NUT-440 Midterm Revision Sheet PDF

Summary

This document covers enteral nutrition support, including different types of feeding tubes and formulas used to deliver nutrition. It details the advantages and disadvantages of each method, considering patient factors and potential complications. The document also provides information on when enteral nutrition might be contraindicated.

Full Transcript

NUT-440 Midterm Revision Sheet Chapter 20: Enteral Nutrition Support Specialized nutrition support (SNS): llnesses may interfere with food consumption, digestion, or absorption, therefore SNS provides nutrients via feeding tube or intravenous infusion. Types Include: enteral and parenteral nutrition...

NUT-440 Midterm Revision Sheet Chapter 20: Enteral Nutrition Support Specialized nutrition support (SNS): llnesses may interfere with food consumption, digestion, or absorption, therefore SNS provides nutrients via feeding tube or intravenous infusion. Types Include: enteral and parenteral nutrition. Oral Nutrition: oral nutrient supplements including tablets, liquids, fortified or nutrient dense foods. • Patients: with loss of appetite or struggle meeting nutritional needs through diet. • Advantages: easier to consume than meals, avoids stress, complications, and expense of tube feedings. • Taste should be taken into consideration when recommending oral supplements. Enteral nutrition: any method of feeding that uses the gastrointestinal (GI) tract to deliver nutrition and calories. It can include the use of tube feedings, which deliver nutrient-dense formulas directly to the stomach or small intestine via a thin, flexible tube. • Patients: Must have a functioning GI track. - Have impaired motility in the upper GI tract. - Have GI obstructions and fistulas that can be bypassed with a feeding tube. - Gone through intestinal/other surgeries. - Are malnourished. - Have extremely high nutrient requirements. - Mechanical ventilation. - Are mentally incapacitated due to confusion, neurological disorders, or coma. • • Advantages: Fewer chances of infection and less expensive. Contradictions: - Severe GI bleeding. - High-output fistulas (abnormal passages between tissue that permit the passage of fluids). - Intractable vomiting or diarrhea. - Severe malabsorption. - Procedure may be contraindicated if the expected need for nutrition support is < 5- 7 days in a malnourished patient or < 7- 9 days in an adequately nourished patient. Enteral nutrition tube feeding routes: chosen depending on patients’ medical condition, expected duration, and potential complications. 1) Transnasal: tube interested through the nose. For patients expected to be tube fed for <4 weeks. Patients are usually awake during the procedure and the final position of the tube is verified via X-ray. Types: • Nasogastric (NG): tube placed into the stomach via nose. • Nonintentional: tube placed into the intestines via nose. Types include: - Nasoduodenal (ND): tube is placed into the duodenum via the nose. - Nasojejunal (NJ): tube is placed into the jejunum via the nose. • Nasoduodenal (ND): the tube is placed into the duodenum via the nose. • Nasojejunal (NJ): the tube is placed into the jejunum via the nose. 2) Orogastric: tube is passed into the stomach via the mouth. • In infants, orogastric placement is preferred because it allows them breathe normally during feedings. 3) Enterostomy: an opening into the GI tract through the abdominal wall. For patients expecting to be tube-fed for > 4 weeks, or if the nasointestinal route is inaccessible. An enterostomy can be made by either surgical incision or needle puncture. Types: • Gastrostomy: an opening into the stomach where a feeding tube can be passed. • Jejunostomy: an opening into the jejunum where a feeding tube can be passed. Selecting a Feeding Route- Gastric vs. Intestinal: Gastric feedings are preferred because they’re easily tolerated and less complicated because the stomach controls the rate at which nutrients enter the intestine. They are not preferred if patients have: • Gastric obstructions. • Motility disorders. • Inadequate stomach volume. • Avoided in patients at high risk of aspiration. Aspiration: when food, liquid, or other material enters a person's airway and eventually the lungs by accident. • Aspiration pneumonia: and infection of the lungs or large airways caused by aspiration. Feeding tubes: Made from soft, flexible materials that comes in various lengths and diameters. Choice is based on patient age and size, feeding route, and formula viscosity. Outer diameter measured in French units (1 French unit= 1/3 millimeter). Enteral Formulas: Most formulas can supply all of an individual’s nutrient requirements when consumed in sufficient volume. The formulas can be used alone or provided along with other foods. Types include: 1) Standard formulas (polymeric formulas): contain intact proteins and polysaccharides. • Patients: individuals who can digest and absorb nutrients without difficulty. • Intact proteins: protein isolates from milk or soybeans. • Blenderized formulas: enteral formulas that are prepared by using a food blender to blend whole foods. 2) Elemental formulas (hydrolyzed): contain macronutrients that have been broken down and require less digestion. They’re Low in fat and provide fat from medium-chain triglycerides (MCT) to ease digestion and absorption. • Patients: those who have compromised digestive or absorptive function. • MCT: triglycerides that contain fatty acids that 6-12 carbons. MCT do not require digestion and can be absorbed in the absence of lipase or bile. 3) Specialized formulas (disease specific): include nutrient combinations that assist in the treatment of certain illnesses. • Patients: for individuals with liver, kidney, and lung diseases; glucose intolerance; severe wounds; and metabolic stress. • Generally expensive and their effectiveness is controversial. 4) Modular formulas: when ideal formulas are unavailable, modular formulas can be prepared by combining individual macronutrient and micronutrient preparations (called modules). • Patients: prepared for patients who require specific nutrient combinations. Formula characteristics: 1) Macronutrients: • Protein: 12-20% - Higher in patients with metabolic stress. - Lower in patients with chronic kidney disease. • Fat: 15-30% • Carbohydrates: 30-60% 2) Energy density: 1.0- 2.0 Kcal/mL of fluid. • Low energy density: appropriate for patients with average fluid requirements. • High energy density: appropriate for patients who have high nutrient needs or fluid restrictions. • Individuals with high fluid: should be given a formula with low energy density or be supplied with additional water. 