Total enteral and Parenteral Nutrition

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Total enteral and Parenteral Nutrition : 

Total enteral and Parenteral Nutrition Presenter :Dr. Manjula Sudhakar Rao Moderator : Dr. Nalini Kotekar

Slide 2: 

The more impure bodies are fed, the more diseased they will become. --Hippocrates

Overview : 

Overview Adaptations to Food Deprivation Energy Expenditure and Caloric Requirements Enteral nutrition Modes of feeding Feeding formulas Regimen Complications Parentereal nutririon Indications Routes Formulations Complications

Physiologic Adaptations to Food Deprivation : 

Physiologic Adaptations to Food Deprivation Short-Term Fasting Complete food deprivation leads to mobilization of body protein to support energy needs. Early in fasting, release of amino acids from skeletal muscle increases as a result of a decrease in protein synthesis and a marked rise in protein degradation. These adaptive changes in muscle protein metabolism seem to result from the low level of circulating insulin, although glucocorticoids also play an essential permissive role.

Slide 5: 

Early in fasting, under the influence of decreased insulin and elevated glucagon, hepatic glycogenolysis provides a limited store (≤100 g) for maintenance of systemic glucose. However, fat constitutes the bulk of calories available and lipolysis and release of free fatty acids occur in response to the low insulin levels. For example, the average adult fat reserve is approximately 10 kg, or 100,000 kcal, 60 times hepatic glycogen stores

Slide 6: 

In peripheral tissues during fasting, utilization of free fatty acids and ketone bodies for production of ATP increases, whereas glucose oxidation is inhibited. BCAA oxidation in muscle rises, thus sparing glucose. gluconeogenesis in the liver and kidney is activated via muscle-derived glutamine and alanine, lactate, and glycerol released from lipid oxidation, with increased production of urea. This process maintains blood glucose levels for tissues that are highly dependent on glucose for energy, such as the brain, erythrocytes, and the kidney

Normal Stores of Available Energy and Rates of Use in a Man Weighing 65 kg : 

Normal Stores of Available Energy and Rates of Use in a Man Weighing 65 kg From Passmore R, Robson JS: A Companion to Medical Studies, vol 3. Oxford, Blackwell Scientific, 1974

Long-Term Fasting : 

Long-Term Fasting In prolonged fasting, gluconeogenesis from body proteins and loss of muscle mass are gradually reduced. The most important factor reducing glucose needs during fasting is a decrease in the brain's requirement for glucose, with ketone bodies being used instead for a large part of ATP production by the brain. As the use of alternative fuels to glucose increases, muscle proteolysis falls below levels seen early in starvation, and eventually proteolysis is lower than in the fed state. In humans, 1 week of fasting is necessary for this adaptation, as indicated by a diminished forearm arteriovenous difference in amino acids and by decreased urinary N-methylhistidine excretion.

Energy Expenditure and Caloric Requirements : 

Energy Expenditure and Caloric Requirements Basal energy expenditure (BEE)—also called basal metabolic rate (BMR)—the energy expenditure on awakening from a 12-hour fast measured in a thermoneutral environment (25°C). Thermogenic effect of food—also called specific dynamic action—the energy expenditure after the ingestion of food. After a meal, energy expenditure may increase 5% to 10%

Slide 10: 

Resting energy expenditure (REE)—the energy expenditure while resting in the supine position with eyes open. Includes the thermogenic effect of food if performed within a few hours of a meal or during continuous infusions of nutrients such as during continuous TPN administration. About 10% greater than BEE. Sleeping energy expenditure (SEE)—the energy expenditure during sleep; it is usually 10% to 15% lower than REE.

Slide 11: 

Activity energy expenditure (AEE)—the energy expended during physical activity. During maximum exercise it can be 6- to 10-fold greater than the BEE. Environmental temperature—energy expenditure increases to warm patients placed in a cold environment. Warming occurs through shivering and increased metabolism of brown fat (neonates).

Slide 12: 

Fever—Fever increases metabolic rate 10% per °C (or 7% per °F). Total energy expenditure (TEE)—total energy expended over 24 hours: the sum of energy expended during periods of sleep, resting, and activity.

Estimating Resting Energy Expenditure (Harris-Benedict Equation) : 

Estimating Resting Energy Expenditure (Harris-Benedict Equation) Males: eBEE (kcal/day) = 66 + (13.7 • W) + (5 • H) - (6.8 • A) Females: eBEE (kcal/day) = 655 + (9.6 • W) + (1.7 • H) - (4.7 • A)

Slide 14: 

eREE = eBEE • stress factor eTEE = eREE • activity factor eBEE, estimated basal energy expenditure; W, weight (kg); H, height (cm); A, age (years); eREE, estimated resting energy expenditure; eTEE, estimated total energy expenditure.

