throbber
REVIEW ARTICLE
`
`Nutrition Vol. 13, No. 10, 1997
`
`The Clinical Management of Short Bowel
`Syndrome: Steps to Avoid
`Parenteral Nutrition
`
`ALAN L. BUCHMAN, MD, MSPH
`
`From the Division of Gastroenterology, University of Texas, Houston Health Science Center,
`Houston, Texas, USA
`
`Date accepted: 19 December 1997
`
`INTRODUCTION
`Short bowel syndrome may result from congenital abnormal-
`ities including
`jejunal or ileal atresia, or may be acquired as in
`cases of massive resection due to mesenteric venous thrombosis or
`arterial embolism,
`trauma, small bowel obstruction, volvulus, nec-
`rotizing enterocolitis,
`inflammatory
`bowel disease with multiple
`resections, carcinoma, or radiation enteritis. There are as many as
`20 000-40 000 patients that receive long-term parenteral nutrition
`in the United States.’ Of these, perhaps 7,000-8,000
`have short
`bowel syndrome.
`
`ADAPTATION
`the prognosis of
`Several factors are important
`for determining
`a patient following massive small bowel resection. These include
`age, length of remaining bowel, the presence or absence of a colon
`and ileocecal valve, adaptation of the remaining bowel, and the
`underlying pathology.2-4 The remaining bowel may be function-
`ally insufficient
`in patients with active Crohn’s disease, radiation
`enteritis, carcinoma or pseudo-obstruction
`in the remaining bowel.
`The minimum
`length of functional bowel necessary
`is generally
`thought to be 100 cm in the absence of an intact colon, and 60 cm
`in the presence of an intact colon. However,
`the degree of adap-
`tation may be highly
`individualized.
`Patients with <lo0
`cm of
`residual
`jejunum may have a net secretory
`response
`to foods5
`Hypovolemia
`and dehydration will occur in the presence of mas-
`sive small bowel
`and colonic
`resections. However,
`there are
`reports of infant survival without
`total parenteral nutrition (TPN)
`with as little as 30 cm or less.6,7
`to re-
`response
`The small bowel has a significant adaptation
`section.
`In animal models
`the intestinal
`surface area increases
`because of slightly increased
`length, but more importantly,
`signif-
`icantly
`increased
`circumference.
`Crypt depth and villus width
`increase
`in rodents, dogs, and humans.a-15 Therefore,
`the absorp-
`tive surface area increases. These effects appear to be most sig-
`
`in the ileum in animal models.li-‘3 Accelerated mucosal
`nificant
`proliferation
`is an important part of the adaptation mechanism.
`These adaptations may occur over a l- to 2-y period in humansi
`Similar morphologic
`changes have been found
`in humans
`in the
`functioning
`loop of bowel following
`jejuno-ileal
`bypass.i6 Fluid
`and electrolyte absorption by the colon (which hypertrophies) will
`increase
`to help compensate
`for intestinal
`losses.17 In addition,
`animal models suggest
`that ileal absorption
`increases within 6-8
`wk following
`resection by an upregulation of enterocyte
`absorp-
`tive capacity.i8
`than
`are less well tolerated
`Massive distal (ileal) resections
`proximal
`resections because
`the remaining
`jejunum cannot adapt
`as efficiently as the ileum, and the enterohepatic
`circulation of bile
`salts will be interupted.
`In addition, vitamin B,, malabsorption
`occurs.
`losses occur due to profound
`fluid and electrolyte
`Massive
`diarrhea during the initial postoperative week or two in patients
`with significant
`small bowel
`resection. Parenteral nutrition and
`fluids are necessary
`in this immediate postoperative
`period. Diar-
`rhea will decrease over the following
`l-3 mo, although TPN is
`generally still necessary.
`In order for enteral feeding
`to be toler-
`ated, intestinal
`transit time must be sufficiently
`slow in order to
`permit nutrient absorption along the remaining
`intestine. In animal
`models,
`intestinal adaptation
`is more rapid and significant
`in the
`presence of luminal nutrients.19J0
`
`MEDICAL MANAGEMENT
`
`to a
`occurs for a few months
`Transient gastric hypersecretion
`year (at most) postoperatively. This is related to hypergastrinemia,
`the etiology of which is uncertain. H, antagonists or proton pump
`inhibitors may be useful for decreasing
`jejunostomy
`output and
`potassium
`losses during this period.21-23 The rate of gastric emp-
`tying is increased. However, with proximal
`resections,
`intestinal
`transit usually
`remains normal because of the normal,
`slowed
`
`Correspondence to: Alan L. Buchman, MD, MSPH, Division of Gastroenterology, University of Texas, Houston Health Science Center, 6431 Fannin, MSB
`4. 234 Houston, TX 77030, USA.
