MEDICAL HISTORY AND PHYSICAL EXAMINATION

Reading a patient’s chart, taking a history, and performing a physical examination allows a good understanding of a patient’s disease status and allows the diagnosis of some nutritional deficiencies. Inquiries regarding a patient’s usual body weight (UBW) versus ideal (IBW) or present body weight (PBW) should be noted at the initial patient encounter because these values have been shown in a number of studies to be predictors of morbidity and mortality.^1,2 Although a simple tool, the most sensitive marker of nutritional risk is the percentage deviation from UBW over the past three to six months.

ANTHROPOMORPHIC MEASUREMENTS

Anthropomorphic measurements allow the estimation of body composition or body stores of energy using relatively simple and inexpensive equipment such as hand-held calipers (Fig. 5-1) and scales. Hand-held calipers allow measurement of a patient’s triceps skinfold (TSF), a marker of body fat stores, and midarm muscle circumference (MAMC), a marker of body protein stores. These measurements are compared with standardized tables to obtain percentages of normal values. Loss of body stores of protein (e.g., reduced MAMC) has been associated with poor patient outcomes.

Figure 5-1. Hand-held calipers. This device helps determine body stores of protein or fat.

Because of the obesity epidemic, emphasis has been placed on evaluating a patient’s weight and body habitus using the body mass index (BMI), which is defined as weight (in kilograms)/height (in meters squared). BMI values help categorize patients as underweight, normal weight, overweight, and obese (see Table 4-18).

BIOCHEMICAL MEASUREMENTS

The plasma proteins albumin, prealbumin, and transferrin are widely used to assess nutritional status. Albumin has been overrated as a predictor of protein malnutrition and, because it has a half-life of 21 days, it is a poor indicator of protein malnutrition. Infections, chronic medical conditions, liver disease, acute physiologic changes, and medications affect serum albumin levels through mechanisms not related to protein malnutrition.³ Low serum albumin levels (<3.5 g/dL) on hospital admission have been correlated with poor prognosis and poor surgical outcome.⁴

Prealbumin has been thought to be a better laboratory marker of nutritional status because of its two-day half-life. Prealbumin often is used by nutrition support teams to assess the adequacy of ongoing nutrition therapy; however, the reliability of prealbumin as a marker of malnutrition has not been validated. Transferrin also has been used to evaluate a patient’s nutritional status because it resides almost completely within the intravascular space and has a half-life of seven days. It is, however, affected by iron deficiency, iron overload, pernicious anemia, and infection. There are no data validating its use as a marker of nutritional status.

IMMUNOLOGIC TESTS

The serum total lymphocyte count has been correlated with changes in nutritional status, especially protein depletion.⁵ However, no prospective study has shown this to be a reliable marker of a patient’s nutritional status.

MUSCLE FUNCTION

An effective tool to evaluate a patient’s nutritional status over time is to measure his or her endurance or muscle strength. A practical method of assessing muscle strength involves hand grip strength,⁶ which is proportional to forearm lean muscle mass (Fig. 5-2). The reliability of this test is reduced for patients who are acutely ill or have hand or arm motor abnormalities.

Figure 5-2. Hand-grip dynamometer. This device measures muscle strength and therefore body protein stores.

GLOBAL ASSESSMENTS

To date, there is no single tool that is an accurate predictor of nutritional status. A variety of validated nutrition scoring systems, incorporating a number of features of the patient’s medical history and physical examination, has been developed to assess nutritional status. One of these, the subjective global assessment (SGA), is a comprehensive nutritional assessment tool that incorporates weight changes, dietary intake, functional capacity and preliminary medical diagnosis to categorize patients as well-nourished, moderately malnourished, or severely malnourished (see Table 4-24).⁷ The SGA has been validated in the oncology population.⁸ Other global nutritional assessment tools include the prognostic nutritional index (PNI), the instant nutritional assessment (INA), the Mini-Nutritional Assessment, the malnutrition universal screening tool, the nutritional risk score, and the nutritional risk index.⁹

RESEARCH AND INVESTIGATIONAL TOOLS

Densitometry, isotope measurements, electric impedance testing, infrared refractance, and absorptiometry all provide very accurate assessment of body composition, but many of these tests are limited by cost or safety considerations. These tools may prove practical in the future to help assess a patient’s nutritional status.

CALORIC ASSESSMENT

Indirect Calorimetry

Direct measurements of a patient’s energy needs can be performed using indirect calorimetry, which measures heat produced by oxidation. A ventilated hood is placed over the resting patient’s head and its oxygen and carbon dioxide content for two hours is analyzed. From this information, the resting energy expenditure (REE) is derived. True caloric needs are calculated by multiplying the REE by an activity or stress factor. In addition, a patient’s respiratory quotient (RQ) is derived. The RQ is equal to Vco₂ (volume of CO₂)/Vo₂ (volume of O₂). An RQ of approximately 0.7 or less is an indication of underfeeding whereas an RQ of approximately 1.0 or more is an indication of overfeeding.¹³ Indirect calorimetry plays a large role in obese or very malnourished patients, for whom determining caloric needs based on total body weight can be inaccurate.¹⁴ More recently, simple hand-held devices have been developed with an oxygen sensor for energy measurement. By breathing through the device for 10 minutes, the patient’s REE can be determined (Fig. 5-3).¹⁵ This tool has been shown to be as effective as the more expensive and laborious indirect calorimetry device in patients who can spontaneously breathe on their own volition, that is, those who are not on a ventilator.¹⁶

Figure 5-3. MedGem calorimetry device for energy measurement.

PROTEIN ASSESSMENT

Determining a patient’s daily protein needs is an important part of writing their nutrition prescription, especially for patients on enteral nutrition (EN) or parenteral nutrition (PN). Protein catabolism occurs at varying rates and is affected by a patient’s disease status, current nutritional state, and diet. Stressed patients may use 15 to 30 g of nitrogen/day. Total body protein needs can be calculated by assessing a patient’s 24-hour urinary urea nitrogen (UUN) excretion. To determine a patient’s daily protein needs, the following formula may be used:

MACRONUTRIENTS

The macronutrients that fuel human metabolism include carbohydrates, fats, and proteins. The major source of energy in the human diet is carbohydrate, which constitutes almost half of the typical American diet. Carbohydrate is consumed as starch, sucrose, or lactose. Starch is made up of the polysaccharides amylopectin and amylose. Sucrose and lactose are disaccharides. Most digestion occurs in the duodenum and small intestine (see Chapter 100).¹⁷ Starch digestion begins in the mouth with the enzyme amylase and continues with the pancreatic enzyme alpha-amylase in the small intestine. Starch is broken down into oligosaccharides. The oligosaccharides and disaccharides are hydrolyzed by the small intestinal brush border to monosaccharides by glucoamylase, sucrase, and amylase. Glucose and galactose are absorbed across the small intestinal mucosa by active transport, whereas fructose moves across by facilitated diffusion.¹⁸

