Complications and Management of Enteral Feedings 46

Introduction

IV. Complications and Management of Enteral Feedings 46–58

S E C T I O N I Fundamentals of Nutrition Support Practice and Management

d) Determine the amount of water being provided with flushes and medications that are being administered via the feeding tube.

e) Subtract the patient’s fluid intake (total of steps a–d) from the daily amount required and provide the remainder throughout the day as water flushes via the enteral feeding tube. Note that if IV fluids are discontinued, water intake by the feeding tube may need to be increased.

f ) Assess the patient’s body weight, presence of edema, BUN, serum sodium, adequacy of intravascular volume, and urine output.

E. Assessment of nutrient intake

1. Assess actual nutrient intake. Calculate the macronutrients and energy being provided from the patient’s oral intake, tube feedings, and dextrose-containing IV fluids. Often patients do not receive their full enteral nutrition prescriptions for various reasons, such as the scheduled administration of medications, tests or proce- dures, or daily therapies.

2. It is important for ongoing assessment of actual intake to determine whether changes in the nutrition support regimen are indicated to provide the daily prescribed volume of formulation more accurately and consistently.

F. Oral stimulation for children

1. Infants and young children who have received exclusive enteral tube feedings or PN for extended periods may experience difficulties when oral foods are introduced.³⁹Early and frequent oral stimulation is necessary in such patients to minimize the potential for developing oral feeding difficulties and aversions.

2. Solid food feedings should be used particularly in infants in the first year of life at developmentally appropriate ages. Even though the nutrients may not be bioavailable, if these behaviors are not initiated and learned at this time, problems such as aversive behaviors toward eating are likely to manifest when the child is physiologically able to eat by mouth.⁴⁰

3. If oral intake of fluids or solids is not medically feasible, non- nutritive sucking (sucking on a pacifier while being tube-fed) should be encouraged in infants.

G. Body weight

1. Ideal conditions. If possible, patients should be weighed in the morning—before eating, drinking, or the infusion of the tube- feeding formula but after voiding—using the same scale, and with minimal clothing.

2. Frequency. Patients should be weighed once or twice per week.

More frequent measurements are useful in critically ill patients, in patients whose fluid status is unstable, or in infants and growing children.

H. Biochemical and hematological indices. The use of laboratory values as monitoring parameters during enteral nutrition support is individ- ualized, and the frequency depends on the severity of the underlying medical condition, degree of malnutrition, level of metabolic stress, and presence of nutrient and electrolyte deficiencies.⁴¹Typically, laboratory monitoring is indicated less frequently in patients receiving enteral nutrition than PN because of the ability of the GI tract to reg- ulate the absorption of electrolytes and minerals. However, baseline metabolic and nutrition assessment parameters should be obtained (see Chapter 1).⁴²Follow-up laboratory work is then obtained based on the patient’s clinical status.

I. Maintaining feeding tube patency 1. Method to irrigate the tube

a) Adults. To keep tubes patent, feeding ports should be flushed with warm water (at least 20–30 mL for adults) every 4 hours for continuous feedings as well as before and after each inter-

mittent feeding or medication.⁴³Medications should be administered separately, and 5 to 10 mL of water should be provided between each one. Gastric acids coagulate most intact protein formulations, so it is recommended that a feeding tube be flushed with 30 mL of warm tap water before and after check- ing for feeding residuals.⁴⁴It is important to subtract the amount of water flushed from the obtained residual volume.

b) Children. Most pediatric tubes are not routinely flushed with water to prevent clogging unless recurrent problems occur. It is important to consider the size of the child when providing flushes. Infants’ feeding tubes should be flushed with only 3 to 5 mL of water before and after medication administration, because they may not tolerate large amounts of calorie-free fluid. Older toddlers are also provided small volumes of flushes following medication administration in an effort to prevent fluid excess.²²

2. Choice of irrigant. No irrigant has been shown to be more effective than water in preventing tube clogging. Water and carbonated beverages were shown to be equally effective in preventing tube clogging, and both were superior to cranberry juice. The lower pH of cranberry juice can cause clogging by precipitating certain proteins.⁴⁵

J. The underlying medical condition(s) should be reassessed on an ongoing basis to evaluate the feasibility of transitional feeding and initiating or increasing oral intake.