Stress Factors : 

Stress Factors Spontaneously breathing, nonsedated patients: Major surgery: 15%-25%   Infection: 20%   Long bone fracture: 20%-35%   Malnutrition: Subtract 10%-15%   Burns: Up to 120% depending on extent   Sepsis: 30%-55%   Major trauma: 20%-35%   COPD: 10%-15% Sedated mechanically ventilated patients: Subtract 10%-15%.

Activity Factors : 

Activity Factors Sedated mechanically ventilated patients: 0-5% Bedridden, spontaneously breathing nonsedated patients: 10%-15% Sitting in chair: 15%-20% Ambulating patients: 20%-25%

Measuring Energy Expenditure : 

Measuring Energy Expenditure Indirect calorimetry involves measuring oxygen consumption (Vo2) and carbon dioxide production (Vco2). The gas exchange method is used to measure Vo2 and Vco2, whereas the Fick method can be used to measure only Vo2.

Slide 18: 

Weir equation: EE (kcal/day) = 1.44 (3.9 • Vo2) + (1.1 • Vco2) Measurements made at rest provide the REE. To determine the TEE: REE • activity factor. Continuous measurement made over 24 hours provides the TEE.

Measuring Nitrogen Balance : 

Measuring Nitrogen Balance N balance = [N intake]-[N output] Negative balance—catabolism; positive balance—anabolism. [N intake] = all protein/amino acid intake over 24 hours whether enteral or parenteral [N output] = [UUN + 4 + EL] UUN, urine urea nitrogen over 24 hours; 4 g average fecal and cutaneous losses; EL, excessive losses, such as protein rich drainages (e.g., pus). 6.25 g protein/amino acids = 1 g nitrogen

Slide 20: 

To gain 1 pound of body weight, one needs an excess above TEE of approximately 3500 kcal.

* RQ, ratio of resting CO2 production to resting O2 consumption

Indications for nutritional support : 

Indications for nutritional support 1.    The patient's premorbid state (healthy or otherwise)    2.    Poor nutritional status (current oral intake meeting <50% of total energy needs)    3.    Significant weight loss (initial body weight less than usual body weight by 10% or more or a decrease in inpatient weight by more than 10% of the admission weight    4.    The duration of starvation (>7 days' inanition)

Slide 23: 

5.    An anticipated duration of artificial nutrition (particularly total parenteral nutrition [TPN]) of longer than 7 days    6.    The degree of the anticipated insult, surgical or otherwise    7.    A serum albumin value less than 3.0 g/dL measured in the absence of an inflammatory state    8.    A transferrin level of less than 200 mg/dL    9.    Anergy to injected antigens

Routes : 

Two routes of administration are possible: the enteral route, via the stomach or preferably the small intestine, and the parenteral route. The enteral route is considered to be more physiologic in that the liver is not bypassed, thereby allowing this organ to efficiently process and store various portally supplied nutrients, and the release of gut hormones and insulin is facilitated. Routes

Enteral Nutrition : 

Enteral Nutrition The enteral route is generally favored over the parenteral one because it is the natural portal of entry for exogenous nutrients. The enteral route obviates the need for intravascular access with its attendant risk of infections and sepsis. In addition, the array of nutrients that can be administered via the gastrointestinal tract is greater than what is available for parenteral use, allowing for better tailoring of nutrient intake.

Slide 26: 

Other advantages of enteral nutrition are ease of preparation and maintenance of gut function. The importance of maintaining gut integrity (the gut derives up to 70% of its nutrients from luminal food) is to reduce the translocation of bacteria from the gut. translocation of bacteria from intestines with reduced integrity and increased permeability leads to local activation of the gut's immune inflammatory system (Peyer's patches and hepatic Kupffer cells). These cells then release cytokines that intensify the already existing systemic inflammatory response, increasing the risk for multiple organ failure. Lack of enteral intake, such as occurs among postoperative and critically ill patients receiving no nutrition or only TPN, is associated with small intestinal villous atrophy, decreased villous cell count, and reduced mucosal thickness

Contra-indications : 

Contra-indications Circulatory shock , intestinal ischemia, complete mechanical bowel obstruction or ileus Total enteral nutrition is not advised in patients with partial mechanical bowel obstruction, severe or unrelenting diarrhoea, pancreatitis or high volume EC fistulas

Feeding tubes : 

