The medical management of intestinal failure: methods to reduce the severity

Proceedings of the Nutrition Society (2003), 62, 703–710
03ociety (2003)0029-6651 Nutrition Society 2003 623 The Annual Meeting of the Clinical Nutrition and Metabolism Group of the Nutrition Society with the British Association for Parenteral and Enteral Nutrition, in conjunction with the 24th Congress of the European Society for Parenteral and Enteral Nutrition, was held at the Scottish Exhibition and Conference Centre, Glasgow on 4 September 2002 Symposium on ‘Intestinal failure’
The medical management of intestinal failure:
methods to reduce the severity
Leicester Royal Infirmary, Leicester LE1 5WW, UK Dr Jeremy Nightingale, fax +44 116 2586985, email jnight@globalnet.co.uk A new definition of intestinal failure is of reduced intestinal absorption so that macronutrientand/or water and electrolyte supplements are needed to maintain health or growth. Severeintestinal failure is when parenteral nutrition and/or fluid are needed and mild intestinal failure iswhen oral supplements or dietary modification suffice. Treatment aims to reduce the severity ofintestinal failure. In the peri-operative period avoiding the administration of excessive amounts ofintravenous saline (9 g NaCl/l) may prevent a prolonged ileus. Patients with intermittent bowelobstruction may be managed with a liquid or low-residue diet. Patients with a distal bowel entero-cutaneous fistula may be managed with an enteral feed absorbed by the proximal small bowelwhile no oral intake may be needed for a proximal bowel enterocutaneous fistula. Patientsundergoing high-dose chemotherapy can usually tolerate jejunal feeding. Rotating antibioticcourses may reduce small bowel bacterial overgrowth in patients with chronic intestinal pseudo-obstruction. Restricting oral hypotonic fluids, sipping a glucose–saline solution (Na concentrationof 90–120 mmol/l) and taking anti-diarrhoeal or anti-secretory drugs, reduces the high output froma jejunostomy. This treatment allows most patients with a jejunostomy and > 1 m functioningjejunum remaining to manage without parenteral support. Patients with a short bowel and a colonshould consume a diet high in polysaccharides, as these compounds are fermented in the colon,and low in oxalate, as 25 % of the oxalate will develop as calcium oxalate renal stones. Growthfactors normally produced by the colon (e.g. glucagon-like peptide-2) to induce structural jejunaladaptation have been given in high doses to patients with a jejunostomy and do marginallyincrease the daily energy absorption.
Intestinal failure: Short bowel: Clinical management: Nutritional support: Water and
electrolyte status
The commonly quoted definition of intestinal failure is of Unfortunately, there is no simple clinical or biochemical ‘reduction in functioning gut mass below the minimum measurement to define and grade the severity of intestinal amount necessary for adequate digestion and absorption of failure (as serum creatinine in renal failure or blood gases in nutrients’ (Fleming & Remington, 1981). This definition respiratory failure), although xylose absorption or post- has often been interpreted as referring only to patients who prandial plasma citrulline (Crenn et al. 2000) measurements need parenteral nutrition. This interpretation would be similar to defining patients as having renal failure only when A new definition of intestinal failure is of reduced they needed dialysis. This definition makes no mention of intestinal absorption so that macronutrient and/or water and water and electrolyte losses and yet this issue dominates the electrolyte supplements are needed to maintain health and/or clinical management of most patients with intestinal failure.
growth (Nightingale, 2001a). Without such treatment or Corresponding author: Dr Jeremy Nightingale, fax +44 116 2586985, email jnight@globalnet.co.uk
compensatory mechanisms undernutrition and/or dehy- While methods for reducing the severity of intestinal failure dration will result. This definition allows the severity of include the judicial use of surgery, the present article only intestinal failure to be graded according to the type of nutri- addresses medical or dietary methods for reducing the tional support needed (Fig. 1) and a wide range of underlying severity of intestinal failure, with particular reference to diagnoses are included (Fig. 2). Acute (or temporary) intes- tinal failure is potentially reversible and most commonlyencountered, with > 90 % of patients with severe intestinal Methods for reducing the severity of acute intestinal
failure being in the peri-operative period (Kennedy et al.
2002). Chronic intestinal failure is less common and mostpatients have a short bowel.