Dietary fat is primarily composed of triglycerides, which consist mainly of four long-chain fatty acids—palmitic, stearic, oleic, and linoleic—with smaller amounts of linolenic acid and medium-chain triglycerides (MCTs). Linoleic and linolenic acids are essential fatty acids; that is, they cannot be synthesized from nondietary sources. Essential fatty acid deficiency can result in a clinical syndrome consisting primarily of a scaly erythematous rash.¹⁹ Clinically, this may be seen in patients completely dependent on PN for their nutrient intake who receive no fat in their daily PN solution over a period of one to two weeks. Triglycerides are hydrolyzed to free fatty acids and beta-monoglycerides by pancreatic lipase and colipase.²⁰ Because fats are insoluble in water, their digestion requires a unique environment involving an emulsification process whereby bile salts enhance their absorption (see Chapter 100). In water, bile salts form a micelle with a hydrophobic core and a hydrophilic periphery. Micellar contents diffuse across the water layer, intestinal mucosa, and cell membrane and enter the cell. Here they are reesterified to triglycerides and linked to an apoprotein to form a chylomicron.

MCTs have a different mechanism of absorption; 30% are absorbed directly as intact triglycerides and the remaining 70% are digested to medium-chain fatty acids, which are soluble in water and directly absorbed by the small intestinal mucosa. MCT-based diets may be helpful for patients with fat malabsorption from pancreatic or liver disease. A diet very high in MCT and low in long-chain triglycerides (LCTs), however, can lead to essential fatty acid deficiency. These patients present with a characteristic diffuse, scaly, erythematous skin rash. Fats provide a long-term energy source for patients who are experiencing starvation. Unfortunately, critically ill catabolic patients lose their ability to use fat for energy efficiently, making them more dependent on their carbohydrate and protein stores.

Protein and amino acid metabolism are essential to provide the building blocks necessary to create a variety of body proteins and nitrogen-containing compounds. Proteins are composed of amino acids joined by peptide bonds. There are 22 amino acids, eight of which are essential: lysine, threonine, leucine, isoleucine, valine, methionine, phenylalanine, and tryptophan; two others, histidine and arginine, are essential for infants and growing children. Dietary proteins are partially digested by pepsin in the stomach to form polypeptides, but most protein digestion is performed in the duodenum and upper jejunum by pancreatic proteases, including trypsin, chymotrypsin, carboxypeptidase, and elastase (see Chapter 100).²¹ Peptides are further hydrolyzed in the small intestine by aminopeptidases, enzymes found in the brush border of the small intestine, to free amino acids and very small peptides. Large peptides must be hydrolyzed by brush border enzymes for absorption to occur, whereas dipeptides and tripeptides can move intact into mucosal cells.²²

MACROMINERALS

Minerals account for only 4% of total body weight, yet they serve as essential cofactors, help maintain fluid osmotic pressures, and provide the proper environment for many chemical reactions (see Chapter 4).

MICRONUTRIENTS

Essential micronutrients are present in minute or trace amounts in the body, sometimes in quantities less than 100 µg (see Chapter 4). Although trace elements are present in very small amounts, they often have dramatic effects; deficiencies are more common than toxicity. Deficiencies can result from reduced intake, decreased bioavailability, decreased transport proteins, excess excretion, or as the result of certain disease states. Many of these deficiencies develop in patients who are on long-term PN or who are severely malnourished. Assessment of trace element deficiency is extremely difficult (Table 5-2) because serum levels may not accurately reflect body stores. Therefore, clinicians may have to depend largely on physical signs and symptoms to detect micronutrient deficiency.

Table 5-2 Daily Trace Element Requirements

From American Society for Parenteral and Enteral Nutrition. Guidelines for the use of parenteral and enteral nutrition in adults and pediatric patients. J Parenter Enteral Nutr 2002; 26:29SA-33SA.

VITAMINS

Vitamins (see Chapters 4, 100) are essential micronutrients involved in basic body functions such as growth, tissue maintenance, and metabolism. They are broadly classified as water-soluble or fat-soluble. Absorption of fat-soluble vitamins requires absorption and transport of lipids. Water-soluble vitamins, except vitamin C, are part of a B-complex group (Table 5-3).

Table 5-3 Daily Reference Intakes* and Sites of Absorption of Vitamins

* Daily Reference Intakes (DRI) were established by the Institute of Medicine between 1997-2001. They are quantitative estimates of nutrient intakes to be used for planning and assessing diets for healthy people. The DRIs include both recommended intakes and tolerable upper intake levels. The RDAs (Recommended Dietary Allowances) are a component of the DRIs and are defined as the daily intake of a nutrient considered sufficient to meet the requirements of 97% to 98% of adults.

† A retinol equivalent is 3.3 IU of vitamin A; 1 retinol equivalent = 6 µg β-carotene or 1 µg retinol.

INTESTINAL FAILURE (SHORT BOWEL SYNDROME)

Intestinal failure or short bowel syndrome results from loss or disease of the intestine, or both, to an extent that precludes adequate digestion and absorption (see Chapter 103); Crohn’s disease (see Chapter 111), intestinal trauma, and intestinal infarction (see Chapter 114) are the most common causes. The patient often presents with weight loss, diarrhea, dehydration, and weakness. Following extensive resection of the small intestine, intestinal rehabilitation (goal of resuming oral nutrition) of the remaining small intestine is more likely to be successful if the colon has been preserved and the ileocecal valve is maintained.³¹ The nutritional management of short bowel syndrome depends on the amount and location of small bowel removed. Initially, proton pump inhibitors are used to reduce gastric hypersecretion and anticholinergic agents are used to slow intestinal transit. Parenteral nutrition is prescribed to meet nutritional needs. Oral feedings are gradually started and the volume of PN is reduced as oral feedings are tolerated. If the patient has had a partial ileal resection and has an intact colon, cholestyramine can be used to reduce bile salt–induced diarrhea. In patients with a small amount of ileum remaining and an intact colon, however, the use of cholestyramine can increase diarrhea by creating a relative bile salt deficiency. Vitamin B₁₂ should be given monthly. In patients with significant small bowel resections (80 to 100 cm remaining), a trial of a small-peptide, low-fat, enteral formula should be attempted to reduce the amount of PN the patient requires. Later, a polymeric enteral formula can be substituted. Patients with less than 80 cm of small intestine remaining and no colon often are PN-dependent. The use of somatostatin to reduce intestinal secretions and slow transit time remains controversial.³² Anticholinergic therapy should be initiated. Patients may require larger doses of anticholinergics than usually are recommended, because absorption of the oral medication is limited.

The use of growth hormone, glutamine, and a rice-based diet in an attempt to cause small bowel mucosal hypertrophy and better absorption is controversial. Early data have suggested very significant improvements in small intestinal absorptive function,³³ not confirmed by subsequent studies.³⁴ The use of a glycoprotein (GL-2) also has been postulated as a small intestine mucosal stimulator for improved absorption. A recent prospective evaluation of its efficacy noted a statistically significant reduction in PN use³⁵; the effectiveness of this therapy is still being evaluated in additional studies.

