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Effects of massive small bowel resection 

Effects of massive small bowel resection
Chapter:
Effects of massive small bowel resection
Author(s):

R.J. Playford

DOI:
10.1093/med/9780199204854.003.151007_update_001

February 27, 2014: This chapter has been re-evaluated and remains up-to-date. No changes have been necessary.

Update:

Management—use of glucagon-like peptide 2 analogues to stimulate bowel adaptation; emphasis on importance of psychological support and attention to fluid/electrolyte balance; expanded notes on small bowel transplantation.

Updated on 30 May 2013. The previous version of this content can be found here.
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Essentials

Major vascular events involving the superior mesenteric artery and Crohn’s disease are two of the main reasons for adults requiring massive intestinal resection. The ability of the residual bowel to adapt after resection varies greatly between patients, with factors influencing the ability to absorb nutrients being (1) the extent and site of resection, (2) the condition of the remaining intestine, (3) the presence of the ileocaecal valve, and (4) the function of other digestive organs.

Clinical problems are more likely to occur following large resections that include most of the ileum and include diarrhoea, fluid, and electrolyte imbalance, malnourishment (protein–energy malnutrition, mineral and vitamin deficiencies), gallstones, and renal stones.

In the initial postoperative period management requires assiduous fluid and electrolyte replacement, with many patients requiring parenteral nutritional supplements while the residual bowel adapts. Oral nutrition, initially consisting of elemental or polymeric diets administered by nasogastric or enteral tube feeding, should ideally be started within the first few days of surgery. Subsequently, small-volume, frequent, solid or semisolid meals with low fat and oxalate content should be introduced. Oral multivitamin and mineral supplements are needed; vitamin B12 injections are required following terminal ileum resection; regular long-term monitoring of fat-soluble vitamins (A, K, and D), vitamin B12, folate, magnesium, zinc, and bone status monitoring is required. Anti-peristaltic drugs are usually required. Growth factor administration, especially GLP-2 analogues, may stimulate bowel adaptation. Long-term intravenous nutrition is sometimes needed. Small bowel lengthening or transplantation is considered for some patients.

Aetiology and prevention

Two of the main reasons why adults require massive intestinal resection are major vascular events involving the superior mesenteric artery, usually thrombosis or embolus, or multiple surgical resections of the small bowel in patients with Crohn’s disease (regional ileitis). Additional causes include intestinal volvulus, mesenteric venous thrombosis and surgery for desmoid tumours. Surgical intervention for vascular catastrophes is usually unavoidable. In regards to Crohn’s disease, the use of biological therapies such as antitumour necrosis factor alpha (anti-TNFα‎) antibodies has had a major impact in inducing remission in severe cases and reduced the number of surgical procedures required. Nevertheless, operative interventions may still be required and as this is a lifelong recurrent disease, it is imperative that the minimum amount of bowel is resected. Stricturoplasty, rather than resection, may be possible and multiple small segments of relatively normal intestine should be retained in situ and joined in series, rather than removed. Preservation of only a few additional centimetres of gut may be enough to allow the patient to be maintained on oral rather than parenteral nutrition.

The principal conditions requiring massive resection in children include segmental volvulus in the prenatal period and necrotizing enterocolitis postnatally. Rarer causes affecting all ages include trauma, retroperitoneal tumours, radiation enteritis, and strangulation, mainly resulting from adhesions.

Physiology

Although digestion and absorption of water, electrolytes, and nutrients occurs throughout the small intestine, there are regional differences. Regional functions of the jejunum include iron and folate absorption and disaccharide digestion and, in combination with the duodenum, the production of cholecystokinin and secretin.

The ileum is the principal site for absorption of vitamin B12 and bile salts and, in contrast to the jejunum, is capable of absorbing sodium against a steep gradient. It also plays a key role, in combination with the proximal colon, in mediating the ‘ileal brake’, in which intestinal transit and secretions are reduced when nutrients reach the terminal small bowel. Hormones, particularly peptide tyrosine tyrosine (peptide YY), probably mediate this phenomenon.