IV. Complications and Management of

S E C T I O N I Fundamentals of Nutrition Support Practice and Management

a) Upper airway complications. Nasopharyngeal erosions and necrosis, sinusitis, otitis media, loosening and evulsion of teeth, bacteremia (especially in immunocompromised patients and patients with poor oral or dental hygiene), and interference with dental hygiene (oral tubes). Many of these complications are more common with the use of larger, stiffer tubes and can be minimized by the use of small-bore feeding tubes and meticu- lous nursing care.

b) Lower airway complications.⁶⁰Feeding into the trachea or lung with resultant pneumonia, respiratory distress, acute respiratory failure, empyema, and adult respiratory distress syndrome. Proper assessment of tube location can prevent these complications.

c) GI injuries. Esophagus: erosions, aggravation of variceal bleeding (rarely occurs with soft, small-bore feeding tubes). Stom- ach: erosions, ulcer bleeding, and gastric outlet obstruction.

Small intestine: erosions, ulcer bleeding, obstruction, and volvulus. Other: buried bumper syndrome (ie, percutaneous endoscopic gastrostomy placement), misplaced fasteners, necrotizing fascitis, wound infection, cellulitis, stomal leakage, hematoma, tube dislodgment, extrusion or migration of feeding tubes, subcutaneous emphysema, and enterocutaneous fistulas (eg, from percutaneous or surgical tube placement).

3. Tube clogging. Tube clogging is caused by viscous formulas, inappropriate medication administration, formula residue, and inadequate flushing.²⁶

a) Tube clogging is more likely with intact protein products and viscous formulas (calorically dense and fiber-containing products).^44,61,62Clogging may also be caused by product microbial contamination that leads to formula coagulation⁶³or by the aspiration of residuals (gastric fluid coming in contact with formulation in the feeding tube).⁶⁴To prevent tube clogging, the tubing should be flushed before and after each intermittent feeding and every 4 to 6 hours with continuous feeds.⁶⁵Other strategies to prevent clogging include flushing the tube after aspirating for residuals, using an infusion pump to infuse viscous formulations, responding to an occlusion alarm on a pump as soon as possible, and using clean technique when administering enteral feedings to minimize contamination.

b) Clogging caused by medications. Inadequately crushed tablets, medications administered together (causing precipitation), interaction with formulation, or inadequate tube flushing can cause clogging. Clogging can be prevented by flushing feeding tubes with water (about 30 mL) before administering medication, as well as between each medication (at least 5 mL), and after the administration of all medications is complete (about 30 mL).⁶⁶Avoid mixing a drug with any enteral formulation unless it has been shown to be compatible. Provide liquid forms of medications whenever possible and use elixirs or suspen- sions rather than syrups (which have a lower pH and can easily clump tube-feeding products).⁶⁷Solid dosage forms, such as simple compressed tablets, should be crushed into a fine powder and diluted with enough water to dissolve the powder.

Enteric-coated or sustained-release tablets should not be crushed. Bulk-forming agents should be avoided because they congeal rapidly when mixed with water and can clog the tube.^43,68,69(See Chapter 9 for further discussion of medication administration via enteral feeding tubes.)

c) Clogging attributable to feeding-tube characteristics. Less clogging occurs with polyurethane tubes than with silicone tubes.^65,69,70

4. Declogging methods. Feeding tubes are more successfully de- clogged when intervention is initiated immediately after the obstruction is noted and if the obstruction is close to the proximal tube opening.^71,72

a) Irrigants. Warm water initially should be used as an irrigant.

If ineffective, enzyme treatments can be initiated.⁷³Papain (meat tenderizer) and carbonated beverages showed no significant advantage over distilled water in dissolving coagu- lated formula. However, a solution of digestive enzymes (pancrelipase) mixed with sodium bicarbonate (to activate the enzyme) has been shown to be fairly effective in dissolving formula occlusions.^73–75

(1) With a 30- to 50-mL syringe, aspirate as much liquid as possible from the feeding tube so that the declogging solution can come in contact with the obstruction.

(2) Instill 5 mL of warm water with a 30- to 50-mL syringe under manual pressure for 1 minute and use a back- and-forth motion with the plunger to help dislodge the occlusion.

(3) Clamp the tube for 5 to 15 minutes.

(4) Try to aspirate or flush with warm water.

(5) If the tube remains clogged, prepare a pancrelipase solution buffered with a sodium bicarbonate tablet (eg, 1 crushed pancrelipase tablet or ¹⁄4teaspoon of pancrelipase powder +1 non-enteric-coated sodium bicarbonate [324 mg] tablet) or ¹⁄8tsp of baking soda dissolved in 5 mL of warm water. Follow steps 1 to 4 with the pancrelipase solution instead of water, and repeat once if necessary. When declogging feeding tubes, be certain the tube tip is not inad- vertently positioned in the lung because enzymes or water can severely damage the pulmonary tissue.

b) Mechanical methods. Insertion of the following instruments into the feeding tube is generally used as a final attempt to declog the tube and should be performed by experienced practitioners only. In each case, the instrument used needs to be premeasured so it does not exceed feeding-tube length.