PANCREATITIS

Nutritional support is imperative for patients with severe acute pancreatitis or relapsing chronic pancreatitis (see Chapters 58 and 59). Early PN appears to be associated with a reduction in the complications and mortality associated with acute pancreatitis compared with maintaining the patient on an NPO regimen.³⁶ However, central line catheter sepsis rates are high and hyperglycemia is common. Enteral nutrition also has been used in patients with pancreatitis in contrast to previous beliefs that complete bowel rest was required. It appears that intrajejunal feedings are safe and well tolerated.³⁷ A standard, fat-containing, polymeric enteral formula can be used.³⁸ Randomized, prospective trials have shown a reduction in overall patient complications, hospital length of stay, and total hospital charges compared with the use of PN.^39,40 The use of jejunal feeding in patients with chronic pancreatitis has been described to improve weight and reduce abdominal pain associated with eating.⁴¹ Gastric feedings also have been used successfully in patients with severe acute pancreatitis,⁴² but are still a topic of investigation.

CROHN’S DISEASE

Crohn’s disease (see Chapter 111) is sometimes associated with malnutrition.⁴³ These patients often are hypermetabolic and may have anorexia because of nausea and abdominal pain. Deficiencies of magnesium, selenium, potassium, and zinc are common in inflammatory bowel disease (IBD) as a result of losses in diarrheal fluids and through fistula tracts.⁴⁴ Dietary therapy in IBD always has been considered important, but no specific diet can be recommended. Fat restriction may be important in patients with ileal disease or those who have undergone an ileal resection. The use of EN can be an important component of IBD therapy for patients who cannot eat. Enteral nutrition has not proven superior to PN in inducing remissions in IBD,⁴⁵ although it is less costly and associated with fewer complications. Enteral nutrition alone has not proven superior to drug therapy for the treatment of Crohn’s disease.⁴⁶ The use of PN in IBD should be restricted to patients who have not responded to conservative medical therapy (EN and medications) or in whom EN cannot be delivered.

LIVER DISEASE

Nutritional deficiencies are common among patients with liver disease, mainly from decreased dietary intake, but also as a result of altered metabolism, decreased nutrient storage, and increased nutrient requirements (see Chapters 72, 92, and 93). Decreased nutrient intake is secondary to anorexia and nausea and is more common in patients with cirrhosis.⁴⁷ Decreased bile salt production results in an intolerance to high-fat foods and the development of fat-soluble vitamin malabsorption. In addition, hypoalbuminemia results in edema of the mucosa of the small intestine, further compromising nutrient absorption. Depletion of muscle mass occurs secondary to a lack of adequate glucose stores and a dependency on protein stores for energy. Normal serum amino acid concentrations are altered, with a rise in aromatic amino acids (tyrosine, phenylalanine, and methionine) and a fall in branched-chain amino acids (valine, leucine, and isoleucine). The aromatic amino acids normally are removed by the liver; it is postulated that the rise in aromatic amino acids precipitates hepatic encephalopathy because they act as false neurotransmitters. Moreover, branched-chain amino acids are used preferentially as a protein source by patients in liver failure because they require minimal liver catabolism. Unfortunately, studies have failed to demonstrate improved outcomes in liver-failure patients fed a branched-chain amino acid–fortified diet or enteral solution.⁴⁸ There is a general tendency to limit protein intake in patients with cirrhosis to prevent encephalopathy; however, these patients have an increased protein demand and further limiting their protein intake will only accelerate protein calorie malnutrition. It is preferable to feed patients according to their protein needs and treat encephalopathy with medications as it develops. Parenteral nutrition should be used with caution in patients with liver failure, because immune dysfunction places these patients at increased risk for catheter sepsis. In addition, the lack of liver glycogen stores can lead to episodes of hypoglycemia when patients are rapidly tapered off PN. Nutritional support prior to liver transplantation has been shown to improve patient outcome, especially in patients who are significantly malnourished prior to the transplantation.⁴⁹

DIVERTICULAR DISEASE

Patients with diverticular disease (see Chapter 117) often are provided with incorrect nutritional information. They are told to avoid nuts or foods that contain seeds because of fear that the hard small particles may lodge in diverticula and precipitate diverticulitis. There are no clinical data to support this concept,⁵⁰ and most data suggest that a high-fiber diet will reduce the occurrence of symptomatic diverticular disease.⁵¹ Patients hospitalized for complicated diverticular disease can remain symptom-free on a high-fiber diet.⁵² Fiber intake should be at least 25 g/day and should be provided as insoluble fiber, such as that contained in wheat bran, bran muffins, and fiber-based cereals. The use of probiotics has had some success in the treatment of and prevention of diverticulitis, although more work needs to be done in this area.⁵³

DUMPING SYNDROME

Dumping syndrome is common after partial gastrectomy and vagotomy. Hypertonic gastric contents empty rapidly into the small intestine, and consequently up to 25% of plasma volume suddenly may be transferred to the small intestine.⁵⁴ Nausea, cramping, diaphoresis, and palpitations develop. Nutritional therapy for dumping syndrome aims to deliver a lower osmolarity solution to the small intestine by the frequent ingestion of small meals containing fat, protein, and complex carbohydrates, but limited in simple sugars. Fluid intake should be restricted and separated from solid food intake to avoid rapid gastric transit. High pectin-containing foods (bananas, oranges) will slow gastric output.

CELIAC DISEASE

Small intestinal mucosal injury and consequent malabsorption in celiac disease (see Chapter 104) occur when a susceptible patient ingests gluten-containing foods such as wheat, barley, rye, or possibly oats. Patients, especially younger ones, present with classic signs of malabsorption, including diarrhea, cramping, and marked weight loss and often develop folate, iron, and fat-soluble vitamin deficiencies. The primary treatment is a gluten-free diet. Wheat starch free of gliadin forms the basis for most bread in a gluten-free diet. Corn, rice, and buckwheat are allowed. Most patients will improve with dietary management. The vast majority of commercially available EN products, if required, are gluten-free.

CANCER

Protein-calorie malnutrition is a common problem in cancer patients. Cancer cachexia is the consequence of multiple metabolic abnormalities induced by the tumor. Appetite stimulation has been used successfully in cancer patients with mild malnutrition.⁵⁵ The routine use of aggressive nutritional support in all patients receiving chemotherapy and radiation is controversial. Prospective randomized studies have failed to show improved tolerance to chemotherapy with the use of nutritional support,⁵⁶ and PN also has failed to show an improvement in morbidity from radiation therapy. Parenteral nutrition has been shown to be beneficial for patients with gastrointestinal obstruction from primary or metastatic tumors.⁵⁷ Parenteral nutrition also has been found to be beneficial in patients following bone marrow transplantation who have developed severe gastrointestinal mucositis.⁵⁸ Enteral nutrition has been used successfully in patients with head and neck cancer to prevent weight loss, reduce hospitalizations, and reduce interruptions in chemotherapy and radiotherapy. In summary, the use of nutritional support in the cancer patient should be restricted to those patients with a reasonable life expectancy who are likely to be unable to maintain their nutritional needs for a prolonged period. It is in these patients that an improved quality of life may occur.