`
`Nutrition 13:907-913, 1997
`OElsevier Science Inc. 1997
`Printed in the USA. All rights reserved.
`
`ELSEVIER
`
`0899-9007/97/$17.00
`PI1 SO899-9007(97)00263-3
`
`Page 1
`
`

`
`908
`
`THE CLINICAL MANAGEMENT OF SHORT BOWEL SYNDROME: STEPS TO AVOID PARENTERAL NUTRITION
`
`transit through the ileum. An intact ileocecal valve will normally
`prolong
`intestinal
`transit and permit greater nutrient contact
`time
`with intestinal epithelium. Resection of the ileocecal valve will
`also permit bacterial colonization of the intestine, with the possi-
`bility of bacterial overgrowth. Bacteria compete with enterocytes
`for nutrients
`(such as vitamin B,,), and malabsorption
`and diar-
`rhea could result. In addition, fat malabsorption may be increased
`because bacteria may deconjugate
`bile salts, resulting
`in more
`significant bile salt malabsorption. 24 Antibiotic
`therapy with either
`metronidiazole
`or tetracycline may be necessary
`to treat bacterial
`overgrowth. o-Lactic acidosis may also rarely occur when anero-
`bit bacteria
`ferment malabsorbed
`simple carbohydrates
`such as
`glucose and lactose.25-27 This condition may be suggested by
`severe changes
`in mental status, including slurred speech, ataxia,
`opthalmoplegia,
`nystagmus,
`stupor, and coma. As with bacterial
`overgrowth,
`a course of antibiotic
`therapy with metroniadazole
`or
`tetracycline may be helpful. However, antibiotic use may cause
`vitamin K deficiency, as well as diarrhea (CEostridium d$fzciZe or
`non-C. di@ciZe). The risk of o-lactic acidosis
`(rare) should be
`balanced with the need to supply soluble
`fiber as an additional
`energy source (addressed
`in a subsequent
`section).
`jeju-
`Digestion
`initially occurs in the duodenum and proximal
`num where pancreatic proteases,
`salivary and pancreatic amylase,
`lipase, bile acids, and intestinal disaccharidases
`aid in the diges-
`tion of macronutrients
`such as protein, fat, and carbohydrate. The
`products of digestion are nearly completely
`absorbed within
`the
`first 100-150 cm of jejunum.28 In addition, minerals such as iron
`and calcium are absorbed
`in the duodenum and proximal jejunum,
`as are the water-soluble vitamins. Resection of cl00
`cm of ileum
`may result
`in cholerrhetic
`diarrhea and steatorrhea because bile
`salts are incompletely
`absorbed
`in the remaining distal ileum and
`enter the colon where they are toxic to colonocytes.29 A bile salt
`sequesterant
`such as cholestyramine may be a useful adjunct in the
`treatment of such resections because
`it may prevent
`the transit of
`unabsorbed bile salts into the colon.30 Resection of > 100 cm will
`result in the massive
`loss of bile salts and cannot be compensated
`by increased hepatic synthesis. Micellar solubilization
`of dietary
`fat will not occur because
`the critical micellar concentration
`is not
`reached, owing to the decreased
`intraluminal bile salt concentra-
`tion. Cholestyramine may worsen diarrhea by increasing malab-
`sorption. Fat intake should therefore be restricted
`in patients with
`jejunostomy
`output appears unaf-
`remaining colon29-31; whereas
`fected by fat restriction.32 However,
`too severe a restriction will
`render meals unpalatable,
`and caloric
`intake may subsequently
`decrease. Bile acid replacement with ox bile has been reported
`to
`improve
`steatorrhea
`in patients with and without
`residual colon
`following
`ileectomy.33-35
`(rodent and canine) have demonstrated
`Many animal studies
`following massive
`resection
`is impaired
`that intestinal adaptation
`in the absence of luminal nutrients. Despite claims to the contrary,
`the available data from humans suggest standard diets and enteral
`formulas are as efficacious
`as so-called “specialty,
`defined-for-
`mula or elemental”
`products
`for the nutritional maintenance
`of
`patients with short bowel syndrome. Woolf et a1.36 randomized
`eight patients (in a cross-over design) with complete
`ileal and right
`colon resections
`(5/8 had no colon remaining,
`and 3/8 had only
`30.4-50.8
`cm of jejunum)