Feeding tubes Feeding tubes that currently fovoured are narrower (8-10 Fr) and more flexible than the standard NGT which are 14-16Fr A rigid stylet is also provided to facilitate insertion. Inserted through the nares and advanced into the stomach or the duodenum. The distance can be estimated by measuring the distance fron tip of the nose to the ear lobe and then to the xiphoid process (50-60cm) Proper placement in the stomach is determined by measuring the pH of the aspirate pH less than 5 indicates the tip of the tube is likely to be in the stomach

Duodenal placement : 

Duodenal placement The feeding tube must be advanced through the pylorus into the duodenum This may be accomplished by specialised bedside maneuvers. Or require endoscopic or fluoroscopic guidence Tube placement in the duodenum can be confirmed by radiographic localisation As previously proposed the studies show no advantage of reduced aspiration with duodenal feeding as compared to gastric feeding

Slide 31: 

Small-bowel feeding is more reliable for delivering nutrition than nasogastric feeding. The disadvantages of the use of nasoenteric feeding tubes are clogging, kinking, and inadvertent displacement or removal of the tube, and nasopharyngeal complications. If nasoenteric feeding will be required for longer than 30 days, access should be converted to a percutaneous one.

Percutaneous Endoscopic Gastrostomy : 

Percutaneous Endoscopic Gastrostomy The most common indications for percutaneous endoscopic gastrostomy (PEG) include impaired swallowing mechanisms, oropharyngeal or esophageal obstruction, and major facial trauma. It is frequently used for debilitated patients requiring caloric supplementation, hydration, or frequent medication dosing. It is also appropriate for patients requiring passive gastric decompression. Relative contraindications for PEG placement include ascites, coagulopathy, gastric varices, gastric neoplasm, and lack of a suitable abdominal site. Most tubes are 18F to 28F in size and may be used for 12 to 24 months

complications : 

complications serious complications occur in approximately 3% of patients. These complications include wound infection, necrotizing fasciitis, peritonitis, aspiration, leaks, dislodgment, bowel perforation, enteric fistulas, bleeding, and aspiration pneumonia.

Percutaneous Endoscopic Gastrostomy-Jejunostomy : 

Percutaneous Endoscopic Gastrostomy-Jejunostomy Although gastric bolus feedings are more physiologic, patients who cannot tolerate gastric feedings or who have significant aspiration risks should be fed directly past the pylorus. In the percutaneous endoscopic gastrostomy-jejunostomy (PEG-J) method, a 9F to 12F tube is passed through an existing PEG tube, past the pylorus, and into the duodenum. This can be achieved by endoscopic or fluoroscopic guidance. With weighted catheter tips and guidewires, the tube can be further advanced past the ligament of Treitz.

Direct Percutaneous Endoscopic Jejunostomy : 

Direct Percutaneous Endoscopic Jejunostomy Direct percutaneous endoscopic jejunostomy (DPEJ) tube placement uses the same techniques as PEG tube placement but requires an enteroscope to reach the jejunum. DPEJ tube malfunctions are probably less frequent than PEG-J tube malfunctions, and kinking or clogging is usually averted by placement of larger-caliber catheters. The success rate of DPEJ tube placement is variable because of the complexity of endoscopic skills required to locate a suitable jejunal site.

Surgical Jejunostomy : 

Surgical Jejunostomy Feeding jejunostomy is done along with a major abdominal surgery where need for long term nutritional support is anticipated The only absolute contraindication to feeding jejunostomy is distal intestinal obstruction. Relative contraindications include severe edema of the intestinal wall, radiation enteritis, inflammatory bowel disease, ascites, severe immunodeficiency, and bowel ischemia.

Slide 38: 

Abdominal distention and cramps are common adverse effects of early enteral nutrition. Some have also reported impaired respiratory mechanics as a result of intolerance to enteral feedings. These are mostly correctable by temporarily discontinuing feedings and resuming at a lower infusion rate.

Slide 39: 

Pneumatosis intestinalis and small-bowel necrosis are infrequent but significant problems in patients receiving jejunal tube feedings. Several contributing factors have been proposed, including the hyperosmolarity of enteral solutions, bacterial overgrowth, fermentation, and accumulation of metabolic breakdown products

Slide 40: 

The common pathophysiology is believed to be bowel distention and consequent reduction in bowel wall perfusion. Risk factors for these complications include cardiogenic and circulatory shock, vasopressor use, diabetes mellitus, and chronic obstructive pulmonary disease. Therefore, enteral feedings in the critically ill patient should be delayed until adequate resuscitation has been achieved.