Patients with acute intestinal failure as the result of a distal There are four aims in the management of patients with entero-cutaneous fistula can often be managed with an enteral feed (often a peptide feed) rather than parenteral nutrition,nil by mouth with or without octreotide (Carlson, 2001).
to provide the nutrition and/or water and electrolytes Intermittent small bowel obstruction can be managed with a necessary to maintain health and/or growth; to reduce the severity of intestinal failure; In a study of patients undergoing a colonic resection for to prevent and treat complications, including those cancer two groups each of ten patients were randomized to related to the underlying disease, intestinal failure itself receive either a ‘normal’ (more than 3 litres water and 154 mmol Na/24 h) or a ‘restricted’ (< 2 litres water and 77 mmol Na/24 h) peri-operative fluid management (Loboet al. 2002). On the second post-operative day patients inthe ‘normal’ group had gained 3 kg weight. Measurements of gut function (solid and liquid gastric emptying, time to pass flatus and stool, and time before eating solid food) weresignificantly slower in the ‘normal’ group (P < 0·03 in allcases). Complications were more frequent and hospital stayslonger in those having the normal regimen. This studydemonstrated that the administration of large amounts offluid, especially saline (9 g NaCl/l), to peri-operative Moderate
patients could cause and prolong the period of acute intes-tinal failure (ileus).
Patients undergoing high-dose chemotherapy, particularly as part of bone marrow transplantation, have traditionallybeen given parenteral nutrition. However, there is increasing evidence that enteral feeding may suffice (and be safer) if the nausea or vomiting is controlled. Jejunal feeding may be Fig. 1. Severity of intestinal failure. An aim of treatment is to reduce
given via a percutaneous endoscopic gastrostomy with a jejunal tube placed through it (Steward et al. 2001).
Fig. 2. Classification of intestinal failure.
Methods for reducing the severity of chronic intestinal
Net ‘secretors’ generally have < 1 m jejunum and have an failure: intestinal dysmotility
intestinal output that is greater than the oral intake, so thatthey are in negative intestinal water and Na balance, and These patients are relatively uncommon and have the thus need parenteral support (Fig. 4). Net ‘absorbers’, on the symptoms and signs of intestinal obstruction without a other hand, have 1–2 m jejunum remaining and have an mechanical blockage. This outcome can be due to an intestinal intestinal output that is less than the oral intake, so that they myopathy (e.g. systemic sclerosis or visceral myopathy) or achieve positive water and Na balance and can be managed neuropathy (e.g. diabetes or visceral neuropathy) or a combi- with oral therapy (Nightingale et al. 1990).
nation (e.g. amyloidosis). Treatment addresses the main Patients with a jejuno–colic anastomosis are often well problems of abdominal pain, vomiting, diarrhoea (consti- after surgery except for diarrhoea, which is worse with food.
pation in the early stages) and undernutrition. Abdominal pain They may feel well after the resection but present later with may be treated with antispasmodics, transcutaneous or severe weight loss due to malabsorption.
sublingual opiates, or octreotide. Vomiting may be helped byprokinetic agents (metoclopramide, domperidone, cisapride,ondansetron or erythromycin) or by antibiotics. Diarrhoea Assessment of a patient with a high-output stoma may be helped by drugs that delay gastrointestinal transit(loperamide or codeine phosphate) or by antibiotics (Powell- A patient with a high-output stoma (usually from the small bowel) is likely to feel thirsty. The patient may have suddenly Undernutrition, in addition to vomiting and diarrhoea, lost > 2 kg in weight and may have a low urine output. The may be considerably helped by using oral antibiotics urea and creatinine levels may be high if the patient is very (rotating every 6–8 weeks or short courses of 1–2 weeks) to dehydrated. A random urine Na concentration of < 10 mmol/l treat small-bowel bacterial overgrowth. Traditionally, metro- suggests Na depletion. Hypomagnesaemia (see p. 706) is nidazole, tetracycline and cephalosporins have been given, common. Measurement of the residual bowel length is useful although an amoxycillin–claevulinic acid combination or and can be performed using an opisometer in a small-bowel ciprofloxacin may be more effective.
Ba study if the length was not measured at the time of surgery(Nightingale et al. 1991a; Carbonnel et al. 1996).