`to receive
`isonitrogenous,
`lactose-free
`diets that were either high fat (75% nonprotein calories as fat), or
`a high-carbohydrate
`diet where the ratio of fat to carbohydrate was
`reversed. There was no difference
`in fecal weight, water excretion,
`osmolality,
`sodium, potassium, chloride, calcium, magnesium, or
`zinc output, or mean
`total calorie,
`fat calorie and protein +
`carbohydrate
`calories absorbed as expressed
`as a percentage of
`intake between
`the two diets. Fecal fat excretion was significantly
`greater during the high-fat diet, but the proportion of fat absorbed
`was similar between
`the two groups. However, neither experimen-
`
`that
`tal diet was compared with a regular diet, and it is possible
`both experimental diets were either equally better or worse than a
`regular diet. McIntyre et al.37 compared a polymeric
`formula diet
`with an isonitrogenous,
`chemically
`defined diet delivered
`via
`nasogastric
`tube (NGT) in five patients, and orally in two others
`with jejunostomies
`(60-1.50 cm remaining
`jejunum). No signifi-
`cant difference
`in stool wet and dry weight, percentage of total
`calorie, nitrogen, or fat absorption was seen between groups,
`although
`there was a wide patient-to-patient
`variation. Stoma1
`output of sodium, potassium, calcium, and magnesium was similar
`between groups. Levy et al. 38 found similar results. On the other
`hand, Cosnes et a1.39 found
`that a peptide-based
`diet enhanced
`nitrogen absorption
`in six patients with a jejunostomy
`(90-150 cm
`of jejunum). However,
`total calorie, fat, electrolyte,
`and mineral
`absorption were unaffected,
`as was jejunostomy
`output. Peptide-
`based enteral formulas may be generally
`ineffective when used for
`the purpose of decreasing
`fecal weight because the major cause of
`the watery diarrhea seen in patients with short bowel syndrome
`is
`carbohydrate, not nitrogen malabsorption.40 Regardless of the diet
`or enteral
`formula used, patients may require double
`their pre-
`dicted caloric and protein requirements
`based on height or body
`surface area in order to avoid reliance on TPN.
`Medium-chain
`triacylglycerols
`(MCT) may also be of value as
`an energy supplement
`in patients with steatorrhea because they do
`not require bile salts for digestion. MCTs are a component
`of
`many enteral products, although they are also available separately.
`MCTs, however, do not supply essential fatty acids, are expensive
`and unpalatable
`to some patients despite modem
`recipe
`innova-
`tions, and excessive
`ingestion may worsen diarrhea. Typically,
`daily doses of >40 g are poorly tolerated.
`It should also be noted
`that in rat studies,
`intestinal hyperplasia
`following
`small bowel
`resection was greater
`in animals
`that received diets containing
`long-chain
`triacylglycerols when compared with MCT.41
`short
`Regardless
`of the diet, patients with newly acquired
`bowel syndrome
`should probably
`receive at least some enteral
`feeding as soon as possible after resection. Usually this is admin-
`istered
`for a postoperative
`period of 7-10 days. Isotonic
`fluids
`should be administered;
`hypotonic
`fluid ingestion will promote
`additional
`salt and water
`loss. If possible, dry solids should be
`consumed
`first, followed by isotonic fluids an hour later. However,
`
`TABLE
`
`I.
`
`FOR PATIENTS
`VITAMIN AND MINERAL SUPPLEMENTS
`WITH SHORT BOWEL SYNDROME*
`
`Vitamin A
`Vitamin B ,s
`
`Vitamin C
`Vitamin D
`
`Vitamin E
`Vitamin K
`Calcium
`Magnesium
`Iron
`Selenium
`Zinc
`Bicarbonate
`
`for those w/terminal
`
`or
`
`units daily
`10,00&50,000
`300 mcg subcutaneously monthly
`ileal resections or disease
`200-500 mg
`1600 units DHT daily; may require 25OH-
`1,25 (OH,)-D,
`30 IU daily
`10 mg weekly
`See text
`See text
`As needed
`60-100 Fg daily
`22&440 mg daily (sulfate form)
`As needed
`
`* The table lists rough guidelines only. Vitamin and mineral supplemen-
`tation must be routinely monitored and tailored
`to the individual patient
`because relative absorption and requirements may vary.