3) Fiber: Helpful for treating diarrhea or constipation and maintaining blood glucose control. However, they are avoided in patients before or after some intestinal examinations and surgeries. 4) Osmolality: concentration of osmotically active solutes in a solution, expressed as milliosmoles (mOsm) per kilogram of solvent. • Isotonic formula: osmolality similar to blood serum (≈ 300 milliosmoles/Kg) • Hypertonic formula: osmolality greater than blood serum. Usually 300-700 milliosmoles/Kg. • Medications: when they’re infused along with enteral feedings, the osmotic load increases and may lead to diarrhea. Factors that influence Formula Selection: Should meet the patient’s medical and nutrient needs with the lowest risk of complications and the lowest cost. Factors include: 1) GI function: a person with impaired GI tract may require an elemental formula. 2) Nutrient & energy needs: adjustments might be required in certain situations. 3) Individual tolerances: For patients with food allergies, check ingredient lists. 4) Availability: health care facilities stock a limited number of formulas. 5) Patient’s response to the formula: the dietitian may reevaluate the decision according to the patient’s response to the formula. 6) Fluid requirements: If fluids need to be restricted, the formula should have adequate nutrient & energy densities to provide required nutrients in the volume prescribed. 7) Fiber modifications: • Formulas that provide fiber may be helpful for managing problems such as diarrhea, constipation, and hyperglycemia. • Some patients may need to avoid fiber because they have an increased risk of bowel obstruction or other complications. Administration of Tube Feedings: 1) Transition to Table Foods 2) Safe Handling of Formula: Safety Protocols and feeding Systems. 3) Meeting Water Needs: formula Water Content, water flushes and parenteral Ffuids. 4) Medication Delivery during Tube Feedings: Medications and continuous feedings, and diarrhea. 5) Tube-Feeding Complications: Gastrointestinal, mechanical, metabolic Complications, and monitoring tube Feedings 6) Initiating and Advancing a Tube Feeding: Tube Placement, delivery methods, Initiating tube feedings general guidelines, and checking the gastric residual volume. Safe Handling of Formula: Individuals who are malnourished often have suppressed immune systems and are vulnerable to infection from foodborne illness. Thus, health practitioners should learn the various procedures that help to prevent formula contamination. 1) Safety Protocols: Facilities have protocols for handling food products and formulas based on the potential hazards in food preparation, referred to as Hazard Analysis and Critical Control Points (HACCP) systems. 2) Feeding systems: • Open feeding system: formula is transferred from its original packaging to a feeding container. High chance of contamination. • Closed feeding system: the sterile formula is prepackaged in a container that can be connected directly to a feeding tube. Lower chance of contamination. Initiating and Advancing a Tube Feeding: 1) Tube placement: • X- ray is used to verify the position of the feeding tube, before a feeding is initiated. • If a transnasal tube is inserted into the respiratory tract or are aspirated into the lungs, it will cause serious complications. • To reduce the risk of aspiration, the patient’s upper body is elevated to a 30-to 45-degree angle during the feeding and for 30-60 minutes after the feeding whenever possible. • Tube placement can be monitored by testing pH of a sample of bodily fluid drawn into the feeding tube. - Stomach: pH ≤5 - Small intestine or respiratory track: pH ≥6 2) Formula Delivery Methods: • Intermittent: 250- 400 ml of formula is delivered over 30- 45 minutes using an infusion pump. - Similar to the usual pattern of eating. - Allow the patient freedom of movement between meals. - Best tolerated when delivered into the stomach. - Because of the relatively high volume of formula delivered at one time, intermittent feedings may be difficult for some patients to tolerate, and the risk of aspiration may be higher than with continuous feedings. • Bolus: Rapid delivery of a large volume of formula (250-500ml) over a 5-15 minutes into the stomach. - Given every 3-4 hours using a syringe. - Rapidly administered, do not require an infusion pump, and allow greater independence for patients. - Can cause abdominal discomfort, nausea, and greater risk of aspiration. Therefore, bolus feedings are used only in patients who are not critically ill. • Continuous: Delivered slowly and at a constant rate over a period of 8-24 hours. - Preferred delivery method for intestinal feedings. - Slower and easier to tolerate, therefore its recommended for critically ill patients or patients who cannot tolerate intermittent feedings. - Infusion pump is usually used to ensure accurate and steady flow rates; which can limit the patient’s freedom of movement and are also more costly. • Cyclic: Continuous feedings conducted for shorter periods (8-16 hours) that allows greater patient mobility and GI rest. 3) General guidelines: Formulas are provided full-strength. If the patient cannot tolerate an increased rate of delivery, the feeding rate is slowed until the person adapts. • Intermittent feedings: starts with 60-120 ml/feeding and be increased by 60-120ml every 8 to 12 hours until the goal volume is reached. • Continuous feedings: starts at rates of about 10-40 ml/hour and be increased by 10-20 ml/hour every 8 to 12 hours until the goal rate is reached. 