Abdominal sepsis and partial small-bowel obstruction Methods for reducing the severity of chronic intestinal
can give rise to a high-output stoma and may be excluded failure: short bowel
clinically with the help of radiology (computerized tomog- Two types of patients with a short bowel are shown in Fig. 3, raphy scans and contrast studies). Occasionally, infective those with a jejunostomy and those with a jejuno–colic enteritis (e.g. by Clostridium difficile), recurrent disease or an internal entero-enteral fistula may cause a high-output Patients with a jejunostomy have a high-output stoma, stoma. Patients who have suddenly stopped corticosteroids which is apparent immediately after surgery, especially (e.g. after a colectomy for ulcerative colitis) can have acute when the patient starts to take food and drink. There are two adrenal insufficiency, which includes an increase in stomal types of patient with a short bowel and a high-output stoma.
08.00 10.00 12.00 14.0016.00 18.00 20.00 22.0024.00 02.00 04.00 06.00 08.00 Fig. 4. Oral intake (---) and stomal output (
in a patient who has 0·3 m residual jejunum. Note the large net Fig. 3. Types of patient with a short bowel: (a) a jejunostomy; (b) a
secretory response to food and drink. (Redrawn from Nightingale 3K\VLRORJLFDO FRQVLGHUDWLRQV IRU D SDWLHQW ZLWK D  1LJKWLQJDOH HW DO E DQG PD\ VWLOO EH SDODWDEOH (DFK GD\  OLWUHV IRRG DQG GULQN DUH FRQVXPHG 7KLV 'UXJ WKHUDS\ $V VWRPDO RXWSXW LV PDLQO\ LQ UHVSRQVH LQWDNH LV GLOXWHG E\ Â OLWUHV VDOLYD Â OLWUHV JDVWULF WR DQ RUDO LQWDNH GUXJ WKHUDSLHV WR UHGXFH RXWSXW QHHG WR EH MXLFH DQG Â OLWUHV SDQFUHDWLFRELOLDU\ VHFUHWLRQV VR WKDW JLYHQ LQ WKH GD\WLPH EHIRUH IRRG $QWLGLDUUKRHDO GUXJV  OLWUHV FK\PH SDVV WKH GXRGHQR±MHMXQDO IOH[XUH HDFK GD\ ORSHUDPLGH DQGRU FRGHLQH SKRVSKDWH PD\ EH JLYHQ Â K 6SLOOHU  7KHVH VHFUHWLRQV FRQVWLWXWH EHIRUH IRRG WR VORZ JDVWURLQWHVWLQDO WUDQVLW DQG DOORZ PRUH PRVW RI WKH VWRPDO RXWSXW IURP D QHW µVHFUHWRU¶ DQG WKHUH WLPH IRU DEVRUSWLRQ /RSHUDPLGH ± PJ LV XVHG LQ SUHI LV OLWWOH RXWSXW DW QLJKW )LJ  1LJKWLQJDOH HW DO  HUHQFH WR FRGHLQH SKRVSKDWH DV LW LV QRW VHGDWLQJ LV QRW 7KH FRQFHQWUDWLRQ RI 1D LQ VPDOO ERZHO IOXLG LV DERXW DGGLFWLYH DQG GRHV QRW LPSDLU SDQFUHDWLF IXQFWLRQ 7\WJDW HW DO  /RSHUDPLGH FLUFXODWHV WKURXJK WKH HQWHUR 7KHUH DUH LPSRUWDQW SK\VLRORJLFDO IHDWXUHV VSHFLILF WR KHSDWLF FLUFXODWLRQ ZKLFK LV GLVUXSWHG LQ SDWLHQWV ZLWK D WKH MHMXQXP QRW SUHVHQW LQ WKH LOHXP 7KH LQWHUFHOOXODU VKRUW ERZHO VR WKDW KLJK GRVHV PD\ EH QHHGHG 2FFDVLRQDOO\ MXQFWLRQV LQ WKH MHMXQXP DUH OHDN\ DQG WKXV MHMXQDO FRQWHQWV LW LV EHQHILFLDO WR DGG FRGHLQH SKRVSKDWH ± PJ WR FDQ RQO\ EH LVRRVPRODU ZLWK SODVPD +RZHYHU WKHUH LV DQ ORSHUDPLGH WUHDWPHQW 7KHVH GUXJV DUH JLYHQ WR DOO W\SHV RI DFWLYH SXPS WKDW