Feeding formula : 

Feeding formula Features Calory density: It is determined primarily by the carbohydrate content. Formula that provide 1 to 1.5 kcals per ml is standard calory density formula. Formula that provides 1.5 to 2 kcals per ml is called high calory density formula High calory density formulas are well suited for patients who are volume restricted and those who have excessive daily energy needs

Standard density formulas : 

Standard density formulas

High calory density formulas : 

High calory density formulas

Slide 44: 

Osmolality The osmolality of liquid feeding formulas varies from 280 to 1100 mOsm per kg It is mainly determined by the carbohydrate content Osmolality and calory density are directly proportional as both parameters are determined by the carbohydrate content Formulas with lowest calory density(1kcal/ml) have lowest osmolality(300mOsm/kg) and are usually isotonic. Formulas with highest calory density(2 kcal/ml) are usually hypertonic with high osmolality(1000mOsm/kg) Hypertonic formulas should be infused into stomach to take advantage of the dilutional effect of the secretions

Slide 45: 

Protien Liquid feeding formulas provide 35 to 40g of protiens per L Protien rich formulas provide 20% more protiens. These formulas often have a suffix HN (high nitrogen) Most formulas contain intact protiens which are broken down to amino acids in upper GIT Since small peptides are more rapidly absorbed than amino acids, some formulas contain small peptides instead of intact protiens They also promote water absorption in the bowel (useful in patients with diarrhoea)

Slide 46: 

Lipids Lipid emulsions used in feeding formulas are rich in long chain triglycerides derived from vegetable oils These provide a concentrated source of calories Since excessive lipid concentration is not well tolerated, lipid content of most formulas is limited to 30% of colories

Slide 47: 

Lipid rich formula Contains high lipid content to provide 55% of total calories (pulmocare) This formula is intended for patients with respiratory failure Lipid metabolism produces less CO2 relative to O2 consumption Thus when lipids replace carbohydrates as primary nutrient substrate, CO2 production declines and there will be less CO2 retension in patients with compromised lung function

Slide 48: 

Alternative lipids PUFA from vegetable oils serve as precurssors for inflamatory mediators which can cause widespread cell injury. As omega 3 fatty acids do not form inflammatory mediators, they are used instead of PUFA in some formulas These are meant for patients with SIRS or ARDS

Feeding formulas with altered lipid composition : 

Feeding formulas with altered lipid composition

Additives : 

Additives Glutamine Is the principal fuel for the bowel mucosa It maintains its functional integrity Although it is not an essential amino acid (produced in skeletal muscle) tissue glutamine stores decline precipitously in acute hypercatabolic states. Hence addition of glutamine helps to maintain mucosal integrity Average glutamine dose is 0.35g/kg/day or 24.5g/day for a 70 kg patient

Glutamine-Enriched Feeding Formulas : 

Glutamine-Enriched Feeding Formulas

Slide 52: 

Dietary fiber It’s a group of plant products that are not degraded by human digestive enzymes Two types based on fermentative propertives Fermentable (cellulose, pectin, gums) these are used as energy substrate for large bowel mucosa It slows gastric emptying time and binds bile salts. Helps to alleviate diarrhoea Non fermentable (lignin) it creates an osmotic force,that adsorbs water from the bowel lumen, reducing tendency for watery diarrrhoea

Fiber-Enriched Enteral Feeding Formulas : 

Fiber-Enriched Enteral Feeding Formulas

Slide 54: 

Branched chain amino acids Isoleucine, leucine, valine, are available and intended for trauma victims and patients with hepatic encephalopathy In trauma, it is used as a fuel source in skeletal muscle, thus sparing degradation of other muscle protiens to provide energy In hepatic encephalopathy, it antagonises the uptake of aromatic amino acids into the CNS and prevent the breakdown of the aromatic amino acids to form false neurotransmitters which are implicated in its pathogenesis. Eg. Nutri Hep and Hepatic Aid 2

Slide 55: 

Carnitine It is necessary for transportation of fatty acids into mitochondria for fatty acid oxydation Humans normally synthesize it from lysine and methionine. Deficiency can occur in prolonged states of hypercatabolism or during prolonged hemodialysis Thus the deficiency can cause cardiomyopathy, skeletal myopathy and hypoglycemia RDA 20 to 30 mg/kg in adults Glucerna, Isocal HN, Jevity and Peptamen are the formulas containing carnitine

Feeding regimen : 

Feeding regimen Tube feedings are usually infused for 12 to 16 hours in each 24 hr period Continuous infusion without a period of bowel rest is an unrelenting stress to the bowel mucosa and promotes mal absorption and diarrhoea