Factors, including adaptation, that influence the metabolic consequences of massive resection

The ability of the residual bowel to adapt after resection varies greatly between patients; it influences the development of symptoms and may determine the long-term requirement for parenteral nutrition. Four main factors influence the patient’s ability to absorb nutrients:

  • Extent and site resected. The length of the small intestine varies between individuals. In general, patients with an intact duodenum but less than 50 cm of additional small bowel if the colon is in situ, or less than 100 cm if the colon has been removed, will require long-term total parenteral nutrition. Conversely, a requirement for parenteral nutrition is unlikely if more than 25% of the small bowel remains.

  • Condition of the remaining intestine. The capacity of the residual bowel to adapt postoperatively is influenced by any underlying condition. Patients in which the residual bowel is damaged or abnormal due to conditions such as Crohn’s disease or radiation enterocolitis are more likely to have metabolic disturbances.

  • Presence of the ileocaecal valve. Removal of the ileocaecal valve has a major impact on subsequent clinical progress and troublesome watery diarrhoea that compounds malabsorption is frequent. Factors contributing to this include faster intestinal transit, possibly related to loss of the ileal brake mechanism, and a much higher likelihood of bacterial overgrowth.

  • Function of other digestive organs. Pancreatic hypofunction, resulting from malnutrition and reduced hormonal stimulation, may exacerbate fat malabsorption; this is sometimes compounded by gastric hypersecretion that inactivates pancreatic enzymes in the lumen.

Pathophysiology

Because regional differences in the function of the small intestine exist, the clinical sequelae of resection vary according to the site removed. Resection of most of the jejunum can usually be compensated for by the distal bowel, and the consequences of proximal resections are usually slight. Patients may experience iron and folic acid deficiency as well as lactose intolerance, resulting in abdominal bloating and watery diarrhoea.

Clinical problems are more likely to occur following large resections that include most of the ileum. Intractable (cholerheic) diarrhoea, often with steatorrhoea, and consequential metabolic abnormalities including vitamin B12 deficiency occur.

Diarrhoea

This is probably the most troubling symptom. Multiple factors are involved in its aetiology (Table 15.10.7.1):

  • Decreased transit time due to the reduced length of bowel and alteration in the control of its motility.

  • Increased luminal osmolality, partly due to reduced absorption of lactose and other carbohydrates, which are then metabolized by colonic bacteria. Severe metabolic (lactic) acidosis may develop—the increased anion gap being due to the microbial generation of d-lactate.

  • Disruption of the enterohepatic circulation of bile salts reduces the total body pool of bile salts. This is initially compensated for by a homeostatic up-regulation of bile salt production by the liver. Increased delivery of bile salts into the colon, however, stimulates colonic adenylate cyclase activity, increasing colonic secretion of water and electrolytes, resulting in watery diarrhoea sometimes termed cholerheic diarrhoea.

  • If most of the ileum has been removed, the compensatory up-regulation of bile salt production may be insufficient to balance losses. This leads to decreased micelle formation in the lumen of the small bowel with a resultant reduction in absorption of water-insoluble fatty acids, causing the patient to have steatorrheic diarrhoea. Resection of the terminal 100 cm of ileum is typically associated with clinically significant malabsorption of bile salts. The presence of excess α‎-hydroxy fatty acids derived from bacterial metabolism in the colonic lumen stimulates adenylate cyclase, further increasing secretion of fluids and electrolytes.

  • In massive intestinal resections, the reduced micellar solubilization of fat and consequential impairment of lipolysis is compounded by the loss of absorptive mucosa, thus aggravating the effects of maldigestion and fluid loss.

Table 15.10.7.1 Aetiology and therapy of diarrhoeal symptoms

Condition

Mechanism, effect

Potential therapy

Shortened bowel

Reduced time and surface for absorption

Antiperistaltic drugs, GLP-2 analogues

Lactose intolerance

Reduced mucosal surface area and lactase, increases luminal osmolality

Reduce dietary dairy products

Bile salt diarrhoea

Increased bile salts in colon stimulates fluid secretion

Bile salt sequestrants

Steatorrhoea

Bile salt deficiency, fatty acids stimulate colonic secretion and contractility, reducing transit time

Reduce fat intake, pancreatic supplements

Pancreatic hyposecretion

Malnutrition, exacerbates steatorrhea

Maintain nutritional support

Gastric hypersecretion

Increases gastric fluid secretion and inactivates pancreatic enzymes

Acid suppressants

Stones

Gallstone formation is two to three times more common after ileal resection and the stones may be of the cholesterol-rich or pigment type. Reduced concentrations of bile salts within the bile due to depletion of the body pool of bile salts, in combination with gallbladder hypomotility, facilitate the formation of cholesterol crystals.