4) Checking the Gastric Residual Volume (GRV): • GRV: volume of formula and GI secretions remaining in the stomach after a previous feeding. • When a patient receives a gastric feeding, the nurse may measure GRV to ensure that the stomach is emptying properly. • Although controversial, experts recommend that feedings be withheld and evaluated if GRV > 500ml • If is issue persists, the physician may recommend intestinal feedings or begin drug therapy to stimulate gastric emptying. Meeting water needs: • Needs: 30- 40 milliliters of water/ Kg of body weight daily. • Formula water content: 70-85% water. • Fluids may be restricted in patients with: kidney, liver, or heart disease. • Additional water is required in patients with: severe vomiting, diarrhea, fever, excessive sweating, high urine output, high-output ostomies, blood loss, or open wounds. • Evaluating hydration status: monitor patients’ weight changes, blood pressure, fluid intake and output, urine specific gravity, and blood levels of creatinine, blood urea nitrogen, and sodium. • Water flushes and parenteral fluids: In addition to the water in formulas, water can be provided by flushing water separately through the feeding tube usually to prevent feeding tubes from clogging. All sources of should be included when estimating fluid intakes. Medication Delivery during Tube Feedings: • Some medications may need to be exposed to the acidic stomach environment, therefore avoid intestinal feeding. • Medications can interact with the components of enteral formulas, however, potential diet-drug interactions must be considered. • Medications and continuous feedings: Continuous feedings usually are stopped before and after medication administration to prevent interactions that may clog the feeding tube or interfere with the medication’s absorption. Some medications may require a prolonged formula-free interval, therefore formula’s delivery rate needs to be adjusted • Diarrhea: Diarrhea is associated with the administration of: sorbitol-containing medications, laxatives, and some types of antibiotics. The high osmolality of many liquid medications can also cause diarrhea, therefore, dilution of hypertonic medications may be helpful. Tube-Feeding Complications: 1) GI complication: • Diarrhea: caused by motility problems, malabsorption, medications, infections, and bacterial overgrowth. • Constipation: caused by motility problems, obstructions, dehydration, certain medications, and low fiber intakes. • Increases aspiration risk due to: impaired gastric motility, or inadequate functioning of the lower esophageal sphincter. 2) Mechanical Complications: • Feeding tube that is: clogged, malfunctioning, dislodged, physical irritant. • Transnasal routes are associated with: dry mouth, sinus or middle ear infections, and injury to GI tissues. • Ostomy patients: leakages of GI secretions develop at tube insertion sites. 3) Metabolic Complications: fluid imbalances, electrolyte imbalances, and hyperglycemia. 4) Monitoring Tube Feedings: • Complications can be prevented by choosing the appropriate feeding route, formula, and delivery method. • Attention to a patient’s primary medical condition and medication use is important as well. • Health practitioners responsible for monitoring body weight, hydration status, and results of laboratory tests to detect problems before complications develop. Transition to table foods: After the patient’s condition improves, the volume of formula can be tapered off as the patient gradually shifts to an oral diet. • Some patients may need an evaluation of swallowing function, • Continuous feedings is often switched to intermittent feedings initially. • Elemental formulas may be replaced by standard formula. • If the patient has not consumed lactose for several weeks, a diet with minimal lactose may be better tolerated. • Oral intake should supply about two-thirds of estimated nutrient needs before the tube feedings are discontinued completely. Chapter 21: Parenteral Nutrition Support Enteral nutrition is preferred over parenteral nutrition if the GI tract is functional, why? Parenteral nutrition is costly and is associated with a number of potentially dangerous complications. To preserve healthy GI function. Parenteral Solutions: • Pharmacies are often for preparing parenteral solutions; therefore: Solutions can be customized to meet patients’ nutrient needs. Solutions have a limited shelf life. • Many premixed parenteral solutions are available for patients with general nutrition requirements. Indications for Parenteral Nutrition: if patients have: • Intractable vomiting or diarrhea • Severe GI bleeding • Intestinal obstructions or fistulas • Paralytic ileus. • Short bowel syndrome • Bone marrow transplants • If using the GI tract would cause harm. • Severe malnutrition and intolerance to enteral nutrition. Contraindications for Parenteral Nutrition: contraindicated in patients at risk of fluid overload, severe hyperglycemia, or significant electrolyte disturbances. • used for <7 days in previously well-nourished patients. Parenteral Nutrition: Access Site 1) Peripheral parental nutrition (PPN): • Location: forearm or hand. • Delivery: limited amounts of nutrients for short periods. • Limitations: not possible if the peripheral veins are too weak to tolerate the procedure. • Patients: who require short-term nutrition support (< 2 weeks) and who do not have high nutrient needs or fluid restrictions. • Complications: veins can be damaged (phlebitis) by highly concentrated solutions. - Phlebitis: inflammation of the vein. - Phlebitis prevention: PPN must be kept below 900 milliosmoles/liter, which limits the amounts of energy and protein the solution can provide. 2) Total parenteral nutrition (TPN): • Location: Large-diameter veins near the heart. • Delivery: supply all a patient’s nutrient needs for longer periods via catheter. The parenteral solutions are rapidly diluted and nutrient concentrations do not need to be limited. - Catheter: thin tube placed within a narrow lumen, used to infuse, or withdraw fluid. • Patients: patients with high nutrient needs or fluid restrictions and for patients who require long term parenteral nutrition. Parenteral Nutrients: Because the nutrients are provided intravenously, they must be given in forms that are safe to inject directly into the bloodstream. Nutrients include: 1) Amino acids: solutions (≥ 8.5%) are used for parenteral solutions, providing 4 kcal/g. Disease-specific amino acid products exist (e.g., for liver and kidney disease) but are rarely used due to limited evidence. 2) Carbohydrates: Dextrose (3.4kcal/g) is the main source of energy in parenteral solutions. Solution concentrations > 10% percent are used only in TPN solutions. Dextrose (3.4kcal/g) is the main source of energy in parenteral solutions. Solution concentrations > 10% percent are used only in TPN solutions. • Example: D5NS: a solution contains 5% dextrose in normal saline. 