WUDQVSRUWV JOXFRVH DQG 1D WRJHWKHU LQWR WKH FHOOV 7UDQVLW WKURXJK WKH MHMXQXP LV IDVWHU WKDQ WKDW WKURXJK $QWLVHFUHWRU\ GUXJV KRZHYHU DUH JHQHUDOO\ RQO\ WKH LOHXP RU FRORQ 7KH MHMXQXP GRHV QRW DEVRUE ELOH VDOWV RU HIIHFWLYH ZKHQ WKH VWRPDO RXWSXW H[FHHGV WKH RUDO LQWDNH LH LQ QHW µVHFUHWRUV¶ $Q RUDO SURWRQ SXPS LQKLELWRU RPHSUD]ROH  PJ GDLO\ 1LJKWLQJDOH HW DO E -HSSHVHQ HW DO  KLJKGRVH KLVWDPLQH UHFHSWRU W\SH  DQWDJRQLVWV HJ 7UHDWPHQWV IRU D SDWLHQW ZLWK D KLJKRXWSXW VWRPD UDQLWLGLQH  PJ EHIRUH EUHDNIDVW DQG VXSSHU DQG RFWUHRWLGH D VRPDWRVWDWLQ DQDORJXH PD\ EH KHOSIXO 7DEOH  7R HVWDEOLVK K\GUDWLRQ WKH SDWLHQW LV NHSW QLO E\ PRXWK DQG 2FWUHRWLGH LV XVXDOO\ QHHGHG LI WKHUH LV LQVXIILFLHQW ERZHO WR LQWUDYHQRXV VDOLQH  J 1D&OO ZLWK RU ZLWKRXW 0J LV JLYHQ WR UHVWRUH K\GUDWLRQ DQG UHGXFH WKLUVW ,Q DGGLWLRQ WKH SDWLHQW¶V VWRPDO ORVVHV HVSHFLDOO\ WKDW RI 1D  PPROO PXVW EH UHSODFHG 7KH PDQDJHPHQW WKDW ZLOO EH RXWOLQHG LV LPSRUWDQW ZKHQ D SDWLHQW UHVXPHV DQ RUDO LQWDNH HYHQ LI WKH\ FRQWLQXH WR QHHG SDUHQWHUDO QXWULWLRQ DQG VDOLQH DQG ZLOO UHGXFH WKH YROXPH RI VWRPDO RXWSXW DQG WKH DPRXQW RI SDUHQWHUDO VXSSRUW QHHGHG 1LJKWLQJDOH F ,I ZDWHU QR 1D RU DQ\ K\SRWRQLF VROXWLRQ LV WDNHQ RUDOO\ 1D ZLOO GLIIXVH LQWR WKH LQWHVWLQDO OXPHQ WR JLYH D OXPHQ FRQFHQWUDWLRQ RI DSSUR[LPDWHO\  PPROO 7KLV 1D LV QRW UHDEVRUEHG DQG LV WKHUHIRUH ORVW YLD WKH VWRPD 7KH DGPLQ LVWUDWLRQ RI K\SRWRQLF IOXLG LV GHWULPHQWDO DV LW LQFUHDVHV 1D ORVVHV 1HZWRQ HW DO  5RGULJXHV HW DO  7KH :RUOG +HDOWK 2UJDQL]DWLRQ FKROHUD VROXWLRQ $YHU\ 6Q\GHU   J JOXFRVH Â J 1D&O DQG Â J 1D+&2 RU Â J VRGLXP FLWUDWH LQ  OLWUH WDS ZDWHU VLSSHG GXULQJ WKH GD\ FROG ZLWK RU ZLWKRXW IODYRXULQJ FDQ UHGXFH 1D ORVVHV :KLOH WKLV :RUOG +HDOWK 2UJDQL]DWLRQ VROXWLRQ ZLWKRXW . )LJ  'DLO\ PHDQ RI  G LQWHVWLQDO VRGLXP EDODQFH LQ VL[ SDWLHQWV KDV D 1D FRQFHQWUDWLRQ RI  PPROO DQG LV FRPPRQO\ ZLWK D MHMXQRVWRP\ XQGHUJRLQJ GLIIHUHQW WUHDWPHQWV WR UHGXFH VRGLXP JLYHQ EDODQFH VWXGLHV VXJJHVW WKDW D 1D FRQFHQWUDWLRQ RI ORVVHV 9DOXHV DUH PHDQV ZLWK WKHLU VWDQGDUG HUURUV UHSUHVHQWHG E\  PPROO JLYHV RSWLPXP 1D DEVRUSWLRQ 5RGULJXHV HW DO YHUWLFDO EDUV 5HGUDZQ IURP 1LJKWLQJDOH HW DO E 7DEOH  7ULDOV RI RFWUHRWLGH LQ SDWLHQWV ZLWK D MHMXQRVWRP\ VF 6XEFXWDQHRXV LY LQWUDYHQRXV EG WZLFH GDLO\ WGV WKUHH WLPHV GDLO\ /LTXLG PHDO RWKHU VWXGLHV LQYROYHG QRUPDO PHDOV absorb a proton pump inhibitor (approximately < 0·5 m large molecules of low osmolality are given (polypeptides, polysaccharides and long-chain triacylglycerols) and extra Fludrocortisone may be effective in reducing stomal output if some terminal ileum remains, as it can directly increase ileal Na absorption (Levitan & Goulston, 1967; advantage as water and electrolytes can be absorbed against Goulston et al. 1963; Kramer & Levitan, 1972).
