NUTRITIONAL ALTERATIONS Assessing Nutritional Status

Assessing the patient includes taking a history and performing a physical examination. A thorough assessment will help confirm good nutrition or detect an alteration in nutritional status and the need for in- depth assessment and follow-up. It will also help you identify potential nutrition related health problems, determine educational needs, and plan realistic patient outcomes. 1) Biochemical Data - A wide range of laboratory tests can provide information about nutritional status, including blood and urine tests often used. No diagnostic tests areperfect, and care must be taken in interpreting the results of the test. Serum Proteins- serum protein levels provide an estimate of visceral protein stores. Tests commonly include hemoglobin, albumin, transferrin, and total iron- binding capacity. A low hemoglobin level may be evidence of iron deficiency anemia. However, abnormal blood loss or a pathologic process must be ruled out before iron deficiency related to diet is confirmed. o Albumin- accounts for more than 50% of the total serum albumin, is one of the most common visceral proteins evaluated as part of the nutritional assessment. Because there is so much albumin in the body and because it is not broken down very quickly, albumin concentrations changes slowly. Thus, a low serum albumin level is a useful indicator of prolonged protein depletion rather than acute or short- term changes in nutritional status. However, many conditions besides malnutrition can depress albumin concentration, such as altered liver function, hydration status, and losses from open wounds and burns. o Transferrin- a protein that binds and carries iron from the intestine through the serum. Because it has a shorter half life than albumin (8-9days), transferrin is likely to respond more quickly to protein depletion than albumin. Serum transferrin can be measured directly by a total iron-binding capacity test, which indicates iron deficiency anemia, pregnancy, hepatitis and liver dysfunction. An increase in TIBC can indicate iron- deficiency: a decrease, anemia. o Pre- albumin- also referred to as thyroxin- binding albumin and transthyretin, has the shortest half- life and smallest body pool, and is, therefore, the most responsive serum protein to rapid changes in nutritional status but unfortunately is expensive to measure.

Urinary Tests Urinary urea nitrogen creatinine are measures of proteincatabolism and the state of nitrogen-balance. Urea, the chief end product of amino acid metabolism, is formed from ammonia detoxified by the liver, circulated in the blood, and transported to the kidneys for excretion in urine. Urea concentrations in the blood and urine, therefore, directly reflect the intake and breakdown of dietary protein, the rate of urea production in the liver, and the rate of urea removal by the kidneys. The state of nitrogen balance is determined by comparing the nitrogen intake to the nitrogen output over a24-hour period. A positive nitrogen balance exists when intake exceeds nitrogen output; a negative nitrogen balance occurs when output exceeds nitrogen intake. Protein intake must be accurately recorded and kidney function must be normal to ensure the validity of urinary urea nitrogen test. Urinary creatinine reflects a persons total muscle mass because creatinine is the chief end product of the creatinine produced when energy is released during skeletal muscle metabolism. As skeletal muscle atrophies during malnutrition, creatinine excretion decreases. Standard for creatinine excretion are developed based on gender and height. Urinary creatinine is also influenced by protein intake, exercise, age, renal function, and thyroid function. Total Lymphocyte Count Certain nutrient deficiencies and forms of PCM can depress the immune system. The total number of lymphocytes decreases as protein depletion occurs.

2) Clinical Manifestations Manifestations That May Indicate Protein- Calorie Malnutrition - Hair- loss; dull, dry, brittle hair; loss of hair pigment - Loss of subcutaneous tissue; muscle wasting - Poor wound healing; decubitus ulcer - Hepatomegaly - Edema Manifestation Often Present In Vitamin Deficiencies. - Conjunctival and corneal dryness (vitamin A) - Dry, scaly skin; follicular hyperkeratosis, in which the skin appears to have gooseflesh continually (Vitamin A) - Gingivitis; poor wound healing (Vitamin C)

Petechiae; ecchymoses (vitamin C or K) Inflamed tongue, cracking at the corners of the mouth (riboflavin [vitamin b2],niacin, folic acid, Vitamin B12,or other B vitamins) Edema; heart Failure (thiamine [Vitamin B1]) Confusion; Confabulation(thiamine [Vitamin B1])