OBESITY

Obesity is a disease that has had explosive growth, simultaneously affecting many individuals in a community without regard to age, gender, or ethnic origin (see Chapter 6).⁵⁹ Traditionally, the gastroenterologist has been involved in the endoscopic management of postbariatric surgical complications, including stomal stenosis, gastrointestinal bleeding, and fistulization (see Chapter 7). Previous endoscopic technologies used to treat obesity endoscopically, such as the gastric balloon, had limited exposure in the United States and were removed from the market because of associated complications, such as balloon deflation with migration and resultant small intestinal obstruction. Internationally, however, balloon endoscopic therapy continues, with a number of favorable outcomes reported.^60,61 Patients with obesity-related gastrointestinal disease, such as gastroesophageal reflux disease, always have been a staple of the gastroenterologist’s practice. Today, gastroenterologists find themselves on the front line with other physicians attempting to combat obesity and its associated complications, including assessment of patients for risk, identification of those who may benefit from weight loss therapy, and determination of the appropriate weight loss intervention, including management of therapy-associated complications.

Assessing patients with obesity generally takes into consideration the BMI, waist circumference, and comorbid disease states. A person with a BMI more than 30 kg/m² is considered obese. Patients who are overweight (BMI, 25 to 30 kg/m²) with comorbid diseases should be offered dietary management, exercise, and behavioral therapy. Patients with a BMI more than 30 kg/m² also should be offered medical management (Table 5-4). If these patients have comorbid diseases, they also should be offered pharmacotherapy (weight loss medications). Patients with a BMI more than 35 kg/m² should be offered medical management and pharmacotherapy. Surgical therapy is recommended for patients with a BMI more than 35 kg/m² with significant comorbid diseases and who have not responded to medical management and pharmacotherapy. Patients with a BMI more than 40 kg/m² should be offered medical management, pharmacotherapy, and surgery.

An enlarged waist circumference also places a patient at higher medical disease risk, separate from comorbid diseases, and correlates well with total body fat.⁶² Men with a waist circumference more than 40 inches or women with a waist circumference more than 35 inches have a higher risk, similar to the presence of significant comorbid diseases in a man with a BMI more than 30 kg/m². These patients would be offered pharmacotherapy in addition to medical management, similar to the management of a patient with a BMI more than 30 kg/m² with significant comorbid disease.

Surgical management of obesity in the United States typically involves a Roux-en-Y gastric bypass, vertical banded gastroplasty, or gastric banding (see Fig. 7-1). In general, most weight is lost in the first year.⁶³ Gastric bypass surgery has a reasonable five-year outcome for maintenance of successful weight loss, but there is an associated mortality (0.5% to 2%) and complications associated with surgical therapy, some of them very significant.^64,65

PARENTERAL NUTRITION

For patients with a nonfunctioning gastrointestinal tract, nutrients can be delivered directly into the venous system via a process referred to as parenteral nutrition (PN); nutrients can be delivered into a central vein (central parenteral nutrition, CPN) or a peripheral vein (peripheral parenteral nutrition, PPN).

PN delivers a solution consisting of water, electrolytes, amino acids, carbohydrates, fats, proteins, vitamins, and trace elements. These compounds are mixed and delivered over a period of time, usually 12 to 24 hours. Table 5-5 details a typical CPN formula. A CPN solution is six times more concentrated than blood (1800 to 2400 mOsm/L) and generally consists of approximately 30 to 50 g of protein and 1000 to 1200 cal/L. Determination of caloric and protein needs is based on a prior nutritional assessment.⁶⁶ Table 5-6 provides an approximation of a patient’s daily protein and calorie needs based on the severity of the disease processes. These needs could be used instead of more complicated formulas presented earlier in this chapter for determining calorie and protein requirements. Overall, daily water requirements are estimated at 20 to 30 mL/kg.

Table 5-5 Sample Central Parenteral Nutrition Order*

* Volume: 2000 mL (83 mL/hr over 24-hr infusion).

Table 5-6 Calorie and Protein Needs Based on Degree of Physiologic Stress

ENTERAL NUTRITION

Enteral Access

In a patient who can eat and drink, EN support focuses on the use of nutritional supplements, dietary counseling, and appetite stimulation. In those patients who will not or cannot eat secondary to some dysfunction of the gastrointestinal tract, an enteral route or feeding tube is necessary to provide feedings. In this situation, obtaining enteral access becomes the foundation of any attempt to provide EN.

The radiologist, gastroenterologist, or surgeon usually places enteral access devices (Table 5-9). This can be done at the bedside, fluoroscopically, endoscopically, or in the operating room, depending on the specific device and the expertise available. Medicare trends from 1997 to 2000 have shown a significant increase in enteral access procedures in the United States. The greatest increase in enteral access procedures was among radiologists, closely followed by gastroenterologists. The percentage of surgeons performing enteral access has decreased over time.⁹³

Table 5-9 Enteral Access Methods

TYPE OF ACCESS	PURPOSE	DURATION OF NEED (MO)
Surgical or Percutaneous
Gastrostomy	Gastric feeding	>1
	Gastric decompression
Gastrojejunostomy	Gastric decompression	>1
	Gastric feeding
	Jejunal feeding
Jejunostomy	Jejunal feeding	>1
Nasal or Oral
Nasal or oral gastric tube	Gastric feeding	<1
	Gastric decompression
Nasal or oral gastrojejunal tube	Gastric decompression	<1
	Gastric feeding
	Jejunal feeding
Nasal or oral small bowel tube	Jejunal feeding	<1

Nasoenteric Tube Access

Nasoenteric tube placement techniques have been developed for placement at the bedside, with endoscopy, with fluoroscopy, or during surgery. These techniques all have their indications, benefits, and risks. The final position of an enteral access tube is the stomach for gastric feedings, or the jejunum for small bowel feedings. A patient who is intolerant of gastric feedings, such as a patient with gastroparesis, gastric outlet obstruction, or who has had the stomach surgically removed, will receive small bowel feedings. Nasogastric and nasojejunal tubes have similar complications (Table 5-10).