3) Lipids: lipid emulsions supply essential fatty acids and energy • Typically contain: triglycerides, phospholipids (emulsifier), & glycerol. • Available in : 10, 20, and 30% solutions, providing ≈ 1.1, 2.0, and 2.9 (or 3.0) Kcal/mL. • Supply ≈ 20-30% of total Kcalories → reduces the need for energy from dextrose and lowers the risk of hyperglycemia. Therefore, should be restricted in patients with hypertriglyceridemia 4) Fluids and electrolytes: • Body’s fluids and parenteral solutions are neutral solutions. • Daily needs: 30-40ml/kg and adjusted according to daily fluid losses. • Electrolytes added to parenteral solutions: Na+, K+, Cl-, Ca+2, Mg+2, PO -3. - Not according to the DRI values because they’re not influenced by absorption - Expressed in milliequivalents (mEq); indicate number of ionic charges provided by the electrolyte. - Electrolyte imbalances can be lethal: blood tests are administered daily to monitor electrolyte levels until patients have stabilized. 5) Vitamins and trace minerals: all vitamin included. • Vitamin K: not included for patients on warfarin (anticoagulant). • Iron: can destabilize parenteral solutions that contain lipid emulsions, and some patients have allergic reactions to infused iron, therefore, special forms of iron may need to be injected separately. Parenteral nutrients medication: medication is added directly to the solution or through a separate port using a Y- connector “piggybacking”. • Piggyback: the administration of a second solution using a separate port in an intravenous catheter. Insulin and Heparin (anticoagulant) are sometimes added by piggyback to avoid potential drug-nutrient interactions. Solution preparation: 1) Parenteral formulations: includes: • Total Nutrient Admixture (TNA) “3 in 1” solution: When a parenteral solution contains dextrose, amino acids, and lipids. - Addition of lipids to the formula may cause formation of enlarged lipid droplets and particulates that can obstruct capillaries or have other damaging effects. • 2-in-1 solution: contains dextrose and amino acids, excludes lipids which is often piggybacked to maintain emulsion and stability. - Lipids are administered separately when they are not a major energy source and are used only to provide essential fatty acids. 2) Osmolarity: • PPN solutions: osmolarity is limited to 900 milliosmoles/L. • TPN solutions: may be as nutrient-dense as necessary. • Lipids emulsion: contributes to osmolarity by increasing the energy provided in PPN solutions. • Amino acids, dextrose, and electrolytes: as concentrations of these nutrients increase, the osmolarity of a solution increases. 3) Safety concerns: • To prevent bacterial contamination and maintain stability, parenteral solutions are compounded in the pharmacy under aseptic (sterile) conditions, shielded from light, and refrigerated. • Prior to infusion, the solutions are removed from the refrigerator and allowed to reach room temperature. • During feedings, the solution and catheter need to be checked frequently for signs of contamination. Many hospitals organize nutrition support teams, consisting of physicians, nurses, dietitians, and pharmacists: Administering Parenteral Nutrition: 1) Insertion and Care of Intravenous Catheters: • Catheters in peripheral veins: may be inserted by skilled nurses • Catheters directly in central veins: must be inserted by a physician. - Patients may be awake for the procedure and given local anesthesia. • Complications: air embolism, blood clotting, clogging, dislodgment of catheter, improper placement, infection, sepsis, phlebitis, and tissue injury. - Prevention: nurses use aseptic techniques. 2) Administration of Parenteral Solutions: differs among different institutions. • Start at a slow rate (e.g. 40 mL/hr for 24 hours) and increase the rate gradually to reach the goal rate over 2-3 days. • Slowly increase concentration of the nutrient dilute solution. • Solutions can be started at full volume and full strength unless there is a risk of complications (fluid overload, hyperglycemia). • Continuous Parenteral Nutrition: continuous administration of parenteral solutions over a 24-hour period. - Patients: actuely ill. • Cyclic Parenteral Nutrition: administration of parenteral solutions over an 8-to 14-hour period each day. - Patients: who require long-term parenteral nutrition. - Allows more freedom of movement during the day. - Patients must be able to start and stop daily infusions without complication and tolerate the nutrient-dense solutions. - Some patients may begin with continuous infusions and transition to cyclic infusions as their condition improves. • Regular monitoring: - The parenteral solution and tubing are checked frequently for signs of contamination. - Routine testing of glucose, lipids, and electrolyte levels helps to determine tolerance to solutions. - Frequent reassessment of nutrition status until a patient has stabilized. - Rapid changes in infusion rate are discouraged in patients at risk of developing hyperglycemia or hypoglycemia. 3) Discontinuing Parenteral Nutrition: • Before parenteral nutrition is stopped and enteral feedings begins, good GI function and minimal aspiration risk are needed. • Appetite remains suppressed for weeks after parenteral nutrition is stopped and transitioning to an oral diet is difficult. • Parenteral infusions are reduced when tube feedings or oral feedings begin, because both supply the needed nutrients. • If GI symptoms (nausea, vomiting, bloating, or diarrhea) develop, oral feedings should be limited in size or frequency until the intestines adapt. • Once about 60-75% of nutrient needs can be provided by other means, the parenteral infusions may be discontinued. 