Manifestations Often Present In Mineral Deficiencies -Blue sclera; pale mucous membranes; spoon- shaped nails (iron) - Hypogeusia, dysgeusia; eczema; poor wound healing( zinc) Manifestations Often Observed With Excessive Vitamin Intake - Hair loss; dry- skin; Hepatomegaly (vitamin A)

3) Nutrition History Information

Inadequate Intake Of Nutrients - Alcohol abuse - Anorexia, severe or prolonged nausea or vomiting - Confusion, coma - Poverty Inadequate Digestion Or Absorption Of Nutrients - Previous gastrointestinal surgeries, especially gastrectomy, jejunoileal bypass, and ileal resection. - Certain medications, especially antacids and histamine H2- receptor antagonists, cholestyramine and anti convulsants Increased Nutrient Losses - Blood loss - Severe diarrhea - Fistulae, draining abscesses, wounds, decubitus ulcers - Peritoneal dialysis or hemodialysis - Corticosteroid therapy (increased tissue catabolism) Increased Nutrient Requirement - Fever - Surgery, trauma, burns, infection - Cancer (some types) - Physiologic Demands ( pregnancy, lactation, growth)

Nursing Diagnoses

1) Diarrhea - Related to impaired absorption, Diarrhea may indicate a problem, such as in dietary intake appetite, or weight or ingestion of irritating or contaminated foods. 2) Risk for Impaired Skin Integrity - Related to nutritional deficiencies, risk for impaired skin integrity may occur with deficiencies of Vitamins A, B, and C; Hypervitaminoses A and D; iodine and zinc deficiencies; and protein- calorie malnutrition. 3) Impaired Physical Mobility - Related to nutritional problems, impaired physical mobility may be associated with B and D deficiencies.

4) Risk for Deficient Fluid Volume - Related to decrease fluid intake or fluid loss, Risk for Deficient Fluid Volume may occur with vomiting, excessive nasogastric tube drainage, diarrhea, or hemorrhage. 5) Imbalanced Nutrition: Less than body Requirements - Related to an inability to ingest adequate amounts of food, Imbalanced Nutrition: Less than body Requirements may occur in any disorder that affects the patients ability to digest or absorb any nutrients.

Total Parenteral Nutrition

Refers to the delivery of all nutrients via IV route. TPN is used when the GI tract is not functional or when nutritional needs cannot be met solely via the GI tract. Likely candidates for TPNinclude patients who have a severely impaired absorption (as in short bowel syndrome, collagen- vascular diseases, and radiation enteritis), intestinal obstruction, peritonitis, and prolonged ileus. In addition, some postoperative, trauma, and burn patient may need TPN to supplement the nutrient intake they are able to tolerate via the enteral route.

Types of Parenteral Route

PN should only be initiated in patients who are hemodynamically stable and who are able to tolerate the fluid volume, protein, carbohydrate, and lipid doses necessary to provide adequate nutrients. -Temporary use -Handles 800-900 mosm/Kg -Uses arm and leg veins for infusion

Conditions warranting cautious use of PN: Azotemia Congestive heart failure Diabetes Mellitus Electrolyte disorders Pulmonary disease Peripheral administration is achieved through peripherally inserted central catheters (PICCs) or standard cannulas, inserted with an aseptic technique. o Tolerance to peripheral lines is increased with feeds of low osmolality and neutral pH and the use of soft paediatric cannulas.

Central PN (TPN) is a concentrated formula which is hyperosmolar and must be delivered into a central vein. -Subclavian central venous catheter into superior vena cava -Requires surgery to place central line -Can use single or double lumen tubes -Infection control v. V. Important -Can be used for long term feeding TPN provides:

Carbohydrates in the form of glucose. Protein in the form of amino acids. Lipids in the form of triglycerides. Electrolytes. Vitamins and trace minerals.

Central catheters and ideally tunnelled subclavian vein central lines, inserted using the full aseptic technique are the optimal method of access. Parenteral nutrition solution is thrombogenic and an irritant to veins. Central access allows delivery of more concentrated formulations into high-flow vessels.