Table 5-10 Complications of Nasogastric or Nasojejunal Tubes

Aspiration pneumonia

Nasal mucosal ulceration

Otitis media

Pharyngitis

Pneumothorax

Sinusitis

Tracheoesophageal fistula

Tube migration

Tube obstruction

The use of small bowel feedings to prevent tube feeding aspiration events is a complicated and contentious issue. Some studies have shown fewer aspiration episodes in patients whose feedings were placed directly into the small bowel than when placed into the stomach.^94,95 A prospective trial by Neumann and DeLegge⁹⁶ directly compared the incidence of aspiration episodes with gastric feedings and small bowel feedings in the intensive care unit and found no difference. It took longer to initiate small bowel feedings, however, because of the difficulty in obtaining adequate tube position. A 2002 consensus conference determined that small bowel feeding is recommended for the prevention of aspiration pneumonia in critically ill patients,⁹⁷ but this debate certainly will continue. Small bowel feedings should be initiated in patients known to have gastroparesis, patients who are intolerant of gastric feedings, or patients who have had a witnessed tube feeding aspiration event with gastric feedings.

Bedside nasoenteric tube placement is the most common enteral access technique used in the hospital and long-term care environments. A nasogastric (NG) or nasojejunal (NJ) tube may be placed, a decision based on concerns with tube feeding tolerance and aspiration risk. There are many techniques available for passing bedside NG tubes. Typically, an 8- to 12-Fr NG tube is lubricated and passed into the stomach with the patient’s head flexed; the patient ingests sips of water to assist in passing the tube into the stomach.⁹⁸ Many centers advise bedside auscultation for confirmation of an adequate position of the NG tube before its use; however, this can be misleading because a tube in an inappropriate location (e.g., lung, pleural cavity, esophagus) may be misinterpreted as being in proper position by improper bedside auscultatory techniques. Roubenoff and Ravich⁹⁹ have reported on a technique to avoid intrapulmonary placement of nasoenteric tubes in high-risk patients. They suggested measuring a length of the tube from the earlobe to the xiphoid process before insertion. Once the tube is passed to this length, an anterior-posterior plain film is obtained to determine that the tube is in the esophagus before passing it further into the stomach or small intestine. Every patient should have a plain film to confirm proper positioning of a NG or NJ tube before initiating feedings.¹⁰⁰

It is not unusual to be faced with a patient who is comatose and therefore unable to assist with the passage of a nasoenteric tube. In this case, the tube can again be passed at the bedside after tube lubrication and head flexion. The patient is monitored for coughing and wheezing consistent with a bronchial placement. Auscultation of the abdominal cavity and an abdominal plain film can confirm proper tube location.

The difficulty of passing a nasoenteric tube at the bedside blindly into the small intestine has prompted development of a variety of techniques. Thurlow has promoted the use of a stylet-filled NJ tube that is advanced with a corkscrew motion.¹⁰¹ Zaloga has confirmed the reliability of this technique, with a more than 90% success rate.¹⁰² Ugo and associates have reported on placing the patient in the right lateral decubitus position and tracking the position of the tube into the small bowel by using a stethoscope and auscultation, a technique that resulted with an 83% success rate.¹⁰³ Lord and coworkers have promoted the use of unweighted feeding tubes for these bedside passages; their success rate for spontaneous small bowel placement was far more than that documented for weighted tubes (92% vs. 56%).¹⁰⁴ The hypothesis here was that the weight at the tip of the feeding tube actually was an impediment to the tube’s spontaneous passage through the pylorus. In Lord’s study, metoclopramide was used to promote passage of the tube from the stomach into the small intestine. Others have reported on positioning a tube beyond the pylorus with the use of pharmacologic agents; results with metoclopramide ranged from no benefit^105,106 to a 90% success rate.^107,108 Silva and colleagues, in a comprehensive literature review, noted that metoclopramide given intravenously or intramuscularly was effective in promoting successful nasoenteric tube placement into the small intestine.¹⁰⁹ Griffith and associates have confirmed the usefulness of another promotility agent, erythromycin, for promoting successful NJ tube placement at the bedside in critically ill patients.¹¹⁰

Newer technologies have been developed for NJ tube placement. Self-propelled NJ tubes have a spiral tip at the distal end. It is hypothesized that the stomach can propel this type of tip through the pylorus easier than with a standard straight tip. Berger and coworkers have reported a 50% success rate in passing the pylorus with the self-propelled feeding tube in 105 critically ill patients.¹¹¹ Magnetically steered NJ tubes also have been reported to show reasonably successful rates of proper placement.¹¹² Concurrent use of narcotics decreased the likelihood of successful tube placement.

If attempts fail to pass an NJ tube blindly at the bedside, fluoroscopic or endoscopic methods of passage are then required. The preference of technique is center-dependent. In centers with available C-arm fluoroscopy and modified fluoroscopy beds, fluoroscopic passage of NJ tubes can be done at the patient’s bedside. Success of fluoroscopic guidance of NJ tube passage can approach 100%.¹¹³ In institutions without bedside fluoroscopic capabilities, however, transport of patients to the radiology suite, especially critically ill patients, can be time-consuming, expensive, and hazardous.¹¹⁴ In these cases, bedside endoscopic passage of NJ tubes is preferable.

NJ feeding tubes can be placed endoscopically at the bedside with moderate sedation. Table 5-11 lists the techniques for endoscopic passage of nasoenteric tubes at the bedside. The “drag-and-pull” method has the longest history. In this technique, a suture or another grabbable item is attached to the end of a NJ tube and used to drag the NJ tube into position in the small intestine with a grasping forceps. Difficulty usually occurs in releasing the suture from the grasping forceps. A second common technique, the “over-the-guidewire” technique, requires the initial endoscopic placement of a guidewire into the small intestine. The endoscope is removed and the guidewire is left in place. A feeding tube subsequently is passed blindly or with fluoroscopic assistance over the guidewire and into position in the small intestine. Patrick and colleagues have reported a 94% success rate using this technique.¹¹⁵ Fang and associates have described the use of an ultrathin endoscope to perform nasal endoscopy and place a guidewire into the small intestine. After the endoscope is removed, a NJ tube is passed over the guidewire into position.¹¹⁶ With this technique, no sedation is required. Other methods of endoscopic NJ placement are used less frequently.

Table 5-11 Endoscopic Methods of Nasoenteric Tube Placement

METHODS	TECHNIQUE
Drag-and-pull	Suture on end of a tube pulled with forceps into position
Over-the-guidewire	Tube pushed into position over a guidewire
Through-the-scope	Tube pushed through biopsy channel of endoscope into small bowel
Nasal endoscopy	Tube passed over guidewire placed through a nasal endoscope

Nasoenteric tube placement is the most common method of enteral access. Unfortunately, nasoenteric tubes may fail early because of tube occlusion or dislodgment, with subsequent interruption of tube feeding and medication regimens. Therefore, nasoenteric tubes should be used in patients requiring NG or NJ access for less than one month. The tip of the NJ tube may be anchored onto the small bowel mucosa using an endoscopic clipping device, a practice that seems to add a few days to the projected longevity of NJ tubes, presumably by reducing the risk for NJ tube migration.¹¹⁷ Patients who have experienced repeated, early failure of nasoenteric tubes should receive more permanent enteral access, such as a percutaneous endoscopic gastrostomy, percutaneous endoscopic jejunostomy, surgical gastrostomy, or surgical jejunostomy.