Renal stones (usually calcium oxalate) commonly result from increased absorption of oxalate and hyperoxaluria. The availability of free oxalate within the colon is increased by excessive complexation of calcium by fatty acids which normally promote formation of insoluble (nonabsorbable) calcium oxalate. Although concentrations of bile salts in the small intestine may be reduced, the failure to reabsorb bile salts in the ileum increases luminal bile salts in the colon; this increases colonic permeability and further promotes oxalate absorption.

Gastric hypersecretion

This phenomenon occurs in some patients, although its severity tends to lessen over time. Hyperacidity may inactivate pancreatic enzymes by precipitating bile salts and lowering intraduodenal pH as in Zollinger–Ellison syndrome.

Nutritional status

Many patients undergoing resections will be malnourished preoperatively and energy consumption increases in the immediate postoperative period. If not appropriately managed, long-term protein–energy malnutrition as well as life-threatening mineral and vitamin deficiencies develop.

Adaptation

Morphological and functional adaptive changes follow resection of the small intestine. The residual bowel undergoes mucosal hyperplasia and its capacity to absorb fluids and nutrients increases over a period of weeks or months. The molecular events that underlie these changes are unclear but may include circulating trophic factors and growth factors present in pancreatic juice or secreted into the intestinal lumen. Early intervention is required to achieve maximal adaptation, and maintenance of a supply of luminal nutrients is a prerequisite for the adaptive changes. It is therefore important that luminal feeding is started as early as possible after surgery even if the patient also requires parenteral nutrition.

Management

Initial therapy

In the initial postoperative period, vigilant oversight including vigorous intravenous fluid and electrolyte replacement is required to prevent dehydration and to compensate for intestinal losses. Many patients will also require parenteral nutritional supplements while the residual bowel adapts. Ingestion of water may exacerbate diarrhoea and be counterproductive. The use of an oral isoosmolar saline–glucose solution containing bicarbonate, similar to that used for the treatment of cholera, may often assist in reducing intravenous requirements without increasing intestinal fluid loss.

Nutrition

Oral nutrition, initially consisting of elemental or polymeric diets administered by nasogastric or enteral tube feeding, should ideally be started within the first few days of surgery. The introduction of luminal nutrition tends, however, to exacerbate the diarrhoea. Many high-calorie enteral supplements for use in malnourished patients who have little or no impairment of small intestinal function have a very high osmolality, thereby inducing catastrophic egress of luminal fluid and diarrhoea in patients with large resections. These preparations must be used with great caution or avoided altogether in patients suffering the effects of massive bowel resections. Subsequently, small-volume, frequent, solid or semisolid meals with low fat and oxalate content should be introduced. Low-fat meals and supplements containing large quantities of medium-chain fatty acids tend to be unpalatable. Compliance of patients with dietary advice is therefore best if symptoms are used as a guide to the amount of fat that is included in the diet. Since much of the energy content of the ingested diet may well be lost in the stool, the daily intake of calories often has to be greater than expected. This is best provided in a complex form, including glucose polymers and starch, which have little osmotic effect in the lumen and are hydrolysed rapidly by brush-border hydrolases at the site of absorption. Lactose intolerance, seen particularly in patients following significant jejunal resections, may induce bloating and exacerbation of diarrhoea but usually responds to reduction in lactose-containing dairy products. Low-fibre diets are helpful in some patients although they may aggravate symptoms in others; treatment must be tailored to the individual. Patients should be encouraged to take multivitamin and mineral supplementation at levels two to five times the normal recommended daily requirements; vitamin B12 injections are required following terminal ileum resection. In all patients, regular long-term monitoring of fat-soluble vitamins (A, K, and D), vitamin B12, folate, magnesium, zinc, and bone status is required.