a concentration gradient, it ferments carbohydrate, slows gastrointestinal transit and promotes adaptive changes.
precarious Mg balance mainly as a result of Na depletion A diet high in polysaccharides, although bulky, is and secondary hyperaldosteronism (Fig. 6). Initially, salt encouraged as the carbohydrate is fermented in the colon and water depletion (and thus secondary hyperaldos- to produce short-chain fatty acids, which when absorbed teronism) are treated, then an oral Mg compound (usually provide a source of energy (Nordgaard et al. 1994; Table 2).
three MgO (4 mmol) capsules at night) is given. If these A diet rich in polysaccharides needs to be of a considerable measures fail, 1-α-hydroxycholecalciferol may be given size (after the ‘malabsorption factor’ has also been taken into (Selby et al. 1984) in gradually-increasing doses, ensuring account). However, as these patients are often fastidious that hypercalcaemia does not occur. Regular Mg infusions, eaters who quickly feel satiated, such a diet is rarely practical.
usually with saline, may be necessary.
A diet rich in mono- and oligosaccharides can occasionally cause D(−)-lactic acidosis. Lactic acid produced by man is the through the stoma occurs only when < 0·50 m jejunum L(+)-isomer; however, abnormal bacterial or fungal coloni- remains (Nightingale et al. 1990). A low serum K level may zation of the colon may form the D(−)-isomer, which after be consequent upon secondary hyperaldosteronism (Night- absorption cannot be metabolized and can cause ataxia, ingale, 2001b) resulting from Na depletion and, thus, large blurred vision, ophthalmoplegia and nystagmus. D(−)-lactic urinary K losses. It may also occur secondary to Mg acidosis is suspected when these symptoms occur and a depletion. Thus, K does not usually need to be given, but Nadepletion and hypomagnesaemia should be corrected.
Table 2. Energy absorption in patients with a short bowel given three
diets, each for 3 d (Nordgaard et al. 1994) Dietary advice, oral or enteral nutritional support for These patients malabsorb 30–60 % of the oral or enteral nutrition given and this ‘malabsorption factor’ needs to betaken into account and more energy than normal consumed.
To keep up with these losses an enteral feed may be given at night to utilize the gut at a time when it is usually inactive.
A patient with a jejunostomy needs a diet or feed that is isosmolar (300 mOsm/kg) and has a Na concen- Mean value was significantly higher than that for the low-carbohydrate diet for tration of about 100 mmol/l. To achieve this requirement the jejunum–colon group: ***P < 0·001.
Fig. 6. Diagram showing the reasons for hypomagnesaemia in patients with a jejunostomy.
(↓), Decreased.
patient has a metabolic acidosis with a large anion gap.
twice daily was given subcutaneously to eight patients with Treatment consists of giving broad-spectrum antibiotics 0·30–1·7 m small bowel remaining (six with Crohn’s disease, (neomycin or vancomycin) and thiamine, and changing the four with home parenteral nutrition) for 35 d. Balance studies diet to one that is high in polysaccharides but low in mono- (3 d) using identical diets showed increases in mean daily and oligosaccharides (Editorial, 1990).
energy absorption of 0·44 MJ (106 kcal; P = 0·09), mean Unabsorbed non-esterified fatty acids resulting from daily wet weight absorption of 0·42 kg (P = 0·04) and solid triacylglycerol digestion cause problems within the colon, as gastric emptying time for 50 % of the meal of 30 min they reduce colonic water and Na absorption, increase the (P = 0·002; Jeppesen et al. 2001). Other growth factors colonic transit rate, are toxic to bacteria (so reducing the include epidermal growth factor, which has been used for amount of carbohydrate fermented) and bind divalent children with necrotising enterocolitis or microvillus atrophy cations (Ca and Mg), thus increasing their loss in the stools.