`
`Page 2
`
`

`
`THE CLINICAL MANAGEMENT OF SHORT BOWEL SYNDROME: STEPS TO AVOID PARENTERAL NUTRITION
`
`909
`
`feeding, bolus
`
`inpractical. When enteral
`is often
`this approach
`feedings
`should be avoided, at least initially.
`All enteral products should be lactose-free. Lactose maldiges-
`tion is common because of the decreased
`intestinal
`surface area
`(and
`lactase-containing
`brush border).42 Other
`foods
`that may
`have laxative effects such as caffeine and osmotically active drugs
`or sweeteners
`(e.g., sorbitol) should be eliminated
`from the diet.
`Multivitamin
`and
`trace mineral
`supplementation
`should be
`routine. Fat-soluble
`vitamin status (A, D, E, and K) should be
`routinely monitored
`in patients who do not require TPN, to which
`these vitamins are routinely
`added. Vitamin A (lO,OOO-50,000
`U/d), vitamin D (1600 U DHT/d), and vitamin E (30 U/d) may be
`necessary
`(Table I). Patients who have concurrent
`renal insuffi-
`ciency may be unable to metabolize 25OH D, to its active form
`(1,25 OH,D,),
`and may require supplementation with the active
`compound. Both water-soluble vitamin A and D supplements
`still
`require micelles for absorption although the water-soluble vitamin
`E supplement does not. Toxicity from either excessive vitamin D
`or vitamin A intake may occur. Therefore,
`serum concentrations
`of these vitamins
`should be monitored during supplementation
`(and calcium
`in the case of vitamin D), and patients should be
`monitored
`for possible signs of toxicity. Vitamin A toxicity may
`be manifested
`in headache, vomiting, diplopia, alopecia, dryness
`of the mucus membranes, hypercalcemia,
`and elevations
`in serum
`hepatic aminotransferase
`concentrations.43 Vitamin D toxicity
`is
`associated with hypercalcemia,
`and subsequent progress
`to renal
`failure
`if not recognized.4 Vitamin K deficiency
`is rare, except
`generally
`in the patient that receives broad-spectrum
`antibiotics or
`in the patient without a colon
`in whom
`there are fewer vitamin
`K-producing bacteria. Vitamin K status is monitored by the pro-
`thrombin
`time (PT), which
`is affected by vitamin K-dependent
`coagulation
`factors. Requirements
`are approximately
`1 mg/d.45
`Water-soluble
`vitamin deficiencies
`are rare, even
`in patients
`with short bowel syndrome, but certainly may occur. Therefore,
`such patients should
`ingest one or two B-complex vitamin sup-
`plements and 200-500 mg of vitamin C daily. Excessive vitamin
`C is to be avoided because of the risk of hyperoxaluria
`related to
`increased endogenous production, because oxalic acid is a product
`of vitamin C metabolism. Toxicity from overdose of other water-
`soluble vitamins has not been recognized. Vitamin B,, should be
`administered
`at a dose of 300 pg every 3 mo (intramuscularly)
`to
`patients with ileal resections, or in those patients who have dis-
`eased ileum (Crohn’s disease,
`radiation enteritis, etc.)
`iron is ab-
`Iron supplements
`are often unnecessary
`because
`sorbed primarily
`in the duodenum, but serum ferritin should be
`monitored. Zinc supplements
`are routinely necessary. Zinc is lost
`in a concentration
`of 17 mg/L of small bowel output.46 Usually
`one or two 220-mg zinc sulfate tablets will be sufficient. Calcium
`supplements may also be necessary,
`especially because
`low-lac-
`tose or lactose-free
`diets will often be low in calcium as well.
`However,
`low plasma calcium concentration may be related
`to
`hypoalbuminemia,
`hypomagnesemia,
`or vitamin D deficiency.
`Alternatively,
`serum calcium concentration may be maintained
`in
`the normal range despite deficiency because
`increased parathyroid
`hormone
`secretion will lead to increased bone resorption. Bone
`disease may also occur because of the metabolic
`acidosis
`that
`results from bicarbonate
`losses from the small bowel.47 BiCitra or
`sodium bicarbonate
`are of value
`to maintain normal acid/base
`status. Magnesium
`deficiency
`is difficult
`to correct using
`the
`enteral route because of the cathartic effect of magnesium
`supple-
`ments, and enteric-coated
`preparations
`are very poorly absorbed.