4) Managing Metabolic Complications: • Hyperglycemia: blood glucose levels >180 mg/dL - High risk patients: Have glucose intolerant, receiving excessive energy or dextrose, undergoing severe metabolic stress, or receiving corticosteroid medications. - Risk can be reduced by: providing insulin along with parenteral solutions, avoiding overfeeding and rapid infusion rates, and restricting the amount of dextrose in the solution. • Hypoglycemia: uncommon - Cause: when parenteral nutrition is interrupted or discontinued or if excessive insulin is given. - High risk patients: young children. - Risks can be reduced by: Feedings may be tapered off over several hours before discontinuation. Infuse a dextrose solution at the same time that parenteral nutrition is interrupted or stopped. • Hypertriglyceridemia: - Cause: dextrose over- feeding or overly rapid infusions of lipid emulsion. - High risk patients: those with severe infection, liver disease, kidney failure, or hyperglycemia, and those using immunosuppressant or corticosteroids. • Refeeding Syndrome: - Cause: when a severely malnourished person is aggressively fed characterized by electrolyte and fluid imbalances and hyperglycemia. Generally, develops within 2 weeks of beginning parenteral infusions. - High risk patients: those who have experienced chronic malnutrition or substantial weight loss. • - Symptoms: edema, cardiac arrhythmias, muscle weakness, and fatigue. - Mechanism: dextrose infusions increase circulating insulin which promotes anabolic processes and quickly remove P, K, and Mg from the blood, altering electrolyte levels which results in fluid retention and life- threatening changes in various organ systems. - Prevention: provide only half of the patient’s energy requirement when initiating nutrition support and gradually advance the dose over several days while monitoring electrolyte levels. Liver Disease: - Cause: Parenteral nutrition often cause fatty liver, but it is usually corrected after the parenteral infusions are discontinued. Long-term parenteral nutrition can cause progressive liver disease and eventual liver failure. - • Gallbladder Disease: - Cause: When parenteral nutrition continues the GI tract remains unused for long periods, this causes thickened bile that may build up in the gallbladder and cause gallstone formation. - • High risk patients: those GI or liver disorders, malnutrition, or severe infection. Signs: Liver enzymes levels are monitored; abnormal values are seen within weeks of beginning the infusions. Prevention: avoid giving the patient excess energy, dextrose, or lipids (which promote fat deposition in the liver). Prevention: initiating oral intakes or tube feedings before problems develop. Metabolic Bone Disease: - Cause: Long-term parenteral nutrition is associated with lower bone mineralization and bone density. May be related to altered intakes or metabolism of calcium, phosphorus, magnesium, and vitamin D. - Treatment: adjustments in parenteral nutrients, medications, and weight-bearing physical activity. Nutrition Support at Home: Current medical technology allows for the safe administration of nutrition support in the home, patients using home nutrition support can continue to receive specialized nutrition care while leading normal lives. • Patients (or caregivers) must be capable of learning the procedures and managing any complications. • The home should be clean and have adequate storage for formulas or solutions and equipment. • Patients: - Home enteral nutrition: people with disorders that prevent food from reaching the intestines/ interfere with absorption. - Home parenteral nutrition: individuals with disorders that impede absorption or interfere with intestinal motility. • Quality-of-Life Issues: - Time-consuming and inconvenient. - Lifestyle: adjustments must be made. - Extra planning: to travel or participate in sports. - Social issues: no mealtime with family/friends. - Nocturnal feedings: disturbed sleep (bathroom visits/noisy pump). - Explaining one’s medical needs to friends may be embarrassing. Nutrition assessment checklist includes: Medical history, medication, dietary intake, anthropometric measurements, lab test, and physical signs. Chapter 28: Kidney Disease Kidneys: The two kidneys sit just above the waist on each side of the spinal column. They filter the blood and remove excess fluid and wastes in the urine. Nephron (kidney): the functional unit of the kidneys, consists of a glomerulus and tubules. • Glomerulus: the filtering unit of the kidneys as urine production begins. • Tubules: As the filtered fluid moves along the tubule, the blood vessel reabsorbs almost all the water, along with minerals and nutrients your body needs. • Filtrate: substance that passes through the glomerulus and tubules that form urine. • Bowman’s capsule: a part of the nephron that forms a cup-like sack surrounding the glomerulus that collects the filtrate. • Collecting duct: collects urine and transports it to the pelvis through ureters where it is temporarily stored in the bladder. How the kidney functions: 1) Glomerulus and Bowman’s capsule function like a sieve by retaining blood cells and most plasma proteins in the blood while allowing fluid and small solutes to enter the tubules. 2) Next, As the filtrate passes through the tubules, some of its components are reabsorbed and returned to the blood via capillaries surrounding the tubules. 3) Eventually, the remaining filtrate enters a collecting duct shared by several nephrons; additional water is reabsorbed to form the final urine product. 4) The urine then travels through the ureters to the bladder for temporary storage. Why are the kidneys important? 1) Secrete the enzyme renin which helps regulate blood pressure. 2) Produce the hormone erythropoietin, which stimulates the production of RBCs in the bone marrow. 3) Convert vitamin D to its active hormonal form (calcitriol), which helps regulate calcium balance and bone. 4) Regulate the extracellular fluid volume and osmolarity, electrolyte concentrations, and acid–base balance. 5) Excrete metabolic waste products (urea and creatinine), various drugs and toxicants. • Urea: nitrogen- excretion product of protein metabolism. • Creatinine: waste product of creatine. Nephrotic Syndrome: syndrome caused by significant urinary protein losses caused by severe glomerular damage. • Damage to the glomeruli increases their permeability to plasma proteins, allowing the proteins to escape into the urine. • Proteinuria: presence of protein in the urine. • Causes: glomerular disorders, diabetic nephropathy, immunological and hereditary diseases, infections, chemical damage, and some cancers. Consequences of nephrotic syndrome: 1) Edema: • Hypoalbuminemia: low albumin concentrations contribute to a fluid shift from blood plasma to the interstitial space causing edema. • Impaired sodium excretion: nephrotic kidney tends to reabsorb sodium in greater amounts than usual causing sodium and water retention within the body resulting in edema. 