(Walker-Smith et al. 1985; Sullivan et al. 1991), and amino- A low-fat diet is theoretically ideal as it will reduce guanidine, an inhibitor of polyamine breakdown that has diarrhoea and malodorous steatorrhoea, but fat yields twice been used in animal studies (Rokkas et al. 1990).
as much energy as comparable weights of carbohydrate and makes food palatable, thus cannot be excessively restricted.
induce functional adaptation by giving peptide YY analogues Medium-chain triacylglycerols are an alternative source of energy that can be absorbed in the colon (Jeppesen &Mortensen, 1998).
Calcium oxalate renal stones occur in 25 % of patients with a retained colon (Nightingale et al. 1992a) because of A new definition of intestinal failure that includes reference increased colonic absorption of dietary oxalate. This situ- to water and electrolytes has been given and the severity of ation results in increased oxalate excretion in the urine intestinal failure graded according to the route by which where it may precipitate. The increased colonic absorption nutrients and fluid are given. An aim in the management of oxalate is partly the result of free unabsorbed fatty of patients with intestinal failure is to reduce its severity.
acids preferentially binding to Ca, which allows oxalate to Acute intestinal failure in the peri-operative period may be become soluble and hence absorbed. Other mechanisms prevented or its duration reduced by avoiding the adminis- include: unabsorbed bile salts directly increasing colonic tration of excessive intravenous saline. A patient with a high- permeability to oxalate; Oxalobacter formigenes, a species output small bowel stoma should restrict oral hypotonic of bacteria that normally metabolize oxalate within the fluids; serum Mg and random urinary Na concentrations colon, may be absent or present in small numbers; urinary should be monitored. The severities of intestinal failure can citrate, which prevents initial nucleation of calcium oxalate, be reduced in terms of water and electrolyte requirements by may be present in a reduced concentration. The formation of careful fluid balance management and the judicial use of calcium oxalate stones is prevented by advice about a low- drugs. The severity of intestinal failure in terms of macro- oxalate diet (avoid rhubarb, spinach, beetroot, peanuts and nutrient requirements is rarely markedly altered by dietary or excessive amounts of tea), reducing or avoiding excess fat in enteral feeding adjustments or the use of growth factors.
the diet, taking oral Ca supplements or a Ca-containingorganic marine hydrocolloid and/or cholestyramine (to bindbile salts; Tomson, 2001).
References
In patients with a colon the absorption of nutrients and Avery ME & Snyder JD (1990) Oral therapy for acute diarrhoea.
minerals may continue to improve for 2 years (Gouttebel The underused simple solution. New England Journal of Medicine 323, 891–894.
Carbonnel F, Cosnes J, Chevret S, Beaugerie L, Ngo Y, Malafosse M, Parc R, Le Quintrec Y & Gendre JP (1996) The role of New treatments to increase energy absorption anatomic factors in nutritional autonomy after extensive small Most new treatments have been aimed at increasing nutrient bowel resection. Journal of Parenteral and Enteral Nutrition 20,
Carlson G (2001) Surgical causes and management. In Intestinal Failure, pp. 39–49 [JMD Nightingale, editor]. London: conjugated bile acid resistant to bacterial deconjugation and dehydroxylation that does not itself cause diarrhoea, Crenn P, Coudray-Lucas C, Thuillier F, Cynober L & Messing B has been given to patients with and without a retained (2000) Postabsorptive plasma citrulline concentration is a marker functioning colon (Gruy-Kapral et al. 1999; Heydorn et al.
of absorptive enterocyte mass and intestinal failure in humans.
1999). Taking 4 g three times daily increased fat absorption Gastroenterology 119, 1496–1505.
from 1·4 MJ/d to 2·2 MJ/d without affecting carbohydrate or Editorial (1990) The colon, the rumen, and D-lactic acidosis. Lancet protein absorption (Heydorn et al. 1999); however, this 336, 599–600.
increase in energy absorption was not enough to change the Fleming CR & Remington M (1981) Intestinal failure. In Nutrition and the Surgical Patient, pp. 219–235 [GL Hill, editor]. NewYork: Churchill Livingstone.