Potential Complications
Mechanical complications Mechanical complications are primarily related to the initial placement of a central venous catheter. Improper placement may cause pneumothorax, vascular injury with hemothorax, brachial plexus injury or cardiac arrhythmia.

Venous thrombosis is one of the two most common problems that occur after central venous access is established. The other is infection. Venous thrombosis is associated with significant morbidity rates. Signs include distended neck veins and swelling of the face and ipsilateral arm. The risk of venous thrombosis is greater if patients are dehydrated, have certain malignancies, have had prolonged bed rest, have venous stasis, have sepsis, or have hypercoagulation. Additional risk factors include morbid obesity, smoking, or ongoing estrogen therapy. Infectious complications PN imposes a chronic breech in the body's barrier system. The infusion apparatus from container to catheter tip may prove a source for the introduction of bacterial or fungal organisms. The operator inserting the venous catheter, the pharmacist compounding the solution, or the care-giver hanging the bag or changing the site dressing may contaminate the patient's "lifeline." Infection is one of the two most common problems that arise after central venous access is established. The other is venous thrombosis, discussed earlier. The mortality rate from catheter sepsis may be as high as 15%. The primary preventive measures include adhering to strict aseptic procedure while establishing access and providing care of the dressing and line, and prohibiting the use of the TPN line for other purposes. Other preventive measures include:

Changing the dressing routinely (every 48-72 hours) or when it becomes soiled, wet or loose. The care-giver should wear a mask and gloves while changing the dressing. Extending the application of antimicrobial solution at least 1 inch beyond the final dressing. Placing a sterile sponge over the catheter, then placing an occlusive dressing. Inspecting the site for tenderness, erythema, edema, loose sutures, or drainage. Changing the TPN intravenous tubing every 48 hours. A 0.22-m inline filter should be used whenever fat is not being infused. Avoiding violation of TPN catheters for central venous pressure monitoring or the administration of intravenous medications or blood products. Reported by: Juliann S. Aragon

References: Fundamentals of Nursing by Kozier Illustrated Manual of Nursing Practice By Lippincot Williams and Wilkins Priorites in Critical Care Nursing by Urden, Lindan, et. al.
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NUTRITIONAL ALTERATIONS Nutrition and Cardiovascular Alterations

Diet and cardiovascular disease may interact in a variety of ways. On the one hand, excessive nutrient intake, manifested by overweight or obesity and a diet rich in cholesterol and saturated fat, is a risk factor for development of arteriosclerotic heart disease. On the other hand, the consequences of chronic myocardial insufficiency may include malnutrition.

Nutrition and Pulmonary Alterations

Malnutrition has extremely adverse effects on respiratory function, decreasing surfactant production, diaphragmatic mass, vital capacity, and immunocompetence. Patients with acute respiratory disorders find it difficult to consume adequate oral nutrients and can rapidly become malnourished. Individuals who have an acute illness superimposed on chronic respiratory problems are also at high risk. Almost three fourths of patients with chronic obstructive pulmonary disease (COPD) have had weight loss. Patients with undernutrition and end-stage COPD, however, often cannot tolerate the increase in metabolic demand that occurs during refeeding. In addition they are at significant risk for development of cor pulmonale and may fail to tolerate the fluid required for delivery of enteral or parenteral nutrition support. Prevention of severe nutritional deficits, rather than correction of deficits once they have occurred, is important in nutritional management of these patients.

Nutrition and Neurologic Alterations

Because neurologic disorders such as stroke and closed head injury tend to be long-term problems, these patients require good nutritional care to prevent nutritional deficits and promote well-being.

Nutrition and Renal Alterations

Providing adequate nutrition care for the patient with renal disease can be extremely challenging. Although renal disturbances and their treatments can greatly increase needs for nutrients, necessary restrictions in intake of fluid, protein, phosphorus, and potassium make delivery of adequate calories, vitamins, and minerals difficult. Thorough nutrition assessment provides the basis for successful nutrition management in patients with renal disease.

Nutrition and Gastrointestinal Alterations

Because the gastrointestinal (GI) tract is so inherently related to nutrition, it is not surprising that impairment of the GI tract and its accessory organs has a major impact on nutrition. Two of the most serious GI-related illnesses seen among critical care patients are hepatic failure and pancreatitis.