Slide 57: 

Gastric retention Before gastric feedings are started, it is necessary to determine how much volume will be retained in the stomach over a one hr period This will determine how fast the feedings can be administered Volume of water that is equivalent to the desired hrly feeding volume should be infused over one hr. Then should be clamped for 30 min Then it is unclamped and any residual volume should be aspirated from the stomach. If a 4 hr gastric residual volume is less than 200 ml, gastric feeding can proceed. If it is excessively high, duodenal or jejunal feeds may be more appropriate

Slide 58: 

Starter regimen The traditional approach to initiate tube feedings is to begin with dilute formulas and a slow infusion rate. This is gradually progressed to higher concentration and higher infusion rate over the next few days until the desired nutrient intake is achieved. This allows the atrophic bowel mucosa to regenerate after a period of bowel rest Disadvantage is that in a malnourished patient this added period of inadequate nutrition adds to the malnutrition This regimen is recommended for jejunal feeds as small bowel does not have reservoir capacity of the stomach Full feeds can be delivered immediately into stomach without troublesome vomiting or diarrhoea

Complications of enteral feeding : 

Complications of enteral feeding Tube occlusion Due to precipitation of proteins in the feeding solution by acid gastric juice that refluxes up the feeding tubes Standard preventive measures include flushing with 30ml of water every 4 hrs and using a 10 ml of water flush after medications are instilled If still obstruction persists, warm water should be injected into the tube and agitated with a syringe

Slide 60: 

If this is ineffective pancreatic enzyme can be used as follows Dissolve one tablet of viokase and one tablet of sodium carbonate 324 mg in 5ml of water Inject this mixture into the feeding tube and clamp for 5 mins Follow with a warm water flush

Slide 61: 

Aspiration Can be prevented by elevating the head end of bed by 30-40 degrees Regurgitation of the feeds is reported in as many as 80% of cases Aspiration of the feeds into the airways can be detected by testing the tracheal aspirates with glucose oxidase reagent strips Glucose content more than 20mg/dL is evidence of aspiration

Slide 62: 

Diarrhoea Occurs in 30% of the patients Although the hypertonicity of the enteral feeds can induce osmotic diarrhoea but it is not responsible in most of the cases The cause in majority of cases is a medicinal elixir that contains sorbitol (osmotic agent) to improve palatability

Sorbitol-Containing Liquid Drug Preparations : 

Sorbitol-Containing Liquid Drug Preparations

Stool osmolal gap : 

Stool osmolal gap Clostridium difficile enterocolitis is also a possible cause of diarrhoea during enteral feedings To differentiate it from osmotic diarrhoea, stool osmolal gap is calculated as follows. Osmolal gap= measured stool osmolality- 2x(stool Na- stool K) Stool osmolal gap greater than 160mOsm/kg suggests osmotic diarrhoea.

Parenteral nutrition : 

Parenteral nutrition Parenteral nutrition is the continuous infusion of a hyperosmolar solution containing carbohydrates, proteins, fat, and other necessary nutrients through an intravenous route Parenteral nutrition is used when the enteral route is unable to provide or sustain sufficient caloric intake.

Indications : 

Indications Gastrointestinal cutaneous fistulas Short-bowel syndrome    Acute burns    Crohn's disease    Acute radiation enteritis   Acute chemotherapy toxicity   Prolonged ileus (>7 to 10 days), Hepatic failure (acute decompensation superimposed on cirrhosis) Anorexia nervosa Chylothorax unresponsive to a medium-chain triglyceride diet.

Routes for TPN : 

Routes for TPN Parenteral nutrition is administered through either central or peripheral venous catheters. Solutions with high osmolality (more than 750mOsmols/kg) should be infused through large central veins. Lower osmolality solutions can be infused through peripheral veins. Parenteral nutrition is administered through either central or peripheral venous catheters.

Central TPN : 

Central TPN Central venous catheters are the main route of TPN administration. The preferred entry location is the subclavian vein, which provides a stable site, good patient acceptability, and lower infection rates than either the internal jugular or femoral routes. The catheter should be a single-lumen catheter used only for TPN. Multiple-lumen catheters and multiple-purpose single-lumen catheters have high infection rates

Peripherally inserted central catheters (PICCs) : 

Peripherally inserted central catheters (PICCs) Introduced via the basilic vein, Can be used both in the inpatient setting and also for longer-term outpatient therapy. PICC line in the outpatient setting has a lifetime of 4 to 6 weeks

Subcutaneously tunneled central catheters (Hickman) : 

Subcutaneously tunneled central catheters (Hickman) The catheter of these devices can be inserted into the vein percutaneously (e.g., the subclavian, internal jugular, or femoral) and then tunneled to the final skin exit site Subcutaneous tract forms a barrier to bacterial encroachment and colonization Tunneled catheters are desirable when frequent access is required

Implanted Venous Access Device (portacath) : 

Implanted Venous Access Device (portacath)

Slide 72: 

Portacath is completely subcutaneous It is accessed by percutaneous insertion of a special low-profile needle (Huber needle) Which passes through the self-sealing diaphragm of the device into the chamber.