In some patients, although nutritional status can be stabilized via the oral route, additional intravenous fluid and electrolyte supplementation may continue to be required. Where nutrition status is unsustainable via the oral route, long-term intravenous nutrition is needed. These patients should be encouraged to continue oral nutrition, for social and psychological reasons, as well as to minimize the amount of parental nutrition required. Psychological and social support, education in self-directed care and patient engagement in clinical decision making add value for long-term outcome.

Drugs

Effects of massive small bowel resectionMost patients will require antiperistaltic drugs to increase the time of contact between luminal contents and residual bowel. A stepwise approach should be used, starting with agents such as loperamide or codeine phosphate. Long-term administration of the more potent constipating, but potentially addictive, opiates should be used only in intractable cases. Since diarrhoea may be particularly troublesome in the initial postoperative period, liquid or occasionally intravenous formulations may be needed.

Administration of H2-receptor antagonists or proton pump inhibitors may reduce diarrhoea and promote digestion, as well as prevent peptic ulceration, by decreasing gastric secretions and preventing inactivation of pancreatic enzymes. Cholerheic diarrhoeas may respond well to bile acid sequestrants such as cholestyramine, especially in those patients whose colon remains in situ. Its use, however, can worsen the fatty component of diarrhoea by exacerbating the deficiency of bile salts. Similarly, the use of long-acting somatostatin analogues can reduce gastrointestinal secretions and fluid loss but may exacerbate steatorrhea and formation of gallstones. In patients with marked steatorrhea who do not respond to restriction of fat intake, the addition of oral pancreatic enzyme supplements to food may assist lipolysis and improve digestion. Glucagon-like peptide 2 analogues may stimulate additional intestinal adaptation and absorption.

Bacterial overgrowth

Colonization (’overgrowth’) of the small bowel by colonic or pathogenic bacteria results in exacerbation of diarrhoea, malabsorption, and nutritional deficiencies. Culture and analysis of small-bowel aspirates is required for definitive diagnosis but is a moderately invasive procedure. Because results from many of the usual noninvasive tests, e.g. glucose or lactulose hydrogen breath tests, are abnormal in all patients after significant resection, empirical trials of antibiotics may be justified.

Surgical options

In patients with severe intractable diarrhoea further surgery such as longitudinal lengthening may be of value, particularly in paediatric patients. Although not in general clinical use, reversal of a small segment of small bowel can delay gut transit; however, if too long a segment is used, obstruction may occur.

Effects of massive small bowel resectionSmall-bowel transplantation is now available in a limited number of centres. Issues around infection and acute and chronic rejection continue to be problematic, although 5-year survival is now similar to that seen in liver transplant patients. Patients who have undergone intestinal transplantation also have an increased risk of lymphoma. Because of the high morbidity and mortality associated with transplantation, it is usually only offered to patients who cannot be maintained on intravenous nutrition for reasons such as progressive intravenous feeding-induced liver damage. Patients therefore require detailed counselling about the risks of any such procedure.

Future directions

Administration of gut trophic factors, such as hepatocyte growth factor, epidermal growth factor, and growth hormone (possibly in combination with glutamine supplements) may increase the rate and extent of mucosal adaptation that occurs in the intestine. A glucagon-like peptide 2 analogue is now clinically licensed in the European Union. These are, however, unlikely to be a panacea: side effects, such as fluid retention, are not uncommon and adaptive changes seem to rapidly disappear when treatment is stopped, meaning that such therapies may be required lifelong. In patients who prove not to adapt adequately, continuing advances in techniques for gut lengthening, small-bowel transplantation and in antirejection therapy offers future hope. In the longer term, advances in tissue engineering technology may allow intestinal mucosa to be obtained from humanized animal gut or to be reconstituted in culture from the patient’s own residual bowel, thereby removing the problems of rejection and immunosuppression.

Further reading

Orlando G, et al. (2012). Cell and organ bioengineering technology as applied to gastrointestinal diseases. Gut, Jan 20. [Epub ahead of print.]Find this resource:

    Thompson JS, et al. (2012). Current management of short bowel syndrome. Curr Probl Surg, 49, 52–115. [An extensive review of the area with good illustrations of surgical procedures.]Find this resource: