient
is able to tolerate them.Consumption of foods high in antioxidants (for example, carotenoids, vitamin E,
vitamin C, and selenium) and omega-3 fatty acids has been associated with
protection against inflammation.
These would include fruits, vegetables, vegetable oils, nuts, and fishes such as
tuna and salmon. Although some reports have indicated that glutamine,short-chain fatty acids, antioxidants, and immunonutrition with omega-3 fatty
acids are an important therapeutic alternative in the management of
inflammatory bowel diseases, the reported beneficial effects have yet to be
translated into clinical practice.
The real efficacy of these nutrients still needs further evaluation throughprospective and randomized trials (Campos et al 2003)
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Foods high in oxalate may increase risk for urolithiasis or kidney stones,
which can occur in IBD. These foods include, for example, cocoa, tea,
wheat germ, strawberries, nuts, spinach, beets and baked beans, peanut
butter, tofu, and high doses of vitamin C supplements (>2 g/day).
As has been previously discussed in this chapter, use of probiotics and
prebiotics enhances the normal flora of the GI tract.
Several recent studies have indicated consumption of foods and
supplements with probiotics and prebiotics has been associated with
decreased symptoms for patients with IBD (Galves,RodriguezCabeas,and Zarzuelo 2005; Gassull 2005; Guarner 2005; Shanahan 2004; Schultz and
Sartor 2000).
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Diverticulosis/Diverticulitis
Definition
Diverticulosis is defined as the abnormal presence of outpockets or
pouches on the surface of the small intestine or colon. Meckelsdiverticulum is a type of diverticulosis present at birth. Meckels
diverticula are usually found near the ileocecal valve and may cause
gastrointestinal bleeding or obstruction for the newborn.
Etiology
Evidence suggest development of diverticulosis is related to low fiberintake, history of constipation, and the resulting long-term increased
colonic pressure. Recently it has been proposed that low fiber intake also
contributes to the incidence od diverticulosis ( Floch and Bina 2004; Ye,Losada and West 2005).
Factors that may increase risk for development of diverticulosis includeobesity, decreased physical activity, steroids, alcohol and caffeine intake,
and cigarette smoking.( Aldoori et al 1995,1998).
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Pathophysiology
Diverticula do occur in the small intestine but are most common in the colon.
Factors that affect integrity of the mucosa of the colon appear to
contribute to development of the diverticula.The aging process and differences within parts of the colon may account for
the pattern of development that has been observed. Specific
pathophysiology indicates that within two or more of the muscular bands
(taeniae coli) contract at the same time. This hinders motility of the colon,
and thus its ability to move waste products. Fecal matter becomestrapped and exerts excessive pressure against the wall of the colon. This
pressure causes development of small pouches on the wall of the colon,
which are referred to as diverticula.(Beitz 2004; West and Losada 2004)
Constipation increases colonic pressure through the excessive straining
involved in bowel movements. This further increases the probability for
development of diverticula.(Stollman and Raskin 1999)
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T t t
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Treatment
Treatment for diverticulosis involves only nutrition therapy, with a specific
focus on fiber intake, and use of probiotic and prebiotic supplementation.
Treatment for acute diverticulitis begins with making the patient NPO with
complete bowel rest until symptoms (bleeding and/or diarrhea) subside.
Antibiotics are used to treat any infection. The most common antibiotic
regimens involve treatment for Gram negative rods and anaerobes.(American Society of Surgeon Colon dan Rectal 2000;Stoolman and Raskin
1999).
For those patients with complications (such as abscess or sepsis), surgicalresections may be necessary.
Nutrition Therapy
Researchindicates that dietary habits may be strongly linked to the etiology
of diverticulosis. Nutrition therapy should then focus on those nutrition
interventions that could impact disease course.
The patient with diverticulosis is not at any more risk for malnutrition than
any other individual. The presence of diverticulitis with infection and
inflammation does impact nutritional requirements if this condition is
prolonged or if other complications, such as sepsis, occur.