Peripheral TPN : 

Peripheral TPN Peripheral veins cannot tolerate an osmolarity of more than 750 mOsm/L (the equivalent of 12.5% dextrose) The fluid volume that can be tolerated limits the caloric intake. Therefore, this route is used mainly for supplementation or short-term feeding. Typically, PPN is used for short periods (<2 weeks).

Intravenous Nutrient Solutions : 

Intravenous Nutrient Solutions Dextrose Solutions the standard nutritional support regimen uses carbohydrates to supply approximately 70% of the daily (nonprotein) calorie requirements. These are provided by dextrose (glucose) solutions, which are available in various strengths. As dextrose is not a potent metabolic fuel, the solutions must be concentrated to provide enough calories to satisfy daily requirements. As a result, the dextrose solutions used for TPN are hyperosmolar and should be infused through large central veins

Intravenous Dextrose Solutions : 

Intravenous Dextrose Solutions

Amino acid solutions : 

Amino acid solutions Amino acid solutions are mixed together with the dextrose solutions to provide the daily protein requirements. A variety of amino acid solutions are available for specific clinical settings. The standard amino acid solutions contain approximately 50% essential amino acids and 50% nonessential + semiessential amino acids

Amino acid cont… : 

Amino acid cont… The nitrogen in essential amino acids is partially recycled for the production of nonessential amino acids So metabolism of essential amino acids produces less of a rise in the blood urea nitrogen concentration than metabolism of nonessential amino acids amino acid solutions designed for use in renal failure are rich in essential amino acids

Standard and Specialty Amino Acid Solutions : 

Standard and Specialty Amino Acid Solutions

Glutamine : 

Glutamine Glutamine is the principle metabolic fuel for intestinal epithelial cells, Glutamine-supplemented TPN has an important role in maintaining the functional integrity of the bowel mucosa and preventing bacterial translocation. Glutamine is formed when glutamic acid combines with ammonia in the presence of the enzyme glutamine synthetase. Glutamic acid is given as exogenous source of glutamine.

Amino Acid Solutions with Glutamic Acid : 

Amino Acid Solutions with Glutamic Acid

Lipid Emulsions : 

Lipid Emulsions Intravenous lipid emulsions consist of submicron droplets (=0.45 mm) of cholesterol and phospholipids surrounding a core of long-chain triglycerides The triglycerides are derived from vegetable oils (safflower or soybean oils) and are rich in linoleic acid, an essential polyunsaturated fatty acid lipid emulsions are available in 10% and 20% strengths (the percentage refers to grams of triglyceride per 100 mL of solution). The 10% emulsionsprovide approximately 1 kcal/mL, and the 20% emulsions provide 2 kcal/mL

Slide 82: 

Unlike the hypertonic dextrose solutions, lipid emulsions are roughly isotonic to plasma Can be infused through peripheral veins. The lipid emulsions are available in unit volumes of 50 to 500 mL They can be infused separately (at a maximum rate of 50 mL/hour) or added to the dextrose–amino acid mixtures. The triglycerides introduced into the bloodstream are not cleared for 8 to 10 hours, and lipid infusions often produce a transient, lipemic-appearing (whitish) plasma.

Intravenous Lipid Emulsions : 

Intravenous Lipid Emulsions

Lipid Restriction : 

Lipid Restriction Lipids are used to provide up to 30% of the daily (nonprotein) calorie requirements. Dietary lipids are oxidation-prone and can promote oxidant-induced cell injury Use of lipids in critically ill patients (who often have high oxidation rates) should be restricted. Minimal amounts (4% of calorie) of lipid infusion is necessary to prevent essential fatty acid deficiency (cardiomyopathy, skeletal muscle myopathy)

Additives : 

Additives Electrolytes Most electrolyte mixtures contain sodium, chloride, potassium, and magnesium; they also may contain calcium and phosphorous. The daily requirement for specific electrolyte can be specified in the TPN orders. If no electrolyte requirements are specified, the electrolytes are added to replace normal daily electrolyte losses.