Feeding-tube stylets should not be used to clear an obstruction, because they may cause tube perforation and trauma to the GI mucosa.⁷⁴

(1) Small-diameter catheter. Introduce a small-diameter catheter into the clogged feeding tube. Instill declogging solution in close proximity to the obstruction.^71,73After feeding-tube length is verified, mark the catheter appropriately and insert it into the feeding tube up to the point of obstruction. Ini- tially, warm water is infused through the catheter and a back-and-forth motion is used to dislodge and dissolve the occlusion. If this method fails, the pancrelipase solution technique (see above) can be used.

(2) Endoscopy/cytology brushes.⁶¹—Insert an endoscopy/

cytology brush through the tube lumen to break up an obstruction. The feeding tube is then flushed with water.

(3) Declogger devices. These devices are made of plastic and come in various lengths and diameters, which conform to various feeding-tube lengths and diameters. The threaded end of the device is inserted into the feeding tube with a twisting motion. After the clog is penetrated, the device is moved in a back-and-forth motion to dislodge the clog. This is followed by a water flush.

5. Aspiration is a potentially lethal complication of enteral feeding.^50,76,77Clinically significant aspiration pneumonia is esti- mated to occur in 5% of gastric-fed patients. It can result in

S E C T I O N I Fundamentals of Nutrition Support Practice and Management

cough, bronchospasm, pulmonary edema, pneumonia, empyema, and respiratory failure.

a) Risk factors include decreased level of consciousness, dimin- ished cough or gag reflex, neurologic injury, incompetent LES, gastroesophageal reflux, supine position, use of large-bore feeding tubes, large gastric residuals, and gastroparesis. Most aspiration is of oral-pharyngeal secretions, not gastric contents.

b) Aspiration of gastric contents may be prevented by providing smaller, more frequent feedings in patients receiving intermittent tube feedings; using small-bowel feeding tubes (and gastric decompression); using promotility agents; periodically assessing gastric residuals; and keeping the head of the bed elevated (≥30°).

6. Miscellaneous. Other mechanical complications are tube knotting; perforation of the feeding tube with the guidewire (which also could perforate the bowel); inability to remove the guidewire because of knotting, kinking, or poor lubrication; tube deteriora- tion; dislodgment; and migration.

B. GI complications

1. Gastroparesis is not a complication of feeding but may be present in patients who require enteral feeding. It predisposes the patient to gastroesophageal reflux and aspiration. Gastroparesis results from altered gut neurologic or muscular function (eg, neu- ropathy in patients with diabetes mellitus) and release of mediators that inhibit gastric emptying (eg, during critical illness).

Consistently high gastric residuals may be an indicator of gastroparesis. For patients with impaired gastric motility, the use of promotility agents such as metoclopramide and erythromycin should be considered.

2. Gastroesophageal reflux occurs in most patients at some time.⁷⁸ Reflux can occur when gastric pressure exceeds LES pressure.

Gastric pressure is increased by large gastric volumes and increased abdominal pressure due to fluid (eg, ascites). Reflux may be greater when the patient is in the supine position, especially if a large-bore feeding tube is in place.³⁰Complications of reflux include esophagitis, vomiting, and aspiration. Gastroesophageal reflux and secondary aspiration can be minimized by maintaining low gastric volumes, keeping the head of the bed elevated, and using agents that increase LES pressure (eg, metoclopramide).

3. Duodenal-gastric (DG) reflux is common but does not usually present a clinical problem. The finding of bile or small-bowel feedings in the stomach is not a contraindication to enteral feedings. It is important to evaluate the clinical significance of the DG reflux.

Large-volume DG reflux may indicate impaired small-bowel motility and can increase gastric residual volume. DG reflux is reduced by promotility agents and more distal placement of small- bowel feeding tubes. It is usually minimal when the feeding tube is beyond the ligament of Treitz.⁷⁹

4. Diarrhea occurs in 2% to 63% of enterally fed patients, depend- ing on how it is defined.^80–87Diarrhea is generally defined as the passage of more than 200 grams of stool per day, but it is frequently defined clinically as three or more liquid stools per day.⁸⁶ It is important to note that the stool is usually pasty in patients fed non-fiber-containing liquid formulas. Many patients also develop rectal incontinence as a result of their illness. Thus, a patient with multiple small-volume bowel movements does not necessarily have diarrhea. Impaction should be ruled out in patients with ooz- ing stools. Diarrhea rarely results from the enteral formula but rather indicates malfunction of the GI tract (eg, malabsorption, excess secretion), bacterial overgrowth, or the presence of toxins.