Goulston K, Harrison DD & Skyring AP (1963) Effect of mineralo- hypertrophy of the jejunal mucosa. The initial enthusiasm for corticoids on the sodium/potassium ratio of human ileostomy combined treatment with growth hormone, glutamine and fluid. Lancet ii, 541–543.
fibre has waned (Scolapio et al. 1997; Szkudlarek et al.
Gouttebel MC, Saint Aubert B, Colette C, Astre C, Monnier LH & 2000). Synthetic glucagon-like peptide 2 at a dose of 400 µg Joyeux H (1989) Intestinal adaptation in patients with short bowel syndrome. Measurement by calcium absorption. Digestive Nightingale JMD, Lennard-Jones JE, Walker ER & Farthing MG Diseases and Sciences 34, 709–715.
(1990) Jejunal efflux in short bowel syndrome. Lancet 336,
Gruy-Kapral C, Little KH, Fortran JS, Meziere TL, Hagey LR & Hofmann AF (1999) Conjugated bile acid replacement therapy Nightingale JMD, Lennard-Jones JE, Walker ER & Farthing MJG for short-bowel syndrome. Gastroenterology 116, 15–21.
(1992b) Oral salt supplements to compensate for jejunostomy Heydorn S, Jeppesen PB & Mortensen PB (1999) Bile acid losses: comparison of sodium chloride capsules, glucose replacement therapy with cholylsarcosine for short-bowel electrolyte solution and glucose polymer electrolyte solution syndrome. Scandinavian Journal of Gastroenterology 34,
(Maxijul). Gut 33, 759–761.
Nightingale JMD & Spiller RC (2001) Normal intestinal Jeppesen PB, Hartmann B, Thulesen J, Graff J, Lohmann J, Hansen anatomy and physiology. In Intestinal Failure, pp. 15–36 BS, Tofteng F, Poulsen SS, Madsen JL, Holst JJ & Mortensen PB [JMD Nightingale, editor]. London: Greenwich Medical Media (2001) Glucagon-like peptide 2 improves nutrient absorption and nutritional status in short bowel patients with no colon.
Nightingale JMD, Walker ER, Burnham WR, Farthing MJG & Gastroenterology 120, 806–815.
Lennard-Jones JE (1989) Octreotide (a somatostatin Jeppesen PB & Mortensen PB (1998) The influence of a preserved analogue) improves the quality of life in some patients with a colon on the absorption of medium chain fat in patients with short intestine. Alimentary Pharmacology and Therapeutics 3,
small bowel resection. Gut 43, 478–483.
Jeppesen PB, Staun M, Tjellesen L & Mortensen PB (1998) Effect Nightingale JMD, Walker ER, Farthing MJG & Lennard-Jones JE of intravenous ranitidine and omeprazole on intestinal absorption (1991b) Effect of Omeprazole on intestinal output in the short of water, sodium, macronutrients in patients with intestinal bowel syndrome. Alimentary Pharmacology and Therapeutics 5,
resection. Gut 43, 763–769.
Kennedy JF, Baker ML & Nightingale JMD (2002) Appropriate Nordgaard I, Hansen BS & Mortensen PB (1994) Colon as a parenteral nutrition – the role of the hospital nutrition support digestive organ in patients with short bowel. Lancet 343,
team. Clinical Nutrition 21, Suppl. 1, 35.
Kramer P & Levitan R (1972) Effect of 9 α-fluorohydrocortisone O’Keefe SJD, Peterson ME & Fleming R (1994) Octreotide as an on the ileal excreta of ileostomized subjects. Gastroenterology adjunct to home parenteral nutrition in the management of 62, 235–241.
permanent end-jejunostomy syndrome. Journal of Parenteral Ladefoged K, Christensen KC, Hegnhoj J & Jarnum S (1989) Effect and Enteral Nutrition 18, 26–34.
of a long acting somatostatin analogue SMS 201–995 on Powell-Tuck J, Martin J, Domizio P & Wingate D (2001) Small jejunostomy effluents in patients with severe short bowel bowel dysfunction. In Intestinal Failure, pp.123–139 [JMD syndrome. Gut 30, 943–949.
Nightingale, editor]. London: Greenwich Medical Media Lemann M, de Montigny S, Mahé S, Thuillier F, Huneau JF, Tomé D, Rambaud J-C & Messing B (1993) Effect of octreotide on Rodrigues CA, Lennard-Jones JE, Thompson DG & Farthing MJG water and electrolytes losses, nutrient absorption and transit in (1988) What is the ideal sodium concentration of oral short bowel syndrome. European Journal of Gastroenterology rehydration solutions for short bowel patients? Clinical Science and Hepatology 5, 817–822.