2) Blood lipid abnormalities: blood clearance of lipids decline causes elevated levels of LDL, VLDL, and the more atherogenic LDL variant known as lipoprotein(a). 3) Blood clotting abnormalities • Deep vein thrombosis: caused by Urinary losses of proteins that inhibit blood clotting, and elevated levels of plasma proteins that favor clotting • Increased risk of atherosclerosis, heart disease and stroke. 4) Rickets in children: due to loss of vitamin D binding protein, which causes lower vitamin D and calcium levels. 5) Infections: caused by loss of antibodies. 6) Proteinuria: may cause protein energy malnutrition (PEM) which may cause muscle wasting. Nephrotic syndrome treatment: Complications are managed with medications and nutrition therapy depending on the diagnosis. 1) Protein and energy: • Meeting protein and energy needs helps to minimize losses of muscle tissue. • High-protein diets can exacerbate urinary protein losses and result in further kidney damage. • Recommended intake: - Protein: 0.8-1.0g/ kg - Energy: 35kcal/ kg 2) Sodium and potassium: • Limiting sodium controls edema. • Diuretics prescribed for edema may cause potassium loss. • Recommendation: - Sodium: 1-2g/day - Potassium: consume foods rich in potassium. 3) Lipids: • A diet low in saturated fat, trans fats, and refined sugars may help to control elevated LDL and VLDL levels. • If dietary measures are inadequate, lipid lowering medications (statins) may be used. 4) Vitamins and mineral: supplementation can help patients avoid nutrient deficiencies • Nutrients at risk: iron and vitamin D. • Calcium supplementation is recommended to reduce bone loss. Acute kidney injury: Rapid, often reversible, deterioration of kidney function, which occurs over a period of hours or days. Causes: 1) Prerenal factors: conditions that cause a severe reduction in blood flow to the kidneys (heart failure, shock, or blood loss). 2) Intrarenal factors: factors that damage kidney tissue (infections, toxicants, drugs, or direct trauma). 3) Postrenal factors: factors that prevent urine excretion due to urinary tract obstructions (prostate disorder, or pregnancy). Consequences: 1) Decline in renal function: alters the composition of blood and urine. 2) Reduced urinary output: cause a rise in serum creatinine levels. • Oliguria: abnormally low amount of urine, often <400 mL/day. • Anuria: absence of urine, urine output that is < 50-75 mL/day 3) Reduced excretion of fluids and electrolytes leads to: • Edema (fluid retention): due to sodium retention & reduced urine output. • Hyperkalemia: high serum potassium levels. Can alter heart rhythm, causing heart failure • Hyperphosphatemia: high serum phosphate levels. Causes excessive secretion of parathyroid hormone, causing losses of bone calcium. 4) Uremia: nitrogen-containing compounds and waste products accumulate in the blood. 5) Uremic syndrome: clinical outcome of uremia, complications include hormonal imbalances, electrolyte and acid–base imbalances, disturbed heart and GI functioning, neuromuscular disturbances, depressed immunity. Treatment: 1) Oliguric patients: recovery sometimes begins with diuresis (fluid intake up to 3 L/day) are excreted. 2) Avoid nephrotoxic (toxic to the kidneys) drugs until kidney function improves. Instead, use different medication, for example: • Inflammatory conditions: immunosuppressants. • Edema: diuretics (e.g. Lasix). • Acidosis: bicarbonate. 3) Energy and protein: • Protein recommendations: - Non-catabolic patients who don’t require dialysis: 0.8 -1.0 g/Kg. - Patients at risk of muscle wasting including catabolic patients, or treatment includes dialysis: 1.0-1.7 g/Kg. • Energy recommendations: 20-30 Kcal/Kg. 4) Fluids: • Status assessments: weight fluctuations, urine output, blood pressure, serum sodium concentration… • Fluid balance: must be restored in patients who are overhydrated or dehydrated. • Daily fluid needs: urine output+ 400- 600 mL/ day - Additional fluid for patients with fever, vomiting, or diarrhea. 5) Electrolytes: Depending on assessment results restrictions may be necessary for potassium, phosphorus, and sodium. • Dialysis patients: less restrictions. • Oliguric patients on diuretics: may need electrolyte replacements to compensate urinary losses. 6) Enteral nutrition: Formulas designed for patients with acute kidney injury are calorically dense and have either higher or lower protein and electrolyte concentrations than standard formulas. 7) Total parenteral nutrition (TPN): necessary if severely malnourished or tolerate tube feedings for an extended period. Chronic kidney disease (CKD): gradual, irreversible loss of kidney function that results from long-term disease or injury. • The kidneys have a large functional reserve therefore, they can increase their workload to meet demands. Chronic kidney disease typically progresses over many years without causing symptoms. Patients are often diagnosed late, after most kidney function has been lost. Causes: diabetes mellitus, hypertension, inflammatory, immunological, and hereditary diseases that involve the kidneys. Consequences: 1) In early stages: functional nephrons compensate for those that are lost/damaged. They enlarge and filter blood more rapidly to handle the extra workload. 2) As the disease progress: the overworked nephrons continue to degenerate; until the kidneys are unable to function adequately, resulting in kidney failure. 3) Altered Electrolytes & Hormones: • Hormonal adaptations help to regulate electrolyte levels, at a cost: - Increased aldosterone secretion: prevents increases in serum potassium but contributes to fluid overload and hypertension. - Increased parathyroid hormone secretion: helps to prevent elevations in serum phosphate, but contributes to bone loss and renal osteodystrophy. • Develops during 54th/5th stage when: GFR is very low, hormonal adaptations are inadequate, intakes of water or electrolytes are restricted or excessive. • Acidosis: a condition in which there is too much acid in the body fluids, caused when kidneys trying to maintain acid- base balance. May worsen renal bone disease. 