Hepatic Failure Because the diseased liver has impaired ability to deactivate hormones, levels of circulating glucagon, epinephrine, and cortisol are elevated. These hormones promote catabolism of body tissues and cause glycogen stores to be exhausted. Release of lipids from storage deposits is accelerated, but the liver has decreased ability to metabolize them for energy. Furthermore, inadequate production of bile salts by the liver results in malabsorption of fat from the diet. Therefore body proteins are used for energy sources, producing tissue wasting. The branced-chain animo acids (BCAAs) leucine, isoleucine, and valine are especially well used for energy, and their levels in the blood decline. Conversely, levels of the aromatic amino acids (AAAs) phenylalanine, tyrosine, and tryptophan rise as a result of tissue catabolism and impaired ability of the liver to clear them from the blood. The AAAs are precursors for neurotransmitters in the central nervous system (serotonin and dopamine). Rising leels of AAAs may alter nerve activity within the brain, leading to symptoms of encephalopathy. In addition, the damaged liver cannot clear ammonia from the circulation adequately, and ammonia accumulates in the brain. The ammonia may contribute to the encephalopathic symptoms and also to brain edema.

Pancreatitis The pancreas is an exocrine and endocrine gland required for normal digestion and metabolism of proteins, carbohydrates, and fats. Acute pancreatitis is an inflammatory process that occurs as a result of autodigestion of the pancreas by enzymes normally secreted by that organ. Food intake stimulates pancreatic secretion and thus increases the damage to the pancrease and the pain associated with the disorder. Patients usually present with abdominal pain and tenderness and elevations of pancreatic enzymes. A mild form of acute pancreatitis occurs in 80% of patients requiring hospitalization, and severe acute pancreatitis occurs in the 20%. Patients with the mild form of acute pancreatitis do not require nutrition support and generally resume oral feeding program

Nutrition and Endocrine Alterations

Endocrine alterations have far-reaching effects on all body systems and thus affect nutritional status in a variety of ways. One of the most common endocrine problems, both in the general population and among critically ill patients, is diabetes mellitus.

ADMINISTERING NUTRITION SUPPORT Enteral Nutrition

Whenever possible, the enteral route is the preferred method of feeding. Patients with abdominal trauma in particular have lower morbidity and mortality rates if fed enterally rather than parenterally. There are a variety of commercial enteral feeding products, some of which are designed to meet the specialized needs of the critically ill. Products designed for the stressed patient with trauma or sepsis are usually rich in glutamine, arginine, and antioxidant nutrients (e.g., vitamins C, E, and A; selenium). The antioxidants help to reduce oxidative injury to the tissues (e.g., from reperfusion injury). Some products can be consumed orally, but it can be difficult for the critically ill patient to consume enough orally to meet the increased needs associated with stress. Potential benefits of enteral nutrition over PN include: 1. Physiologic Nutrients are metabolized and utilized more effectively via the enteral than the parenteral route. The gut and liver process enteral nutrients before their release into systemic circulation. The gut and liver help maintain the homeostasis of the amino acid pool as well as the skeletal muscle tissue. 2. Immunologic Gut integrity is maintained by enteral nutrients through the prevention of bacterial translocation from the gut, sytemic sepsis, and potential increased risk of multiple organ failure. Lack of GI stimulation may promote bacterial translocation from the gut without concurrent enteral nutrition. Provision of early enteral nutrition may minimize risk of gut related sepsis. 3. Safety (avoid complications related to intravenous access): Catheter sepsis Pneumothorax

Catheter embolism Arterial laceration Cost of EN formula is less than PN. Cost of equipment and personnel for preparation and administration is less.

4. Cost

However, there are contraindications to enteral nutrition support:

Expected need less than 5-10 days Severe acute pancreatitis High-output proximal fistulas Inability to gain access Intractable vomiting or diarrhea

Formula selection
Selection of an enteral formula must be patient specific. The functioning and capacity of the GI tract, underlying disease states and patient tolerance must be assessed to determine which formula should be selected. Many formulas are very similar in composition, varying only slightly in nutrient content. It is important to be familiar with the properties of commonly used enteral formulas.