Nutrition Intervention
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Nutrition Intervention
Nutrition therapy to treat and prevent diverticulosis will include a high-fiber
diet of 6 to 10 grams above and beyond the recommendations of 25 to 35
grams/day.It is common practice to avoid nuts, seeds, and hulls, which
are sharp enough, hard enough, or large enough to irritate or get caughtin diverticula. This will prevent opportunity for these foodstuffs to lodge in
diverticula and pottentially result in diverticullitis. Foods to omit include
caraway seeds, nuts, popcorn hulls, and sunflower, pumpkin, and
sesame seeds.A food with small seeds such as a tomato, squash,
cucumber, strawberry, or rapsberry is ussuallly tolerated.Many patients, especially the elderly, will need to use a fiber supplement if
they are unable to consume adequate fiber from foods.
The patient with acute diverticulitis will be progressed from bowel rest to
clear liquids. The patient can then move toward a low-residue diet until
inflammation and bleeding are no longer a risk.
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Nutr i tion Therapy for I leostomy and Colostom y
When a certain part of the intestinal tract is removed, normal physiology
and function of that portion is lost to the individual.
This loss of function will produce changes in motility, in absorption, and inhow waste products are handledall of which potentially can impact
nutritional status.
Resections of the terminal ileum and loss of the ileocecal valve tend to
result in significant fluid, electrolyte, vitamin, and mineral deficiencies.
The ileocecal valve controls the rate of movement from the small
intestine to the large; hence, when it is absent, motility is much faster,
interrupting normal absorption.
Nutrition Intervention
Goals for nutrition therapy include decrease risk of obstruction, maintainnormal fluid and electrolyte balance, reduce excessive fecal output and
minimize gas and flatulence (to reduce odor and inflation of the
appliance).(American dietetic association 2000).
After surgery, the patient will be transitioned to an oral diet.
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This begins with clear liquids and progresses as tolerated to a low-residue
diet with four to six small feedings each day.
Foods that may not be completely digested and that can cause stoma
obstruction should be avoided for the first 6 to 8 weeks after surgery.
These include tough fibrous meats; vegetables such as spinach, corn, and
peas; dried fruits such as raisins; fruit skins and seeds; and popcorn.
The patient will need to be instructed to eat slowly, chew thoroughly, and
drink adequate fluids. Generally, oral intake should resemble the regular
diet, meeting all nutritional needs by the eighth week postoperatively.
If the patient experiences excessive or watery fecal output, the amount of
insoluble fiber should be reduced while increasing the amount of soluble
fiber. Applesauce, bananas, tapioca, potatoes, oatmeal, oat bran, rice,
and pasta may help decrease diarrhea.
Use of yogurt, parsley, and buttermilk may decrease gas and odor.
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Recent research has focused on absorption of vitamin and minerals in the
diets for patients with colostomy. It was that most vitamins, minerals, and
phytochemicals appear to have adequate absorption in this population.(Chen et.al 2004; Faulks et.al 2004).
Livny and colleagues did find beta-carotene was best absorbed from cooked
carrots rather than raw carrots in these patients.( Livny 2003). However,
since most patients intake and tolerance varies widely, a general
multivitamin is recommended. Vitamin B12 supplementation may also be
required.
Short Bowel Syndrome
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Short Bowel Syndrome
Definition
Short bowel syndrome (SBS) (also known as short gut syndrome) results
from a large resection of the small intestine.
Spesific definitions vary, but Buchman (2004) describes the most important
concerns of this condition: patients who are the greatest nutritional and
dehydration risk generally have less than 115 cm of residual small
intestine in the absence of colon in continuity or less than 60 cm of
residual small intestine with colon in continuity (Buchman 2004).
Patient with less than 100 cm of residual jejenum often have a net secretory
response to food and may actually secrete more fluid than they ingest.
The American Gastroenterologi and Association states in its clinical
guidelines that Short bowel syndrome occur when, after surgery or
congenitally, a patient is left with less than 200 cm of functional small
intestine
Those patients who also experience resections of the large intestine will
have additional symptoms that contribute to complications of their SBS.
Etiology
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Etiology
Surgical resections of the small intestine and colon due to disease and
trauma can result in extensive loss of surface area of the small intestine
and colon. Without normal anatomy and physiology, malabsorption of
nutrients, fluids, and electrolytes will resultPathophysiology
Several factors will determine the prognosis of this condition: extent of
remaining small intestine, presence of the colon, presence of the
ileocecal valve, health of the remaining gastrointestinal tract, and any
comorbid conditions the individual may have. Though each case ishighly individualized, most research agrees that a resection of more than
70% of the GI tract will result in severe nutritional and metabolic
complications. (American Gastroenterological Association 2003; Buchman2004; Lykins and Stockwell 1998).