The decision to use a jejunostomy (J) tube warrants specific instructions regarding the tube’s care. The lumen of a J tube is usually much smaller than that of a gastric tube and therefore is prone to clogging. Jejunal feeding tubes should never be checked for residual content because this measure is a poor indicator of the residual content of the small bowel. In addition, checking residuals through these small-bore tubes increases their probability of clogging. J tubes should be flushed after every tube feeding and medication instillation. Only liquid medications, or completely dissolved medications, should be placed through a J tube to reduce the chances of tube occlusion. Care should be taken to stop tube feedings during infusion of certain medications, such as theophylline or potassium chloride, products that are known to coagulate tube feedings and obstruct the J tube.

Percutaneous Endoscopic Enteral Access

If a patient will require enteral access for longer than one month, percutaneous procedures are preferred. The endoscopic procedures include percutaneous endoscopic gastrostomy (PEG), percutaneous endoscopic gastrojejunostomy (PEG/J), and direct percutaneous endoscopic jejunostomy (DPEJ). All these procedures require the use of moderate or deep sedation and can be performed in the endoscopy suite, in the operating room, or at the bedside. In comparison to NG access, PEG has been shown to be a more reliable enteral access tube, allowing patients to receive more calories daily because of a reduction in tube dysfunction.¹¹⁸

Percutaneous Endoscopic Gastrostomy

PEG was developed by Gauderer and coworkers in the early 1980s.¹¹⁹ The procedure involves the placement of a percutaneous gastrostomy tube after endoscopic transillumination of the abdominal wall for an appropriate gastrostomy site. The use of prophylactic antibiotics before the procedure is important to prevent postprocedure infections.¹²⁰ Placement of a PEG tube can be accomplished by the Sachs-Vine (push) or Ponsky (pull) techniques, depending on physician preference. Prospective evaluations of PEG placement have found this procedure to be associated with few procedure-related complications.¹²¹ An older technique, the push-dilator technique, has started to make a resurgence. In this technique, the endoscope is used as a viewing port during PEG tube placement. T fasteners are placed percutaneously to attach the wall of the stomach to the abdominal wall; an incision is made in the abdominal wall and a fistula into the stomach is created and sequentially dilated. Ultimately, a PEG tube with a balloon internal bolster is passed through the newly created insertion site, as is done with balloon replacement tubes (Fig. 5-4).¹²²

Figure 5-4. Introductory percutaneous endoscopic gastrostomy (PEG) kit. This kit uses T fasteners to tack the stomach to the abdominal wall, followed by PEG tube tract serial dilations.

PEG tubes are indicated for patients who will be unable to consume sufficient nutrition for longer than one month, despite a functional gastrointestinal tract. Patients requiring PEG placement often are older and have numerous comorbid diseases. In one study of older patients referred for PEG placement, there was a 48% mortality at seven days if the patient had a prior aspiration episode or urinary tract infection, or was older than 75 years, compared with a 4% mortality if none of these risk factors was present.¹²³ In addition to providing access for nutrition, PEG tubes are indicated for hydration and administration of medications as well as for gastric decompression. Some of the more common medical indications for PEG placement are described here.

Cancer

One area of oncology in which PEG tubes are beneficial is head and neck cancer. The benefit of PEG tubes in this setting was illustrated in a retrospective study that had 40% (32 of 88) of head and neck cancer patients receiving a PEG tube prior to chemotherapy and radiotherapy. Those who received a PEG lost an average of 3.1 kg compared with 7 kg of weight loss for those without a PEG. The same PEG group had significantly fewer hospitalizations for dehydration and malnutrition and had no interruption in treatment of their cancer compared with the group which did not receive PEG.¹²⁴

Stroke

Data support the use of PEG tubes in patients with stroke-related dysphagia. In one study, the authors reported a 1-, 8-, and 48-month survival of 78%, 35%, and 27%, respectively, when the most common indication was a hemispheric stroke.¹²⁵ Compared with NG feeding, early PEG placement was found to be associated with a lower incidence of ventilator-associated pneumonia.¹²⁶ In contrast, Dennis and colleagues have reported an increase in the death rate and poor outcome in stroke patients randomized to PEG tube feedings as opposed to nasoenteric tube feedings.¹²⁷ In this same study, patients receiving early tube feeding by any means had a reduction in overall mortality compared with patients who did not receive early enteral nutrition.

Dementia

Dementia is a frequent disorder of older adults and a common indication for referral for PEG. More than 36,000 older patients with dementia receive a PEG tube each year.¹²⁸ The benefit of providing EN in these patients, however, is less clear.¹²⁹ No large, prospective, randomized trials have been performed to evaluate the usefulness of PEG tube placement for this patient population. One retrospective analysis has suggested that mortality among dementia patients does not differ, regardless of whether a PEG tube is placed,¹³⁰ although this study did not address whether the use of PEG tubes in this population for hydration and medication delivery would be appropriate. The use of PEG in the dementia population remains a subject of great debate¹³¹ and ultimately a prospective randomized trial will be required to answer the question definitively.

Disabling Neurologic Conditions

The use of PEG tubes for the patient with disabling motor neuron disease, such as amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS), has been examined. Both these diseases are associated with progressive dysphagia, leading to reduced oral intake, weight loss, and an increasing risk of oral aspiration. Langmore and coworkers did an extensive literature search of patients with ALS receiving PEG and only identified retrospective studies and prospective cohort studies.¹³² Using these data, they concluded that survival and nutritional status could be improved with PEG placement in ALS. There was a trend for improved quality of life although this required further study. Small case reports have demonstrated an improvement in comorbid disease states, such as pressure ulcer healing, in patients with MS and dysphagia who receive tube feedings.¹³³

PEG Procedure

PEG kits are commercially available from a number of manufacturers. The most common sizes for adult patients range from 16 to 24 Fr. Most tubes are made of silicone, although some are constructed of polyurethane. In general, PEG tubes start to degrade one to two years after placement, usually from yeast implantation and degradation of the PEG tube wall.¹³⁴ PEG tubes are less likely to clog than nasoenteric tubes because of their larger size. Obstructed PEG tubes may be cleared by flushing them with warm water. In some cases, pancreatic enzymes mixed in a bicarbonate solution also can be effective.¹³⁵ There are no data to support the use of juices, soft drinks, or meat tenderizers to unclog a PEG tube. Commercially available PEG tube cleaning brushes also are available.