Slide 86: 

Vitamins Aqueous multivitamin preparations are added to the dextrose–amino acid mixtures. One unit vial of a standard multivitamin preparation will provide the normal daily requirements for most vitamins Enhanced vitamin requirements in hypermetabolic patients in the ICU may not be satisfied. Some vitamins are degraded before they are delivered. Some examples are riboflavin and pyridoxine (which are degraded by light) and thiamine (which is degraded by sulfites used as preservatives for amino acid solutions)

Slide 87: 

Trace Elements A variety of trace element additives are available Most trace element mixtures contain chromium, copper, manganese, and zinc, but they do not contain iron and iodine. Some mixtures contain selenium, which has a role in proctection against oxidation injury Routine administration of iron is not recommended in critically ill patients because of the pro-oxidant actions of iron

Trace Element Preparations and Daily Requirements : 

Trace Element Preparations and Daily Requirements

Creating a TPN Regimen : 

Creating a TPN Regimen Step 1 The first step is to estimate the daily protein and calorie requirements Daily calorie requirement will be 25 kcal/kg, and the daily protein requirement will be 1.4 g/kg. Therefore, for the 70-kg patient, the protein and calorie requirements are as follows: Colorie requirement=25 X 70= 1750kcal/day Protein requirement=1.4 X 70= 98g/day

Slide 90: 

Step 2 The next step is to take a standard mixture of 10% amino acids (500 mL) and 50% dextrose (500 mL) and determine the volume of this mixture that is needed to deliver the estimated daily protein requirement. Dextrose–amino acid mixture is referred to as A10–D50,which actually contains 5% amino acids (50 grams of protein per liter) and 25% dextrose (250 grams dextrose per liter). Therefore, the volume of the A10–D50 mixture needed to provide the daily protein requirement is Volume of A10–D50= 98g/day = 1.9L/day 50g/L If this mixture is infused continuously over 24 hours, the infusion rate will be 1900 mL/24 hours = 81 mL/hour

Slide 91: 

Step 3 Using the total daily volume of the dextrose–amino acid mixture determined in Step 2, the total calories that will be provided by the dextrose in the mixture is calculated. Amount of dextrose= 250g/L X 1.9L/day=475g Dextrose calories= 250 X 3.4 = 1615kcal/day The remaining 135kcalories can be provided by intravenous lipid emulsion.

Slide 92: 

Step 4 If a 10% lipid emulsion (1 kcal/mL) is used to provide 135 kcal/day, the daily volume of the lipid emulsion will be 135 mL/day. The volume can be infused at half the maximum recommended rate (50 mL/hour) to minimize the tendency to develop lipemic serum during the infusion.

Slide 93: 

Step 5 The daily TPN orders for the previous example can then be written as follows: 1. Provide standard TPN with A10–D50 to run at 80 mL/hour. 2. Add standard electrolytes, multivitamins, and trace elements. 3. Give 10% Intralipid: 150 mL to infuse over 6 hours.

Total nutrient admixture : 

The example just presented applies to the separate administration of dextrose–amino acid mixtures and lipid emulsions. Another practice that is gaining popularity is to add the nutrient solutions and additives together to form a total nutrient admixture (TNA). Advantages of TNA are Limits the number of central venous catheter violations and chance for contamination    Produces a hyperosmolar environment in the TNA solution that protects against bacterial growth Allows continuous infusion, thereby ensuring lipid administration at a safe rate (<0.11 g/kg/hr) Total nutrient admixture

Complications of TPN : 

Complications of TPN Complications of central venous catheterization pneumothorax hemothorax, brachial plexus injury catheter misplacement in the azygos vein, right ventricle, or retrograde into the jugular vein Peripheral venous access whether via a short peripheral venous catheter can result in thrombophlebitis

Catheter-related infections : 

Catheter-related infections These are the major venous access complication encountered with TPN Infections are uncommon during the first 72 hours after insertion but then increase in incidence Most often caused by Staphylococcus epidermidis or Staphylococcus aureus or Candida species. The incidence of central venous catheter–related bloodstream infections ranges from 0.3 to 30 per 1000 catheter-days Mortality attributed to catheter-related infections is as high as 25% To prevent infective complications, Any manipulation of the catheter or line must be performed using sterile procedures Manipulation of the line should be kept to a minimum The site must be examined regularly for signs of erythema and infection.