`A recent
`report
`suggests oral administration
`of the
`injectable
`formulation
`of magnesium
`sulfate may be preferred,
`although
`expensive.48 Selenium deficiency may occur because of chronic
`stool losses.49 Plasma selenium concentration
`can be monitored
`and replacement
`supplements
`used. Daily
`intake should be 60-
`
`100 pg. Deficiency may be associated with myositis, pseudoalbi-
`nism, macrocytosis,
`and cardiomyopathy.50Ji
`Copper deficiency
`is very rare, but copper status should also be monitored. Defi-
`ciency has been associated with anemia, neutropenia,
`testicular
`atrophy, neuropathy, osteoporosis,
`retinal degeneration,
`and car-
`diomyopathy.52x53
`Patients who have short bowel syndrome, but have an intact
`colon, should be placed on a low oxalate diet (Table II). It has
`been generally
`thought
`that oxalate
`is absorbed
`in the colon, but
`not in the small intestine. Normally, dietary calcium binds oxalate
`(and bile acids), rendering
`it unavailable
`for colonic absorption.
`When steatorrhea occurs, dietary calcium preferably binds unab-
`sorbed fatty acids, rather than oxalate. This allows the oxalate to
`enter
`the colon where
`it is absorbed. This absorption may be
`enhanced because of colonic damage caused by unabsorbed bile
`salts.54 The systemically
`absorbed oxalate
`is then filtered
`in the
`kidney, where it is free to bind calcium and form calcium oxalate
`kidney stones. Foods such as chocolate,
`tea, cola, spinach, celery,
`and carrots should be avoided. Oral calcium supplements may also
`be useful.55 In the absence of a colon, calcium oxalate nephroli-
`thiasis
`is unlikely
`to occur, and these patients do not require
`dietary oxalate restriction.
`Other dietary
`interventions may also be of value in patients
`with short bowel syndrome who have an intact colon. The role of
`the colon has often been
`thought
`to be limited
`to fluid and
`electrolyte absorption. However,
`the colon may play a significant
`role in energy absorption. Soluble
`fiber (e.g., pectin, not wheat
`bran or soy) and starch that is malabsorbed
`in the small intestine
`is metabolized
`to short chain acids (SCFA) by colonic bacteria.
`These SCFA, most notably butyrate, are the prefered
`fuel for the
`human colonocyte.56 In fact, the colon can absorb up to 1000 kcal
`daily via SCFA absorption.52s57 Although
`these studies seem to
`refute
`the previous data that high-carbohydrate
`diets are not su-
`perior
`to standard or high-fat diets, at least for patients with an
`intact colon,
`it may simply be that only high-carbohydrate
`diets
`that contain significant
`amounts of soluble and some
`insoluble
`non-starch polysaccharides
`are efficacious.
`supplementation
`Preliminary
`data suggest
`that oral calcium
`(2.4-3.6 g elemental Ca) may significantly
`reduce
`the amount of
`diarrhea
`in jejunol-ileal
`bypass patients.58
`It therefore may be
`helpful in patients with short bowel syndrome, although definitive
`evidence
`is lacking.
`(ORS) are of use in prevention of
`solutions
`Oral rehydration
`excessive
`fluid losses
`in patients with short bowel syndrome.59sm
`Long used in cash-starved
`third-world countries, and routinely by
`pediatricians
`in their treatment of children with acute diarrhea
`in
`the United States, internists and gastroenterologists
`rarely resort to
`such relatively simple
`inexpensive
`therapy when intravenous
`so-
`lutions and emergency
`rooms are so accessible. Although ORS
`may be more expensive
`than intravenous dextrose,
`there is no cost
`for administration
`(such as an emergency
`room or home nursing
`visit with intravenous catheter
`insertion
`for fluid administration).
`Loperamide hydrochloride
`(4-16 mg total daily), diphenoxylate,
`codeine (30-60 mg up to three times a day), or tincture of opium
`(10 drops two or three times a day) may be required
`to control
`diarrhea or ostomy output (Table III).
`The long-acting
`somatostatin
`analogue, octreotide, has been
`used to decrease output of jejuno- or ileostomies.61-63 However,
`despite
`the statistically
`significant
`results,
`there is little clinically
`apparent significance, because
`the patients studied still had sub-
`stantial
`intravenous
`fluid requirements
`in addition
`to their TPN.
`There are also concerns
`that octreotide use may result in nutrient
`malabsorption
`and gallstone
`formation
`(for which short bowel
`patients are already at increased risk). Therefore, octreotide should
`be used only in patients with high output ileostomies
`as a tempo-
`
`Page 3
`
`

`
`910
`
`THE CLINICAL MANAGEMENT OF SHORT BOWEL SYNDROME: STEPS TO AVOID PARENTERAL NUTRITION
`
`TABLE II.