4) Uremic Syndrome (uremia complications): uremia may develop, when GFR <15 mL/L. includes: • Hormonal imbalances: - Anemia: caused by reduced erythropoietin production. - Bone disease: cause by reduced active vitamin D production. • Altered heart function: - Heart diseases: caused by fluid and electrolyte imbalances. - Arteries and heart issues: caused by excessive parathyroid hormone secretion. • Neuromuscular disturbances: - Initial symptoms (mild): malaise, irritability, altered thought processes. - Later symptoms: muscle cramping, restless leg syndrome, sensory deficits, tremor, and seizures. • • • Defects in platelet function and clotting factors: causing prolonged bleeding time, bruising, GI bleeding, and anemia. Skin changes: increased pigmentation, severe itchiness. Suppressed immune responses: high risk of developing infections. 5) Malnutrition: • Nutrient losses: a consequence of dialysis, frequent blood draws, or bleeding abnormalities. • Protein-energy wasting: losses of muscle mass and energy reserves due to chronic inflammation, metabolic acidosis, and hormonal disorders causing breakdown of body proteins. - Patients at risk: patients with anorexia, dietary restrictions, depression… Evaluation: 1) Glomerular filtration rate (GFR): the rate at which the kidneys form filtrate • Normal GFR: 125 mL/min in young adults and declines with age. Stage GFR (ml/min per 1.77m2) CKD1: kidney damage >90 CKD2 60-89 CKD3 30-59 CKD4 15-29 CKD5: kidney failure <15 2) Degree of albuminuria: amount of albumin lost in urine daily reflects the extent of kidney damage and correlates well with disease progression and health risks. Treatment: Once kidney disease reaches the end stages dialysis or a kidney transplant is necessary to sustain life. 1) Drug therapy: • Antihypertensive: for hypertension. • Erythropoietin: for anemia. • Phosphate binders: reduces elevated serum phosphate levels. - Gastrointestinal effect: constipation. - Metabolic effect: electrolyte imbalances. • Sodium bicarbonate: reverses acidosis • Cholesterol-lowering medications: lowers elevated serum lipids Levels. 2) Dialysis: replaces kidney function by removing excess fluid and wastes from the blood. • Hemodialysis: blood is circulated through a dialyzer (artificial kidney), where it is filtered by a dialysate. • Dialysate: a solution that selectively removes excess fluid and wastes from the blood. • Peritoneal dialysis: the dialysate is infused into a peritoneal cavity, and the blood is filtered by the peritoneum. After several hours, the dialysate is drained, removing unneeded fluid and wastes. - Peritoneum: membrane surrounding the abdominal cavity. 3) Kidney transplant: alternative to dialysis in patients with end stage renal disease that restores kidney function, allows a more liberal diet, and frees the patient from routine dialysis. • Demand is high than supply. Less than 20% of patients in need receive a kidney transplant. • Immunosuppressive drug therapy: prevents tissue rejection following transplant surgery. Food safety guidelines should be provided to patients and caregivers to avoid foodborne infection. • Nutrition therapy after kidney transplant: Most nutrients can be consumed at levels of the RDA. - Corticosteroids: increases urinary calcium losses, therefore needing calcium supplementation. - If drug treatment leads to hyperglycemia: patients should limit refined carbohydrates and concentrated sweets. CKD Nutrition Therapy: 1) Energy: • Malnutrition: patients at risk should consume foods with high energy density. Oral nutrition supplements or tube feedings may be needed. • Peritoneal dialysis: Most dialysates contain glucose. 64% of this glucose is absorbed (600 Kcal/day) and must be included in estimated energy intake. May cause weight gain. 2) Protein: Moderate protein restriction slows disease progression, reduces nitrogenous wastes, and risk of hyperphosphatemia. However, diet must protein meet needs to prevent wasting. Recommendations: • During later stages (0.6-0.75 g/Kg): To meet essential amino acids needs ≥ 50% of protein consumed should come from high-quality(animal) sources. • During dialysis (1.2 g/Kg): Protein restrictions can be relaxed because dialysis removes nitrogenous wastes and results in some amino acid losses. 3) Lipids: to control elevated blood lipids, limit saturated and trans fats, refined sugars, alcohol, and consume unsaturated fats. 4) Sodium and fluids: • Weight: weight gain can be caused by fluid retention and weight loss can be caused by excessive fluid loss. • Sodium restriction: beneficial for CKD patients since they tend to retain sodium. • Fluid restriction: Only when urine output decreases. • Fluid intake: daily fluid intake should match the daily urine output. • During dialysis: sodium and fluid intakes should be controlled; 2 pounds of water weight are gained daily which is then removed during the next dialysis treatment. 5) Potassium: • Restrictions: for patients who develop hyperkalemia, diabetic nephropathy, end stage CKD, or are treated with hemodialysis. • Restriction not necessary: for those undergoing peritoneal dialysis. 6) Calcium, Phosphorus, and Vitamin D: Serum phosphate & calcium levels are monitored to minimize bone disease risk • Vitamin D supplementation: only for patients with suspected deficiency. • Elevated serum phosphate levels: need dietary phosphorus restriction, phosphate binders might be needed. However, many phosphate binders are calcium salts which increased hypercalcemia risk. • Calcium-rich food: are usually phosphorus-rich, therefore are restricted. Patients may rely on calcium supplements to meet their calcium needs. 7) Vitamin and minerals: • Restrictive renal diet: interferes with intakes and increases risk of deficiencies • Dialysis: causes loss of water-soluble vitamins/some trace minerals, therefore they need to be supplemented. • Recommendations: - Folic acid: 1mg/ day. - Vitamin B6: 10mg/ day. - Vitamin C: <100mg/day. Too much causes risk of kidney stones. - Vitamin A: not recommended since they increase as kidney function worsens. - Iron: deficiency common in hemodialysis patients. IV iron administration is more effective than oral supplements. 