Relative contraindications for PEG placement include the presence of gastric varices, severe obesity, major gastric resection, significant disease of the gastric or abdominal wall, ascites, and coagulopathy. Absolute contraindications include the inability to transilluminate the anterior abdominal wall and an ineffective digital intrusion of the abdominal wall to locate a safe gastric access site.¹³⁶

Once a PEG tube malfunctions, degrades, or is no longer needed, it can be removed at the bedside with a traction pull force of seven to 10 pounds; such removable PEG tubes are labeled as traction removal tubes.¹³⁷ Some PEG tubes, labeled as endoscopic removal tubes, have a stiff internal bolster and can be removed only with an endoscope. Although there is an increase in cost with the use of endoscopic removal PEG tubes because of the need for a repeat upper endoscopy at removal, they may be safer to use in patients who are confused or combative and at risk for pulling their PEG tube out after initial placement. Some authors have suggested cutting the PEG tube at the abdominal wall level and allowing the remaining tube and internal bolster to pass through the gastrointestinal tract; this should not be done because there have been cases reported of these cut internal bolsters leading to a small bowel obstruction.¹³⁸

Most post-PEG complications arise from a patient’s comorbidities, such as poor wound healing, aspiration, or coagulopathy.^139–141 Caregivers must raise the head of the patient’s bed to 30 to 45 degrees during and for one hour after feeding to reduce the risk of aspiration.¹⁴² The most common complication is peristomal wound infection.¹⁴³ Excessive tightening of the PEG tube external bolster against the abdominal wall can cause tissue ischemia, wound leakage, and necrotizing fasciitis.¹⁴⁴ To minimize this complication, the external bolster of the PEG tube should be maintained 1 to 2 cm from the anterior abdominal wall to avoid tissue compression and wound breakdown.¹⁴⁵ Peristomal wound infections often are treated for seven days with an oral antibiotic such as cephalexin to cover skin-related microorganisms. The infected area should also have daily topical cleansing with or without antibiotic ointment. The PEG tube should be removed in cases of worsening infection. Other common complications include pneumoperitoneum, fever, ileus, cutaneous or gastric ulceration, and tube extrusion or migration.^146–148 Pneumoperitoneum is common after PEG placement and is not diagnostic of a perforation. Careful clinical evaluation of a patient after PEG placement with questionable peritonitis from perforation or leak should include a contrast study through the PEG tube to avoid unnecessary surgical exploration.¹⁴⁹ Major complications are rare and include intra-abdominal bleeding or hematoma formation, peritonitis, necrotizing fasciitis, gastric or colonic perforation, and hepatogastric, gastrocolic, and colocutaneous fistula. A colocutaneous fistula results from the inadvertent placement of a percutaneous feeding tube through the colon before it enters the stomach. When a colocutaneous fistula is documented, the tube should be removed and the patient’s condition should be monitored for appropriate closure of the fistulous tract. If the tract does not heal, surgery may be warranted to repair the fistula.

If a PEG tube dislodges within four weeks of placement, fluoroscopy can be used to replace it at the bedside or endoscopy may be repeated. The concern in this situation is that the abdominal and gastric wall have separated from one another when the PEG tube was dislodged. If the PEG tube is dislodged more than four weeks after placement, the tract may be mature enough to replace the PEG tube blindly at the bedside without fluoroscopy or endoscopy. Proper placement can be confirmed by aspirating gastric contents from the replacement PEG tube. If there is any question that the replacement tube tip is not in the gastric lumen, a contrast radiologic study through the PEG tube should be obtained.

Replacement PEG tubes are divided broadly into two categories, replacement gastrostomy tubes and low-profile devices. Replacement gastrostomy tubes usually have a balloon-type internal bolster (Fig. 5-5). These balloon tubes can be inserted blindly through the gastrostomy site into the gastric lumen. The balloon is inflated to serve as the internal bolster and an external bolster is slid down the external tube against the abdominal wall to keep the PEG tube from migrating. There also are replacement PEG tubes with a distensible internal bolster (Fig. 5-6). The internal bolster is stretched with a stylet and pushed blindly through the gastrostomy site and the stylet is then removed, allowing the internal bolster to assume its previous shape. The direction of the gastrostomy tract should be known so that the stylet does not damage or rupture the tract.

Figure 5-5. Replacement gastrostomy tube.

Figure 5-6. Replacement percutaneous endoscopic gastrostomy device with distensible internal bolster.

PEG tubes also may be replaced with low-profile gastrostomy devices (Fig. 5-7). These devices provide a skin level access to the gastric lumen, and may be particularly useful for disoriented patients who may habitually tug at their bedclothes and pull out their tube connections. The internal bolster of these low-profile devices may be an inflatable balloon or a distensible internal bolster that requires a stylet for placement. Low-profile PEG tubes come in predetermined lengths and the gastrostomy tract length must be measured in order to choose the correct length of the device. To access the low-profile device for feeding or gastric decompression, a separate access tube must be used to engage a valve in the top of the device. Although these tubes are cosmetically appealing, the small internal diameter of the access tubing and the valve make them more prone to valve and access tube occlusion.

Figure 5-7. Low-profile percutaneous endoscopic gastrostomy device.

Percutaneous Endoscopic Gastrojejunostomy

In patients in whom small bowel feedings are desired, endoscopic percutaneous small bowel access may be obtained by two methods. With the first method, percutaneous endoscopic gastrojejunostomy (PEG/J), a PEG is placed in the standard fashion, after which various techniques may be used to place a jejunal feeding tube through the PEG into the small bowel.^150–152 Usually, a 9- or 12-Fr J tube is passed through the existing PEG and into position in the small bowel over a guidewire (Fig. 5-8). DeLegge and colleagues have reported a 100% success rate and no major complications using the over-the-guidewire technique for PEG/J placement, with a procedure time of 26 minutes.¹⁵⁰ This PEG/J system allowed for concurrent gastric decompression and small bowel feeding. The average longevity of this tube system was approximately 120 days when patients who died from comorbid diseases were excluded from the analysis. A one-piece gastrojejunostomy (G/J) system does exist and is generally used as a replacement device that is passed through a preexisting PEG tube tract (Fig. 5-9). This tube can be dragged into position by a suture at the end of the G/J system during endoscopy or passed over a guidewire during endoscopy or fluoroscopy. The internal bolster on this system is a balloon.

Figure 5-8. Percutaneous endoscopic gastrojejunostomy showing over-the-guidewire placement technique.

Figure 5-9. Combination gastrojejunostomy balloon feeding tube (one piece).

The management of PEG/J tubes is similar to that of PEG tubes. Jejunal tubes need to be flushed aggressively to avoid clogging. Reported clogging rates of J tubes have ranged from 3.5% to 35%.^153,154 Administration of semidissolved medications and bulking medications such as fiber through the J tube, and checking J tube residuals, leads to an increased incidence of tube occlusion. In contrast, medications may be given through the gastrostomy tube because of its larger diameter; the gastrostomy tube also may be used for decompression of gastroparesis or gastric outlet obstruction.