`
`OXALATE CONTENT OF FOODS FOR LOW OXALATE DIET, RESTRICTED TO 40-50 MG DAILY
`
`Little or no oxalate
`<2 mg/serving
`Eat as desired
`
`Moderate oxalate content
`2-10 mg/serving
`Limit: 2 (l/2 cup) servings day
`
`High oxalate
`> 10 mg/serving
`Avoid completely
`
`Coffee, any kind (8 oz)
`Cranberry juice (4 oz)
`Grape juice (4 oz)
`Orange juice (4 oz)
`Tomato juice (4 oz)
`Nescafe powder
`
`Draft beer, stout,
`Juices containing berries
`Ovaltine and other beverage mixes
`Tea, cocoa
`
`Sardines
`
`Baked beans canned in tomato sauce
`Peanut butter
`Soybean curd (tofu)
`
`Food group
`
`Beverages
`
`Meat group
`
`Fruits and vegetables
`
`Apple or pineapple juice
`Bottled beer
`Colas (12 oz limit/d)
`Distilled alcohol
`Grapefruit juice
`Lemonade or limeaid (no peel)
`Wine, red, rose
`Tap water
`Milk, yogurt
`
`Eggs
`Cheese, cheddar
`Lean lamb, beef, or pork
`Poultry
`Seafood
`
`Avocado
`Brussels sprouts
`Cauliflower
`Cabbage
`Mushrooms
`Onions
`Peas, green
`Potatoes (Irish)
`Radishes
`
`Bananas
`Cherries, Bing
`Grapefruits
`Grapes, Thompson seedless
`Mangoes
`Melons
`Cantaloupe
`Casaba
`Honeydew
`Watermelon
`Nectarines
`Peaches, Hiley
`Plums, green/golden
`
`Asparagus
`Broccoli
`carrots
`Corn
`Cucumber, peeled
`Green peas, canned
`Lettuce, iceberg
`Lima beans
`Parsnips
`Tomato, 1 small
`Turnips
`
`Apples
`Apricots
`Black currants
`Cherries, red sour
`Orange
`Peaches, Alberta
`Pears
`Pineapples
`Plums, Damson
`Prunes, Italian
`
`Beans: green, wax, dried
`Beets: tops, root, greens
`Celery
`Swiss chard
`Chives
`Collards
`Dandelion greens
`Eggplant
`Escarole
`Kale
`Leeks
`Mustard greens
`Okra
`
`Blackberries
`Blueberries
`Concord grapes
`Red currants
`Dewberries
`Fruit cocktail
`Gooseberries
`Lemon peel
`Lime peel
`Raspberries
`Rhubarb
`Strawberries
`Tangerines
`
`Fruit cake
`Grits, white corn
`Soybean crackers
`Wheat germ
`
`Nuts
`Peanuts
`Pecans
`Chocolate, cocoa
`Pepper (in excess of 1 tsp/d)
`Vegetable soup
`Tomato soup
`
`Breads and other
`starches
`
`Miscellaneous
`
`Cornflakes
`Macaroni
`Noodles
`Oatmeal
`Rice
`Spaghetti
`White bread
`Mayonnaise
`Salad dressing
`Vegetable oils
`Jelly or preserves (made w/allowed fruits)
`Salt, pepper (1 tsp/d)
`Soups made w/allowed ingredients
`sugar
`
`Cornbread
`Sponge cake
`Spaghetti, canned in
`sauce
`
`tomato
`
`Chicken noodle soup,
`dehydrated
`
`From Denise M. Ney, R.D., The Low Oxylute Diet Book for the Prevenfion of OxyZate Stones, University of California, San Diego, California, 1981
`and UCLA Manual of Clinical Dietetics, University of California, Los Angeles, 1986.
`
`Page 4
`
`

`
`THE CLINICAL MANAGEMENT OF SHORT BOWEL SYNDROME: STEPS TO AVOID PARENTERAL NUTRITION
`
`911
`
`rary solution until other methods for the prevention of dehydration
`resulting
`from excess fluid loss are successful.