Medications have been reported to cause 61% of the cases of diar-

rhea in tube-fed patients.^81–87Antibiotics, H2-receptor antagonists, antineoplastics, laxatives, antacids, and potassium and phosphate supplements are medications that commonly contribute to the development of diarrhea. The cause of diarrhea is often multi- factorial (Table 5-1). The best treatment for diarrhea remains unclear. It is rarely necessary to stop enteral feedings; diarrhea usually subsides as the cause is eliminated (eg, infection, drug, toxin, fecal impaction). However, in infants, increases in stool volumes of greater than 20 mL/kg per day are often an indication for less aggressive enteral feeding advancement.⁴⁰Whenever possible, the offending medication(s) should be discontinued. It is important to rule out infection or the presence of enteric pathogens such as C difficilebefore using antimotility agents, because increased bowel motility is one mechanism for eliminating infecting organ- isms and toxins from the GI tract. Antimotility agents may enhance bacterial growth and toxin absorption. Agents used include adsorbents (eg, kaolin, pectin) and antimotility agents (eg, lop- eramide, diphenoxylate/atropine, paregoric, tincture of opium).

Pancreatic enzymes may be useful in patients with pancreatic insufficiency. If diarrhea persists despite treatment of enteric pathogens or disease-related causes, antidiarrheal therapy, and medication adjustments, the enteral formulation should be evaluated. The addition of fiber to the enteral formulation may help bulk up the stool and promote more normal bowel function. Peptide- based and elemental enteral formulas have been associated with improved GI tolerance but should be used judiciously due to their higher cost.⁸⁷Diluting the feeding formula or administering parenteral albumin rarely improves feeding tolerance and is not recommended. Hypoalbuminemia does not cause diarrhea but rather serves as a marker for patients with underlying inflammatory disease, increased gut permeability, and hypercatabolism.

Non-formula-related diarrhea

Medications (sorbitol-based elixirs, antibiotics, H2-receptor antagonists, laxatives, magnesium, and phosphorus) Mediators released during inflammatory syndromes and sepsis Pancreatic insufficiency

Delayed feedings causing bowel atrophy or long-term parenteral nutrition only

Increased bowel motility

Pathogenic bacteria (Clostridium difficile,enterotoxins) Bacterial overgrowth

Cytomegalovirus

Inflammatory bowel disease Impaction

Short-bowel syndrome Formula-related diarrhea Rapid infusion rate

Rapid initiation and progression of feedings in the small bowel High fat intake

Lactose intolerance

Microbial contamination of formula

TABLE 5-1. Possible Causes of Diarrhea in Tube-Fed Patients

S E C T I O N I Fundamentals of Nutrition Support Practice and Management

5. Constipation can result from inactivity, decreased bowel motility, decreased fluid intake, impaction, or lack of dietary fiber. Poor bowel motility and dehydration may lead to impaction and abdominal distension (from obstruction). Other common causes include the use of antimotility agents such as anticholinergics, opioids, calcium-channel antagonists, and certain chemotherapy agents such as vincristine. Neuromuscular blockers do not paralyze gut smooth muscle but may slow bowel motility via anticholinergic actions. Constipation is often improved by the provision of adequate hydration and the use of fiber-containing formulas, stool sof- teners, and bowel stimulants. Laxatives and enemas may improve symptoms in these patients. An abdominal roentgenogram may be needed as a diagnostic tool.

6. Malabsorption without diarrhea. The most common causes are medications (eg, antibiotics, sorbitol-containing medications, H2 antagonists), impaired digestion (pancreatic insufficiency, dimin- ished gut mucosal enzymes, insufficient bile secretion), and impaired absorption (due to underlying injury or disease of the gut).

C. Metabolic complications. Metabolic complications are less prevalent with enteral than parenteral feedings due to the buffering effects of the gut and liver, which can help to prevent rapid metabolic changes.³⁴However, it is still prudent to perform thorough ongoing assessments of patients receiving enteral nutrition support.