Types of Enteral Route

Long-term nutrition:

Gastrostomy Gastrostomy tubes are placed into the stomach and are used for long term feeding-for example, after a stroke. They are commonly placed endoscopically-that is, by percutaneous endoscopic gastrostomy-but can also be placed during surgery or radiologically. Insertion of the tube in percutaneous endoscopic gastrostomy involves insufflation of the stomach to permit apposition to the abdominal wall, percutaneous cannulation of the stomach, and delivery of the gastrostomy tube through the oropharynx and oesophagus out of the percutaneous hole. The tube is kept in place by an intragastric bumper. Complications include damage to intra-abdominal structures, bleeding, infection and peristomal leakage. Buried bumper syndrome is an uncommon but important complication. Tension between bumpers used to secure the tube to the skin and gastric wall can lead to gastric ulceration. The bumpers are then

displaced anywhere between skin and gastric wall. Feed will subsequently leak about the tube and ultimately the buried bumper will need to be removed.

Jejunostomy Jejunostomy tubes are placed directly into the jejunum through the abdominal wall. They are used when the oesophagus or stomach is absent, after oesophagogastric surgery, or if gastric emptying is impaired and there is a high risk of aspiration. They are commonly placed surgically but can be placed endoscopically (percutaneous endoscopic gastrojejunostomy) or radiologically. Specific complications include damage to intra-abdominal organs, bleeding, and infection.

Short-term nutrition:

Nasogastric feeding - feeding consisting of delivering liquid nutrients through a tube passing through the nose and into the stomach A nasogastric feeding tube or NG-tube is passed through the nares (nostril), down the esophagus and into the stomach. This type of feeding tube is generally used for short term feeding, usually less than a month, though some infants and children may use an NG-tube long-term. Individuals who need tube feeding for a longer period of time are typically transitioned to a more permanent gastric feeding tube. The primary advantage of the NG-tube is that it is temporary and relatively non-invasive to place, meaning it can be removed or replaced at any time without surgery. NG-tubes can have complications, particularly related to accidental removal of the tube and nasal irritation.

Nasoduodenal feeding - Nutrition support provided via a tube inserted via the nose, esophagus and stomach into the duodenum. A nasoduodenal feeding tube is a fine bore weighted tube passed into the duodenum via the nose which is used for short or medium term nutritional support. It is particularly indicated in patients with abnormal pylorus function, problems with aspiration or in patients with delayed gastric emptying.

Nasojejunal feeding - Nutrition support provided through a tube inserted through the nose via the esophagus, stomach and duodenum into the jejunum. A nasojejunal feeding tube or NJ-tube is similar to an NG-tube except that it is threaded through the stomach and into the jejunum, the middle section of the small intestine. In some cases, a nasoduodenal or ND-tube may be placed into the duodenum, the first part of the small intestine. These types of tubes are used for

individuals who are unable to tolerate feeding into the stomach, due to dysfunction of the stomach, impaired gastric motility, severe reflux or vomiting. These types of tubes must be placed in a hospital setting.

Potential Complications
Gastrointestinal complications Nausea and vomiting Approximately 20% of patients receiving enteral tube feedings experience nausea and vomiting. Vomiting increases the risk of aspiration. Causes are multifactorial but delayed gastric emptying is the most common problem. If delayed gastric emptying is suspected, consider reducing narcotic medications, switching to a low-fat formula, administering the feeding solution at room temperature, reducing the rate of administration, and administering a promotility agent. If the patient appears distended, check gastric residuals before the next bolus feeding, or every four hours for continuous feeding. If gastric residuals are low yet nausea persists, consider antiemetic medications. Diarrhea Diarrhea is common in tube fed patients, occuring in 2% to 63% of patients depending on how it is defined. If clinically significant diarrhea develops during enteral tube feeding, consider the following options:

Add fiber, e.g., psyllium Consider an enteral formula with fiber Change the formula Use an antidiarrheal agent

Constipation 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. A standard abdominal x-ray is often effective for diagnosis and will clearly differentiate constipation from bowel obstructions.