`Recent data suggest
`that a combination
`of growth hormone,
`glutamine,
`and fiber enhances
`adaptation of the remnant bowel
`following
`resection.@JjS
`In the initial study by Byrne et al.,65
`significantly
`improved
`nitrogen,
`sodium, water,
`and caloric
`absorption were observed after 4 wk of treatment
`in six patients
`compared with baseline
`in an open-labeled
`study. The patients
`averaged 44 y of age and had a mean
`length of approximately
`45 cm of jejunum and ileum remaining. All had intact colon. In
`the second,
`larger study from the same group, 10 patients with
`a similar age (and possibly
`including,
`it seems, most or all of
`the same patients) were
`found
`to exhibit
`increased
`calorie,
`protein,
`carbohydrate,
`water,
`and sodium
`absorption.
`Stool
`output also decreased. However,
`closer
`inspection
`of the report
`indicates
`only 6/10 patients
`actually
`required TPN at the be-
`ginning of the study, and all patients had an intact colon. This
`suggests
`that conventional
`therapy as discussed previously may
`have been equally
`effective
`for these patients;
`there was no
`control group for either study. Soluble
`fiber and ORS were also
`used in the study. Only l/10 patients was at or above their ideal
`body weight
`(IBW), with 5/10 under 85% of their IBW, despite
`over 6 y of home TPN. This suggests
`that the patients may have
`been
`inappropriately
`managed before entering
`the study, and
`protein malnutrition
`could have resulted
`in increased malab-
`sorption. Therefore,
`despite
`seemingly
`dramatic
`and exciting
`results,
`these studies
`should be interpreted with caution until
`more data, and data
`from
`randomized,
`controlled
`trials are
`available. Recent data presented
`from a placebo-controlled
`trial
`at the Mayo Clinic
`indicates
`three-week
`therapy with growth
`hormone, oral glutamine,
`and a high complex carbohydrate
`diet
`lead to modest
`improvements
`in sodium and potassium
`absorp-
`tion, but no change
`in fat or nitrogen absorption,
`no decrease
`in
`stool volume, no improvement
`in 0-xylose
`absorption,
`and no
`improvement
`in small bowel morphology.75
`
`IN SHORT BOWEL SYNDROME
`MEDICATION DELIVERY
`Patients with short bowel syndrome not only have nutrient
`malabsorption,
`but may have medication malabsorption
`as well.
`Therefore,
`significantly
`greater
`than conventional
`doses may be
`required. The clinician may also be forced
`to explore alternative
`routes of medication
`administration
`in the patient with severe
`malabsorption
`and rapid
`intestinal
`transit. These may
`include
`topical, buccal,
`intravenous, or aerosol. Oral doses may be effec-
`tive, but often only with substantially
`increased doses (e.g., war-
`farin).66Jj7 However, one must also be aware that patients may be
`very sensitive
`to small doses of warfarin in the presence of vitamin
`K deficiency
`that may occur because of fat malabsorption
`and
`bacterial overgrowth.
`If a patient requires TPN or tube feeding,
`compatibility
`issues of nutrients and medications must be consid-
`ered.
`
`SURGICAL MANAGEMENT
`to
`or other means
`attempts at bowel
`lengthening
`Numerous
`transit and thereby
`increase absorptive
`time (in-
`slow intestinal
`cluding the use of aperistaltic
`segments, colonic interposition,
`and
`recirculating
`small intestine
`loops) have been made for patients
`with short remaining
`small bowel remnants.68,69 None have been
`considered
`routinely
`successful. Success has been reported
`for
`interposition
`of a reversed bowel loop in a preliminary
`study for
`patients with approximately
`50 cm of remnant bowel.70
`More
`recently,
`small bowel
`transplantation
`has been per-
`formed, primarily
`for patients dependent
`on long-term TPN.
`Small bowel
`transplantation
`has greater
`similarity
`to bone
`marrow
`transplantation
`than to solid organ transplants. There is
`a significant
`risk of rejection, graft-versus-host
`disease, as well
`
`to over
`related
`that appear
`disease
`as a lymphoproliferative
`prob-
`These complex
`immunological
`immunosuppression.7L~7*
`lems do not appear
`to be easily
`controlled with currently
`available
`therapies. One-, 2-, and 4-y survival
`rates are 62%,
`48%, and 37%, respectively,
`in the University
`of Pittsburgh
`experience
`(71 patients at the time of publication), where by far
`the greatest
`experience
`has been generated.72 A recent
`report
`from transplant
`centers
`throughout
`the world
`that included 170
`patients
`reported
`l- and 3-y survival of 57% and 50%, respec-
`tively, for isolated small intestine
`transplants when cyclosporin
`was used.72 Survival was increased
`to 83% at 1 y and 47% at
`3 y when
`tacrolimus was used as the primary
`immunosuppres-
`sive agent.71 Survival was substantially
`less for those with a
`combined
`small bowel-liver
`transplant
`or patients undergoing
`multivisceral
`transplantation. However, 78% of survivors were
`able to discontinue TPN.