Metabolic Complications : 

Metabolic Complications Hyperglycemia is a common problem, especially with severe stress, steroid use, and diabetes mellitus requiring treatment with insulin. It is preferable to administer insulin than to reduce the glucose intake unless there is excessive hyperglycemia (>250 mg/dL) despite high insulin doses. Insulin treatment can reduce serum potassium and phosphate concentrations, which require repletion. As the stress response abates, the degree of glucose intolerance lessens and insulin requirements drop. The blood glucose should be closely monitored to prevent hypoglycemia.

Slide 98: 

Hypoglycemia can occur on the abrupt discontinuation of continuous feedings containing significant amounts of carbohydrate. Continuous feedings result in high blood insulin concentrations so that hypoglycemia intervenes when the carbohydrate intake stops. Therefore, when stopping continuous parenteral and enteral nutrition, any concomitant insulin infusion must be stopped, intravenous glucose should be infused, and blood glucose monitored frequently. The practice of using TPN solutions containing lower glucose:lipid ratios (70:30 to 50:50) has reduced the incidence of hypoglycemia after abrupt discontinuation

Slide 99: 

Refeeding syndrome Hypophosphatemia occurs when tissues begin to rebuild and is especially problematic if inadequate phosphate intake is provided in malnourished patients when TPN or enteral feeds are started. Hypophosphatemia may lead to major muscle (including respiratory muscle) weakness and glucose intolerance because phosphate is a vital component of tissue membranes, enzymes, and nucleosides, especially ATP. Concurrent hypomagnesemia, hypocalcemia, and hypokalemia may exacerbate the muscle weakness. Chronic alcoholics are especially prone to hypophosphatemia.

Consequences of Overfeeding in Parenteral and Enteral Nutrition : 

Consequences of Overfeeding in Parenteral and Enteral Nutrition

Consequences of Overfeeding in Parenteral and Enteral Nutrition : 

Consequences of Overfeeding in Parenteral and Enteral Nutrition

Hepatic dysfunction : 

Hepatic dysfunction Hepatic dysfunction is commonly observed in patients receiving TPN These disorders occupy a spectrum ranging from simple elevations in liver function test results to cirrhosis. Most often, if hyperbilirubinemia occurs acutely in a patient receiving TPN, the cause is generally sepsis. Factors responsible for liver disease attributable primarily to TPN administration, remain unclear. Hepatic steatosis, cholestasis (presumably from lack of enteral stimulation and reduced release of cholecystokinin), and the presence of chronic inflammation have all been implicated as relevant mechanisms TPN-specific factors include excessive glucose or insulin administration (with increased hepatic lipogenesis), excessive lipid administration (sequestration in hepatocytes), and alterations in fatty acid metabolism leading to the release of arachidonate-derived inflammatory leukotrienes

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Deficiencies in particular nutrients, such as carnitine, choline, taurine, cysteine, and S-adenosyl methionine, have also been implicated in TPN-related liver disease Addition of 1 to 2 g of carnitine to standard TPN, especially during long-term administration is recommended to prevent liver dysfunction. The use of oral ursodeoxycholic acid (e.g., 500 mg at bedtime or twice daily) is useful to resolve cholestasis when liver function test abnormalities are observed during chronic TPN administration

Mucosal Atrophy : 

Mucosal Atrophy The absence of bulk nutrients in the bowel produces atrophy and disruption of the bowel mucosa. These changes can predispose to translocation of enteric pathogens across the bowel mucosa and subsequent septicemia. Because TPN is usually accompanied by bowel rest, one of the indirect complications of TPN is bacterial translocation and sepsis of bowel origin. Glutamine-supplemented TPN may help reduce the risk of this complication.

Acalculous Cholecystitis : 

Acalculous Cholecystitis The absence of lipids in the proximal small bowel prevents cholecystokinin-mediated contraction of the gallbladder. Bile stasis Acalculous cholecystitis

Metabolic Bone Disease : 

Metabolic Bone Disease Patients administered TPN over prolonged periods have decreased bone mineral density (BMD) Patients at greatest risk are postmenopausal women, patients with long-standing malnutrition or malabsorption (e.g., Crohn's disease), those with preexisting liver disease, or patients receiving steroids TPN-associated deficiency states, such as calcium, magnesium, copper, boron or silicon, have been suggested to play a role. Use of bisphosphonates which prevents osteoclast-mediated bone resorption is being tried

References : 

References Paul L Marino, The ICU Book, 3rd Edition Ronald D. Miller , Miller's Anesthesia, Seventh Edition Schwartz's Principles of Surgery, Ninth Edition Sabiston Textbook of Surgery, 18th ed. Harrison's principles of internal medicine Seventeenth Edition

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Thank u