The postoperative period for SBS generally follows three distinct phases.The first period ranges anywhere from 7 to 10 days and is characterized
by extensive fluid and electrolyte losses within large volumes of diarrhea.
During this phase, patients are dependent on parenteral nutrition, which
not only provides required nutrients but manages fluid and electrolyte
balance.
The second postoperative phase may last for several months and is
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The second postoperative phase may last for several months and is
characterized by reduction in diarrhea volumes with the initial stages of
adaptation of the remaining bowel. It is during this phase that enteral
nutrition can be introduced with a gradual transition to an oral diet. ( Rees-
Parrish 2005).During the third phase, there is continued adaptation of the remaining
bowel. There is some evidence the intestinal tract increases in both
length and diameter with additional increase in villous height. This time
frame varies, but may range from 1 to 2 years. ( Buchman 2004).
The amount of remaining bowel determines the extent of this condition.Loss of the ileum prevents B12 absorption and reabsorption of bile salts.
Reduction in bile salts further contributes to fat malabsorption.
No other part of the intestinal tract can compensate for these losses. The
ileocecal valve not only controls intestinal motility but also prevents
translocation of bacteria from the colon to the small intestine.When this control is lost, nutritional and metabolic complications are much
more prominent.
Vit i d i l l j i i SBS Wh th i f t
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Vitamin and mineral losses are major issues in SBS. When there is fat
malabsorption, there is an inability to absorb adequate amounts of
vitamins A, D, E, and K. These will need to be supplemented
appropriately, and levels within the body will need to be evaluated.
Other nutrients often deficient include sodium, magnesium, iron, zinc,selenium, and calcium, because they are often lost in the large volumes of
diarrhea.(Rees- Parrish 2005)
Treatment
Initially, medical treatment will focus on managing fluid and electrolyte
balance. This is generally managed by parenteral nutrition and
intravenous support initially, and then as the patient is able, by oral
rehydration solutions. Motility is controlled by medications used to treat
symptoms of diarrhea.
Nutrition Therapy
Maintenance of nutritional and hydration status is critical for individuals with
SBS.
Aggressive nutrition support and careful progression to an oral diet require
careful attention by the entire health care team.
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One item at a time is added to the diet to ensure tolerance If GI symptoms
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One item at a time is added to the diet to ensure tolerance. If GI symptoms
are exacerbated, the food added should be removed from the diet. It may
be added again at a later date, depending on the patients adaptation
after surgery.
Lykins and Stockwell suggest it may be best to retry categories of restrictedfoods even as long as 6 months, since bowel adaptation can take as long
as 1 to 2 years (Lykins and Stockwell 1998).
Many patients with SBS are discharged on home parenteral nutrition (PN) or
home enteral nutrition support (EN) in addition to the limited oral diet. PN
or EN is usually cycled over 10 to 12 hours at home, which will allow apatient to resume normal activity.
Bacterial Overgrowth
DefinitionBacterial overgrowth syndrome results from cross-contamination of bacteria
from the colon to the small intestine. This may be a result of surgery,
disease, or trauma to the GI tract.
Pathophysiology
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Pathophysiology
In this condition, motility of the gastrointestinal tract is delayed due to
disease, surgery, or trauma, and stasis develops. There is a high risk for
development of small bowel bacterial overgrowth for those individuals
with short bowel syndrome. Bacteria numbers increase and begin tocompete with the host for nutrients. Malabsorption, maldigestion, and
malnutrition can result. ( Parisi et al 2003; Singh and Toskes 2003)
Clinical Manifestations
Signs and symptoms are similar to all conditions of malabsorption.
Diarrhea, steatorrhea, anemia, and weight loss all may be present in this
condition.
Treatment
Bacterial overgrowth syndrome is treated by both correcting the underlying
cause and administering broad spectrum antibiotics. ( Singh and Toskes2003)
Nutrition Therapy
Nutrition therapy will be consistent with the level of malabsorption that is
present. Nutrients most commonly malabsorbed (fat and lactose) should