1. Hyperglycemia. Most enterally fed patients do not develop hyperglycemia. Hyperglycemia may occur in some patients because of underlying diabetes mellitus or insulin resistance (precipitated by the illness or by medications such as glucocorticoids). Carbohy- drate feeding can increase blood glucose concentrations in these patients. Hyperglycemia should be treated because it impairs immune function, increases the risk of infection, increases post- ischemic neuronal damage, and results in fluid and electrolyte losses. In critically ill patients, hyperglycemia increases in-hospital mortality, bloodstream infections, incidence of acute renal failure requiring dialysis or hemofiltration, need for red cell transfusions, and critical illness polyneuropathy.⁸⁸Blood glucose levels should be monitored at periodic intervals in all patients receiving enteral nutrition support. It is important to treat the underlying disease (eg, infection, inflammation), maintain intravascular volume, and prevent electrolyte disturbances. If blood glucose concentrations remain elevated (>110 mg/dL) in critically ill patients at the carbohydrate level needed by the patient, insulin should be administered and titrated to achieve blood glucose concentrations that are below this range. In nonacute hyperglycemic patients who have not been previously diagnosed with diabetes mellitus or are not being treated with corticosteroids, a workup for diabetes mellitus should be initiated.

2. Electrolyte and mineral deficiencies⁸⁹(Table 5-2)

a) Electrolytes are lost via stool, ostomies, fistulae, urine, and skin.

Patients with excessive losses may need increased intake of various electrolytes. Potassium, magnesium, and phosphorus are required for optimal protein synthesis. The kidneys are primarily responsible for excretion of potassium, magnesium, and phosphorus; intake of these ions may need to be decreased in patients with renal insufficiency or failure. Serum concentrations should be monitored at intervals based on patient acuity, and electrolytes and minerals should be replaced as needed to keep serum levels within the normal range.

b) Sodium is the primary extracellular cation in the body and the major controller of osmolality. Clinical features of hyponatremia and hypernatremia relate to the nervous system and include depressed mentation, confusion, irritability, obtunda-

tion, coma, seizures, nausea, vomiting, anorexia, and headache.

Altered circulating levels of sodium primarily reflect the status of body water. An excess intake of water compared with sodium results in hyponatremia, while an excess intake of sodium compared with water results in hypernatremia. The most common cause of hyponatremia in hospitalized patients is the syndrome of inappropriate antidiuretic hormone (SIADH), which results in retention of water in excess of sodium. SIADH can result from a variety of causes, including intracranial hemorrhage, trauma, tumor, or encephalitis; carcinoma of the lung, duode- num, pancreas, thymus, or lymph nodes; and pneumonia, tuber- culosis, lung abscess, cystic fibrosis, or certain medications.

The most common cause of hypernatremia is dehydration due to water losses in excess of sodium (eg, excess sweating, excess urinary loss of water because of osmotic diuresis, limited water intake). Thus, hypernatremia is treated primarily by administration of fluid, and hyponatremia is treated by fluid restriction.

Hypernatremia and hyponatremia also can be caused by high and low sodium intake, respectively, in relation to output. Most enteral formulas contain low amounts of sodium. Patients with increased sodium losses require replacement. Table salt may be judiciously added to the formula or the flush solution. The amount of salt used is based on the sodium deficit, the volume of fluid losses, and the organ from which the fluids came. Con- versely, the sodium content of IV fluids needs to be calculated when hypernatremia is evaluated.

c) Potassium is the primary intracellular cation in the body and is the major determinant of electrical membrane potential.

Decreased concentrations of potassium result in cardiac arrhythmias, muscle weakness, and impaired protein synthesis.

Potassium deficiency results from losses in the stool, GI secretions, and urine (especially with diuretics).

d) Calcium is the primary divalent cation of the extracellular fluid and is essential for regulating processes that require movement in the body (eg, excitation-contraction coupling in cardiac, smooth, and skeletal muscle; neurotransmission; hormonal secretion; ciliary motion; or cell division).⁸⁹Calcium circulates in the blood in three fractions: ionized, chelated, and protein bound. The ionized fraction is physiologically active and home- ostatically regulated. Total calcium levels (measured by most laboratories) may not accurately reflect the ionized calcium status of sick patients. The best measure of circulating calcium status is the ionized calcium level. Ionized calcium levels are usually obtained with a parathyroid hormone level when serum total calcium values are persistently low despite attempts to normalize them. In the absence of an ionized calcium mea- surement, practitioners often use the following equation to determine a corrected value:

If adequate dietary calcium is not received over the short term, it will be mobilized from bone. However, long-term depletion of dietary calcium may lead to osteopenia or osteoporosis.

Conversely, excess calcium administration during ischemic and septic states can cause cellular injury. Calcium should be administered to patients in only the amounts required to maintain normal concentrations. Some experts believe that calcium intake should be decreased or completely restricted for a short

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