Diseases of the Lower Gastrointestinal Tract

8/13/2019 Diseases of the Lower Gastrointestinal Tract

1/56

Winda, Agustus 2012

DISEASES OF THE LOWER

GASTROINTESTINAL TRACT


2/56

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.


3/56

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.


4/56

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.


5/56

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


6/56

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)


7/56

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


8/56

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.


9/56

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.


10/56

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) .


11/56

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.


12/56

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


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)


13/56

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.


14/56

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).


15/56

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.


16/56

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.


17/56

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.


18/56

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.


19/56

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


20/56

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.


21/56


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-


22/56

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)


23/56

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).


24/56

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).


25/56

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.


26/56

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)


27/56


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.


28/56

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.


29/56

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


30/56

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.


31/56


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).


32/56

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.


33/56

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.


34/56

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.


35/56

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.


36/56

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.


37/56

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).


38/56

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)


39/56

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.


40/56

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)


41/56

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).


42/56

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).


43/56

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)


44/56

T t t


45/56

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


46/56


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.


47/56

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.


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.


48/56

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.


49/56

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


50/56

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


51/56

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


52/56

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


53/56

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.


54/56

One item at a time is added to the diet to ensure tolerance If GI symptoms


55/56

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


56/56

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)


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

Documents

Diseases of the Lower Gastrointestinal Tract