Complications of PEG/J tubes include those already discussed for a PEG tube. In addition, the jejunal tube may migrate in a retrograde direction or become kinked so that it no longer functions. Tube migration occurs most commonly in patients who have persistent vomiting or in cases in which the J tube has been placed improperly.^150,155

Direct Percutaneous Jejunostomy

The second method of jejunal access, direct percutaneous endoscopic jejunostomy (DPEJ), directly places a J tube into the small bowel using an endoscope. This procedure requires the use of an enteroscope or a pediatric colonoscope to reach a puncture position beyond the ligament of Treitz. Success with this procedure has been reported by Shike and associates;^156,157 minor complications included local site infection, but no instance of peritonitis or bowel infarction. One of the difficulties with DPEJ placement is the frequent migration of the small bowel away from the introducer trocar needle once an adequate entry site on the abdominal wall has been located. Varadarajulu and DeLegge¹⁵⁸ have resolved this problem with the use of a two-needle stick technique (Fig. 5-10). In this procedure, a smaller, sharper, 19-gauge needle (finder needle) first is passed through an appropriate abdominal site into the small intestine. This finder needle is grasped by a snare, thus anchoring the small bowel against the abdominal wall. The larger introducer catheter is passed alongside the 19-gauge needle into the small bowel without pushing the small bowel into the abdominal cavity. The snare is removed from the 19-gauge needle and placed around the introducer catheter. A guidewire is passed through the introducer catheter into the small bowel, where it is then grasped by the snare and pulled out via the oral cavity. A J tube is attached to the guidewire and pulled into place in the small bowel similar to how a PEG tube is placed. Adequate positioning of the internal bolster of the J tube is confirmed with endoscopic visualization.

Figure 5-10. Finder needle insertion and snare fixation in two-needle stick technique.

Knowing what the patient’s needs are for jejunal access can help decide which enteral access is appropriate. Short-term access is probably best achieved by a nasojejunal (NJ) tube. Patients requiring jejunal access for less than six months or those requiring concomitant gastric decompression would do well with a PEG/J system. Long-term jejunal access (i.e., more than six months) is best achieved with a DPEJ tube. Comparisons of PEG/J and DPEJ for jejunal access have found fewer tube-related complications, such as jejunal tube migration and jejunal tube occlusion, with the DPEJ tube.^159,160

Immediately after DPEJ placement, it is helpful to leave the J tube unclamped so that the substantial amount of air that was insufflated during the procedure may escape and thereby decompress the small bowel. Management of DPEJ tubes is otherwise similar to that of PEG tubes. Complications and technical failures have been presented in three retrospective series on DPEJ outcomes. Technical failure rates ranged from 12% to 28%. Complications included bleeding, abdominal wall abscess, colonic perforations, peristomal infections, enteric ulcers, small bowel torsion, and intraperitoneal leakage; tube-related malfunctions similar to those with PEG tubes also have occurred.^157–159

Surgical Enteral Access

A number of studies have compared surgical gastrostomy with PEG and have shown cost savings, operative time savings, or a reduction in morbidity with PEG.^160,161 In the standard surgical gastrostomy tube placement, a gastrotomy is formed and a gastric tube is placed into the gastric lumen. The gastric wall is then fixed to the abdominal wall. Surgical gastrostomy first was described by Stamm in 1894 and has not changed significantly since that description.¹⁶²

Surgical jejunostomy was performed first by Bush in 1858 in a patient with nonoperable cancer¹⁶³ and, in 1891, Witzel described the most well-known technique for jejunostomy, which subsequently has undergone a number of modifications.¹⁶⁴ Laparoscopic placement of J tubes and G tubes began in the early 1990s because it was believed that these procedures would be associated with less morbidity and operative stress than the standard surgical jejunostomy and gastrostomy. It was soon learned that these laparoscopic techniques did not add any significant advantage over standard surgical gastrostomy or jejunostomy with regard to operative time or associated procedure morbidity. Needle catheter jejunostomy (NCJ) involves the placement of a 5- or 7-Fr catheter into the jejunum via a submucosal tunnel. It was hypothesized that this technique would have fewer procedure-related complications than standard jejunostomy because of the smaller entrance created to the jejunum. Multiple studies have reported reduced infectious complications of NCJ compared with standard surgical jejunostomy; however, there is a significant increase in tube occlusions and dislodgment with the smaller NCJ.

Fluoroscopic Percutaneous Enteral Access

Placement of percutaneous gastrostomy and gastrojejunostomy tubes with fluoroscopic guidance has continued to gain acceptance since the introduction of this technique in the early 1980s.^165,166 These procedures usually are performed by radiologists in the fluoroscopy suite. After topical anesthesia to the abdominal wall, occasionally with additional moderate sedation, the inferior margin of the liver is identified by ultrasonography and marked on the patient’s abdominal skin surface. An NG tube is passed into the stomach, after which the stomach is insufflated and punctured with an introducer catheter; some but not all radiologists then attach the stomach to the anterior abdominal wall with T fasteners. A guidewire is placed into the stomach through the introducer and the puncture site is serially dilated over a guidewire to a size of 10 to 14 Fr. A gastrostomy tube is passed over the guidewire, through the dilated puncture site, and into the stomach or the small intestine if a gastrojejunostomy tube is desired.

This fluoroscopic approach to enteral access has a reported technical success rate of over 95%.¹⁶⁷ Most of the complications involve inadvertent puncture of contiguous abdominal organs or separation of the abdominal and gastric wall during gastrostomy tract dilation; the latter may lead to peritonitis, intraperitoneal leakage, and even death. Frequent occlusion of these feeding tubes, because of their typically smaller internal lumen size, has been shown to be avoidable if larger gastrostomy tubes (18 to 22 Fr) are used.¹⁶⁸

ORAL DIET THERAPY

A general diet is designed to provide optimal nutrition to patients who do not require a therapeutic diet. A healthful diet contains a variety of foods that are low in fat and cholesterol, contain moderate salt content, and has an abundance of fruits, grains, and vegetables. Low-carbohydrate diets have been promoted for weight loss,¹⁷⁹ but the long-term outcomes of this dietary regimen for weight loss vary significantly among individuals (see Chapter 6).

PROBIOTICS

Probiotics are microorganisms that on ingestion may help improve microbial balance and the health of the host. Probiotics must survive passage through the gastrointestinal tract and have the ability to adhere to human epithelial cells to populate the intestine. Three basic mechanisms are believed responsible for the action of probiotics:

Probiotics adhere to the colon mucosa, thereby reducing sites at which pathologic bacteria can attach. Probiotics also may release bacteriocins that are detrimental to pathogenic bacteria, but not to the organisms of the ingested probiotic.¹⁸⁴ Probiotics have been shown to decrease the production of inflammatory cytokines, such as tumor necrosis factor-α, interferon-γ, and interleukin-1, and to increase the production of the anti-inflammatory cytokines interferon-α and interleukin-10.¹⁸⁵ Probiotics enhance the intestinal barrier function by binding with Toll-like receptors on the epithelial cells and activating protein kinase C, which results in tightening of the tight junctions of the epithelial cells.¹⁸⁶

Probiotics mainly have been used as treatment in four areas of gastrointestinal disease: symptomatic diverticular disease and recurrent diverticulitis (see Chapter 117), irritable bowel syndrome (IBS; see Chapter 118), inflammatory bowel disease (see Chapters 111 and 112).