8) Nutrition support: for renal patients who cannot consume adequate amounts of food. • Enteral formulas for CKD: higher energy density, lower protein and electrolyte concentrations than standard formulas. • Intradialytic parenteral nutrition: a technique that combines parenteral infusions with hemodialysis treatments. Not proven to be better than oral supplements 9) Dietary Compliance: Adjustments in nutrient intake are required as the disease progresses, once multiple dietary restrictions become necessary, patients often require extensive counseling. • Depending laboratory values, the renal diet may limit: protein, fluids, sodium, potassium, and phosphorus. Kidney stones: crystalline masses that form in the urinary track. Most kidney stones are made of calcium oxalate. • Asymptomatic. • More common in men. Kidney stone development risk factors: • Renal disease • Metabolic abnormalities • Dehydration or low urine volume: promotes minerals crystallization. • Changes in urine acidity: some stones form more readily in acidic urine, whereas others form in alkaline urine. • Obstruction: prevents urine flow and encourages salt precipitation. Types of kidney stones: 1) Calcium Oxalate Stones: • Hypercalciuria, hyperoxaluria and hypocitraturia: promote the formation of calcium oxalate stones. • Hypercalciuria: elevated urinary calcium levels; causes calcium oxalate stones. - Causes: excessive calcium absorption, impaired calcium reabsorption in kidney tubules, elevated serum levels of parathyroid hormone or vitamin D. • Hyperoxaluria: elevated urinary oxalate levels, also promote the formation of calcium oxalate stones. - Oxalate: product of metabolism that binds to calcium. - Causes: increase in the body’s synthesis of oxalate or increased absorption from dietary sources. • Hypocitraturia: low urinary citrate levels; increase the risk of forming calcium stones. - Urinary citrates: form complexes with urinary calcium which inhibit calcium’s tendency to crystallize with oxalates. 2) Calcium Phosphate Stones: Calcium phosphate is a constituent of calcium oxalate stones, but less commonly, some individuals form kidney stones where calcium phosphate is the main constituent. • Patients at risk: people with hypercalciuria who produce alkaline urine. 3) Uric acid stones: associated with gout, a metabolic disorder characterized by elevated uric acid levels in the blood and urine. • Cause: acidosis. • Purines-rich diet: Purines are found in animal proteins that degrade to uric acid in the body, causing high uric acid levels. This promotes the crystallization of uric. acid 4) Cystine stones: high concentrations of urinary cystine causing subsequent crystallization and stone formation. • Prevention: High fluid intakes for some patients, others require drug therapy like potassium citrate to reduces urine acidity. • Patients at risk: people with cystinuria. - Cystinuria: inherited disorder in which the renal tubules are unable to reabsorb cystine. 5) Struvite stones: crystals of magnesium ammonium phosphate. Can accompany chronic urinary infections or disorders that interfere with urinary flow. • Prevention: Preventing/ treating urinary tract infections. Some patients require antibiotic to prevent further stone formation. Consequences of Kidney stones: 1) Renal colic: pain caused by passing a kidney stone through the ureter. Begins in the back and intensifies as the stone travels toward the bladder. • Treatment: some need medication. • Hematuria (blood in the urine): may happen due to damage to the kidneys or ureter lining. 2) Urinary tract complications: caused when stones are unable to pass through the ureter. • Symptoms: urination urgency, frequent urination, or inability to urinate. Kidney stone prevention/ treatment: sones are less likely to form in dilute urine. 1) Adequate fluids intake: drink >12 cups of fluid daily to maintain a urine volume ≥2 L/day. 2) Dietary measures: • Calcium binds oxalate in the intestines which reduces oxalate absorption and helps control hyperoxaluria. - Recommendation: 800-1200 mg/day • • Oxalate: Low-calcium diets promote oxalate absorption causing higher urinary oxalate levels, which could be beneficial. High protein intake and sodium increase urinary calcium excretion. - Protein recommendation: 0.8-1.0g/kg. - Sodium recommendation: 2000-3000mg/day. • Restricting purines: helps to control urinary uric acid levels. 3) Medication: Medications that relax the ureter (α-blockers, calcium-channel blockers) and increase urine volume (e.g. diuretics) may facilitate stone passage. • Thiazide diuretics: prevents calcium oxalate stones. • Allopurinol: reduce uric acid levels • Potassium citrate: reduce urine acidity 4) Stent (thin, flexible tube): can be placed in the ureter to promote stone passage, may cause excessive bleeding. 5) Fragmentation: some kidney stones can be fragmented into pieces that are small enough to pass in the urine; commonly using extracorporeal shock wave lithotripsy. • Extracorporeal shock wave lithotripsy: procedure that uses high-amplitude sound waves to degrade the kidney stone. 6) Surgical: involve physical removal of kidney stones have a higher success rate but are also more invasive. Calculations For parenteral nutrition: Amino acid%= amino acid%/ 100ml = amino acid (g) Amino acid needs= (amino acid (g)/ 100 (ml)) x fluid needs (ml) Example: Amino acid: 5%. = 5/100ml = 5g Fluid needs: 1250ml/ day Amino acid needs: = (5g/100ml) x 1250ml = 62.5g amino acids Carbohydrate needs= dextrose% = (dextrose%/ 100ml) x fluid needs (ml) Example: Dextrose: 25% Fluid needs: 1250ml/ day Dextrose (g)= (25/ 100 (ml)) x 1250ml =312.5g Lipid needs= lipid% emulsion kcal x lipid emulsion (ml) Lipid % Emulsion kcal/ ml 10% 1.1 kcal/ ml 20% 2 kcal/ ml 30% 2.9 or 3 kcal/ ml Example: Lipid emulsion%: 20% Emulsion ml: 250ml Lipid kcal= 250ml x 2kcal/ ml= 500kcal Estimating osmolarity (m0sm/L): 1) Amino acids osmolarity= amino acid (g) x 10 • Example: amino acid= 40g = 40 x 10 = 400 m0sm/L 2) Dextrose osmolarity= dextrose (g) x 5 • Example: Dextrose= 250g = 250 x 5 = 1250 m0sm/L 3) Lipid osmolarity (20%) = lipid (g) x 0.71 • Example: Lipid= 40g = 40 x 0.71 = 28.4 m0sm/L 4) Electrolyte osmolarity= electrolyte (mEq) x 1 • Example: Calcium= 5 mEq =5x1 = 5 m0sm/L 5) Total osmolarity: add all the previous osmolarity results together. Enteral nutrition: planning feeding tube schedule Formula ml= (Kcal/ day) / (Formula kcal/ ml) Remaining fluid needs= total fluid need (ml)- formula (ml) Milliliter of formula per feeding= formula (ml)/ amount of feeding per day Example: Formula= 2kcal/ ml Total kcal/ day= 2000 kcal/ day Fluid needs ml/ day= 2000ml/ day Feeding per day: 6 intermittent feedings Formula ml: = 2000/ 2 = 1000 ml Remaining fluid needs: = 2000- 1000 = 1000 ml Millimeter of formula per feeding: = 1000/ 6 = 167 ml 1 French unit= 1/3mm

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