74, Suppl. 18, 69.
Levitan R & Goulston K (1967) Water and electrolyte content of Rodrigues CA, Lennard-Jones JE, Walker ER, Thompson DG human ileostomy fluid after d-aldosterone administration.
& Farthing MJG (1989) The effects of octreotide, soy Gastroenterology 52, 510–512.
polysaccharide, codeine and loperamide on nutrient, fluid and Lobo DN, Bostock KA, Neal KR, Perkins AC, Rowlands BJ & electrolyte absorption in the short bowel syndrome. Alimentary Allison SP (2002) Effect of salt and water balance on recovery of Pharmacology and Therapeutics 3, 159–169.
gastrointestinal function after elective colonic resection: a Rokkas T, Vaja S, Murphy GM & Dowling RH (1990) Amino- randomized controlled trial. Lancet 359, 1812–1818.
guanidine blocks intestinal diamine oxidase (DAO) activity and Newton CR, Gonvers JJ, McIntyre PB, Preston DM & Lennard- enhances the intestinal adaptive response to resection in the rat.
Jones JE (1985) Effect of different drinks on fluid and electrolyte Digestion 46, Suppl. 2, 447–457.
losses from a jejunostomy. Journal of the Royal Society of Scolapio JS, Camilleri M, Fleming CR, Oenning LV, Burton DD, Medicine 78, 27–34.
Sebo TJ, Batts KP & Kelly DG (1997) Effect of growth Nightingale JMD (editor) (2001a) Introduction. Definition and hormone, glutamine, and diet on adaptation in short-bowel classification of intestinal failure. In Intestinal Failure, pp.
syndrome: a randomized, controlled study. Gastroenterology 113,
xix–xx. London: Greenwich Medical Media Limited.
Nightingale JMD (editor) (2001b) The short bowel. In Intestinal Selby PL, Peacock M & Bambach CP (1984) Hypomagnesaemia Failure, pp. 177–198. London: Greenwich Medical Media after small bowel resection: treatment with 1 alpha-hydroxylated vitamin D metabolites. British Journal of Surgery 71, 334–337.
Nightingale JMD (editor) (2001c) Management of a high output Steward W, Hunter A, O’Byrne K & Snowden J (2001) Chemo- jejunostomy. In Intestinal Failure, pp. 375–392. London: therapy and haemopoietic stem cell transplantation. In Intestinal Failure, pp. 65–86 [JMD Nightingale, editor]. London: Nightingale JMD, Bartram CI & Lennard-Jones JE (1991a) Length of residual small bowel after partial resection: Correlation Sullivan PB, Brueton MJ, Tabara ZB, Goodlad RA, Lee CY & between radiographic and surgical measurements. Gastro- Wright NA (1991) Epidermal growth factor in necrotising intestinal Radiology 16, 305–306.
enteritis. Lancet 338, 53–54.
Nightingale JMD, Lennard-Jones JE, Gertner DJ, Wood SR & Szkudlarek J, Jeppesen PB & Mortensen PB (2000) Effect of Bartram CI (1992a) Colonic preservation reduces the need for high dose growth hormone with glutamine and no change in parenteral therapy, increases the incidence of renal stones but diet on intestinal absorption in short bowel patients: a does not change the high prevalence of gallstones in patients with randomised, double blind, crossover, placebo controlled study.
a short bowel. Gut 33, 1493–1497.
Gut 47, 199–205.
Tomson CRV (2001) Nephrocalcinosis and nephrolithiasis. In Walker-Smith JA, Phillips AD, Walford N, Gregory H, Intestinal Failure, pp. 227–242 [JMD Nightingale, editor].
Fitzgerald JD, MacCullagh K & Wright NA (1985) Intravenous London: Greenwich Medical Media Limited.
epidermal growth factor/urogastrone increases small-intestinal Tytgat GN, Huibregtse K, Dagevos J & van den Ende A (1977) cell proliferation in congenital microvillous atrophy. Lancet ii,
Effect of loperamide on fecal output and composition in well- established ileostomy and ileorectal anastomosis. Digestive
Diseases 22, 669–676.

Source: http://www.luzimarteixeira.com.br/wp-content/uploads/2009/09/artigo12-nutricao.pdf