Constipation usually is improved through adequate hydration and use of fibercontaining formulas, stool softeners, or bowel stimulants. Malabsorption/maldigestion Malabsorption is defined as impaired absorption of one or more nutrients. Clinical manifestations include unexplained weight loss, steatorrhea, diarrhea, anemia, tetany, bone pain, bleeding, neuropath, glossitis, or edema. Causes of malabsorption are many and include gluten sensitive enteropathy, Crohn's disease, diverticular disease, radiation enteritis, enteric fistuals, HIV, pancreatic insufficiency, and short bowel syndrome. Knowledge of the patient's history and selection of an appropriate enteral product should help reduce or prevent malabsorption. However, depending upon the extent of disease, parenteral nutrition may be necessary. Mechanical complications Aspiration Pulmonary aspiration is an extremely serious complication of enteral feeding and can be life-threatening in malnourished patients. The incidence of clinically significant aspiration pneumonia is 1% to 4%. Symptoms of aspiriation include dyspnea, tachypnea, wheezing, rales, tachycardia, agitation, and cyanosis. Aspiration of small amounts of formula may not cause immediate symtoms, but a fever later may suggest development of aspiration pneumonia. Risk factors for aspiration include:

Decreased level of consciousness Diminished gag reflex Neurologic injury Incompetent LES GI reflux Supine position Use of large-bore feeding tubes Large gastric residuals Use of small-bowel feeding tubes, promotility agents, periodic assessment of gastric residuals, and keeping the head of the bed elevated may reduce the risk of aspiration.

Tube malposition Complications may arise during the placement of a feeding tube or simply from the presence of one. Feeding tube placement can cause bleeding, tracheal or parenchymal perforation, and GI tract perforation. Placement of tubes by trained personnel and using appropriate post-placement montoring should minimize these complications. Presence of the feeding tube itself may cause upper and lower airway complications, aggravation of esophageal varices, cellulitis, necrotizing fasciitis, fistulas, and wound infection. Use of a small-bore feeding tube and very attentive nursing care can minimize many of these problems. Tube clogging Tube clogging is more likely with intact protein products and viscous products. Most clogs can be prevented by routine flusing of the feeding tube, use of clean technique to minimize formula contamination, and extreme care when administering medications via the feeding tube. The recommended first line method to unclog a tube is to instill warm water using slight manual pressure. If this fails, a pancrelipase and sodium bicarbonate solution may be instilled in order to "digest" the clog. Metabolic complications Metabolic complications of enteral nutrition are similar to those that occur during PN, although the incidence and severity may be less. Careful monitoring can minimize or prevent metabolic complications. Problem Hyponatremia Hypernatremia Dehydration Hyperglycemia Cause Overhydration Inadequate fluid intake Diarrhea Inadequate fluid intake Too many calories Lack of adequate insulin Treatment Change formula Restrict fluids Increase free water Evaluate causes of diarrhea Increase free water Evaluate caloric intake Adjust insulin

Hypokalemia Hyperkalemia

Refeeding syndrome Diarrhea Excess K intake Renal insufficiency

Replace K Evaluate causes of diarrhea Change formula

Refeeding syndrome Refeeding of severely malnourished patients may result in "refeeding syndrome" in which there are acute decreases in circulating levels of potassium, magnesium, and phosphate. The sequelae of refeeding syndrome adversely affect nearly every organ system and include cardiac dysrhythmias, heart failure, acute respiratory failure, coma, paralysis, nephropathy, and liver dysfunction. The primary cause of the metabolic response to refeeding is the shift from stored body fat to carbohydrate as the primary fuel source. Serum insulin levels rise, causing intracellular movement of electrolytes for use in metabolism. The best advice when initiating nutritional support is to "start low and go slow". Recommendations to reduce the risk of refeeding syndrome include:

Recognize patients at risk o Anorexia nervosa o Classic kwashiorkor or marasmus o Chronic malnutrition o Chronic alcoholism o Prolonged fasting o Prolonged IV hydration o Significant stress and depletion Correct electrolyte abnormalities before starting nutritional support Administer volume and energy slowly Monitor pulse, I/O, electrolytes closely Provide appropriate vitamin supplementation Avoid overfeeding

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