`The survival
`rate for patients on home TPN varies depend-
`ing on age and
`the underlying
`disease.
`For patients with
`Crohn’s disease and congenital bowel defects,
`the 3-y survival
`is approximately
`90%, approximately
`70% for those with isch-
`emit bowel diseases,
`chronic
`adhesive obstructions,
`and mo-
`tility disorders,
`but only 30% for patients with malignancies
`and 20% for those with AIDS.73 These figures are significantly
`better
`than for comparable
`patients who have undergone
`small
`intestine
`transplantation.
`However,
`the longer
`term complica-
`tions of TPN are more recently becoming known. Despite
`this,
`the current
`indication
`for small intestinal
`transplantation
`should
`be only
`for patients with short bowel
`syndrome
`and TPN-
`associated
`hepatic
`failure,
`in whom an orthotopic
`liver
`trans-
`plant
`is necessary.
`Small bowel
`transplantation
`is hazardous
`and extraordinarily
`expensive.
`It is not a true therapeutic option
`for patients who are stable, and satisfactorily maintained
`on
`home TPN. It is extremely
`rare for patients who require
`long-
`term home TPN to lose venous access, although
`thoracotomy
`for line placement may become necessary
`in extremely
`rare
`instances.T4 Because
`in the absence of hepatic
`failure,
`small
`intestinal
`transplantation must be considered
`an elective pro-
`cedure
`and
`the few number of patients
`that would actually
`require such a procedure,
`it is unlikely
`that clinical experience
`will develop
`as rapidly
`as with other organ
`transplants.
`The
`costs of the transplant
`as well as for immunosuppressive
`med-
`ication and treatment
`of transplant-related
`medical
`issues are
`extremely
`expensive
`and have not been fully described. While
`the charges
`for home TPN may range as high as $lOO,OOO-
`$150,000 yearly
`in the United States
`(unpublished
`observa-
`tions),
`in a managed care environment
`it is the actual costs, not
`the charges,
`that become
`important. One day’s supply of TPN
`
`TABLE
`
`III.
`
`TREATMENT OF DIARRHEA IN THE
`SHORT BOWEL PATIENT*
`
`Oral rehydration solutions
`(RehydralyteB,
`PedialyteB,
`RicealyteB, WHO glucose-electrolyte
`formula)
`Loperamide hydrochloride
`Diphenoxylate
`Codein
`
`Tincture of opium
`
`* Suggested
`
`in order of use or need.
`
`As needed
`
`4-16 mg daily
`4-16 mg daily
`Up to 3CMO mg
`three times per day
`10 drops two to
`three times per day
`
`Page 5
`
`

`
`912
`
`THE CLINICAL MANAGEMENT
`
`OF SHORT BOWEL
`
`SYNDROME:
`
`STEPS TO AVOID
`
`PARENTERAL
`
`NUTRITION
`
`daily,
`little as $16-$25
`for as
`solutions may be provided
`obser-
`exclusive of supplies and any nursing care (unpublished
`vations).
`In addition
`to survival and cost, quality of life issues
`
`before
`must also be addressed
`becomes an acceptible
`alternative
`syndrome.
`
`transplantation
`small bowel
`for patients with short bowel
`
`REFERENCES
`
`1. Howard L, Ament M, Fleming CR, et al. Current use and clinical
`outcome of home parenteral
`and enteral nutrition
`therapies
`in the
`United States. Gastroenterology
`1995;109:355
`length of
`Carbonnel F, Cosnes J, Chevret S, et al. What is the minimal
`residual
`small bowel necessary
`to maintain
`autonomy via the oral
`route
`in the short bowel
`syndrome
`(abstract)? Clin Nutr 1993;
`13(suppl):8
`Messing B, Crenn P, Beau P, et al. Parenteral nutrition dependence
`factors
`in adult short bowel syndrome patients
`(abstract). Gastroen-
`terology 1996;l lO:A347
`Kaufman SS, Loseke CA, Lupo JV, et al. Factors affecting duration of
`parenteral
`alimentation
`in children with short bowel syndrome
`(ab-
`stract). Gastroenterology
`1996;l lO:A809
`Nightingale
`JM, Lennard-Jones
`JE, Walker ER, Farthing MJ. Jejunal
`efflux in short bowe

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