Specializes in critical care, hospice, chem dep. Has 10 years experience. Aug 2, That's what causes the confusion, I think. Nov 22, Hi, I wanted to add that Lipids need not to exceed recommended infusion rates under normal circumstances i.
In lipid rescue of anathesia toxicity this would not apply. Also lipids are lovely places for germs to grow in and anything seemingly chunky should NOT be used. Specializes in Vascular Access. Has 32 years experience. Nov 23, As so appropriately said in other posts, TPN should never go into the veins that terminate in the peripheral vascular system. It doesn't matter what your population is.. Thrombus rates skyrocket when a tip stops here, and therefore should not be done.
Midline IV catheters are inches in length and are not central catheters as they stop or terminate before the axillary vein at the shoulder. Dextrose is the most common carbohydrate used in PN solutions. Dextrose for IV use provides 3. Manufacturers cannot supply dextrose and amino acid premixed because these products react when heat sterilized. This product is used as PPN in some institutions. Caloric density of glycerol is 4. Although glycerol may be useful in controlling blood glucose, especially in patients with diabetes, the low concentrations of glycerol and amino acid in ProcalAmine limit its usefulness.
Another method used by manufacturers to facilitate the mixture of dextrose and amino acid solutions is provision in dual-chamber bags. To combine dextrose and amino acids, a septum between two chambers is broken and contents are mixed.
There is room to add fat emulsion if desired. These products are supplied with and without added electrolytes. Lipid is supplied in the U.
These soybean oil or safflower plus soybean oil—based emulsions primarily contain the long-chain fatty acids linoleic and linolenic acid. These products contain egg yolk phospholipids as emulsifiers and glycerol for tonicity.
IV lipid provides 1. Due to concerns that long-chain triglyceride emulsions used in the U. Micronutrient components of PN solutions include electrolytes, vitamins, and trace minerals. The electrolytes usually present include sodium, potassium, magnesium, calcium, phosphorus, chloride, and acetate.
Since these electrolytes are primarily excreted by the kidneys, infused amounts required may be lower in patients with renal insufficiency. Monitoring for serum electrolytes is useful for guiding the amount of electrolyte placed in PN.
It is noteworthy that serum sodium is often not reflective of total body sodium stores, although serial values can be useful for monitoring fluid status. Patients with metabolic alkalosis may benefit from increasing chloride and decreasing acetate in the PN, whereas patients with metabolic acidosis may benefit from the opposite profile of these electrolytes.
Sodium bicarbonate should not be added to PN solutions as an alkalinizing agent because it can interact with calcium to form insoluble calcium carbonate; sodium acetate or potassium acetate should be used instead.
Vitamins are usually added using parenteral multivitamin preparations, which contain 12 or 13 essential vitamins. The number of vitamins in most commercial preparations has recently been reformulated based on FDA guidelines.
The mcg amount of phylloquinone in a daily supply is relatively little and should not clinically affect warfarin anticoagulation when administered consistently.
Nevertheless, the international normalized ratio should be monitored closely in patients receiving warfarin in whom PN is being started or discontinued. Shortages of parenteral multivitamins have occurred in recent years; in such instances, the addition of individual vitamin ingredients such as thiamine and folic acid may be important to avoid complications.
Zinc, chromium, manganese, and copper are the four trace elements most commonly added to PN solutions. Selenium is also added, although not as universally for short-term PN patients. Commercially available products containing a combination of trace elements are frequently used. Some institutions add zinc in quantities beyond those found in commercial mixtures for certain surgical patients.
Copper and manganese undergo biliary excretion and can accumulate in patients with severe hepatic disease; they should be omitted in patients with significantly elevated total bilirubin. Aluminum is a contaminant of parenteral additives that can add up to potentially unsafe amounts in neonates and in patients with renal failure.
This has prompted the FDA to require disclosure of aluminum content of many of the parenteral products used in compounding PN. Although iron is not routinely added to PN, the mineral may be added to PN solutions containing dextrose and amino acids, but not to solutions containing lipid emulsion due to stability issues.
Iron dextran is the form of iron most commonly added to PN. Fluid requirements for patients receiving PN should be monitored. Daily weights are useful in hospitalized patients; weight change of more than 0. Inputs and outputs should be monitored in acute care to gauge fluid status. Serial monitoring of blood for albumin, sodium, and hematocrit may also be helpful in determining fluid status when used in combination with body weight and inputs and outputs; these values can reflect dilution and concentration.
Formulas for estimating maintenance fluid requirements in patients without unusual losses are found in TABLE 3. Compatibility and Stability Issues. Calcium and phosphate solubility is a major issue concerning the compatibility of PN formulations. Solubility is influenced by several factors such as temperature; calcium phosphate solubility decreases with increasing temperature.
Another important factor is pH; calcium phosphate solubility increases as pH decreases. Higher final amino acid and dextrose concentrations are associated with lower pH and thus higher calcium phosphate solubility.
Calcium gluconate is preferred in PN solutions due to superior solubility compared to calcium chloride. The order in which calcium and phosphate are added is important; phosphate is generally added first, while calcium is added near the end of the compounding sequence. The amounts of calcium and phosphate added must be considered, with a greater chance of precipitation if the amount of one or both is increased above standard.
If lipid is admixed with the PN to form a total nutrient admixture TNA , visual detection of calcium phosphate precipitates becomes more difficult. The pharmacist must follow the manufacturer's calcium and phosphate guidelines for specific products and concentrations comprising any PN admixture. Simplified formulas for estimating the maximum amount of calcium and phosphate that can be placed in PN formulas are fraught with error. In-line, 0. Chemical stability can be compromised by excessive cations, particularly divalent cations, resulting in "creaming" or "cracking" of the TNA.
With creaming, lipid can be redispersed with gentle inversion and administered to a patient. A TNA is generally considered microbiologically safe for 24 hours after initial hanging. However, lipid emulsion alone is a better growth medium due to its nearly physiologic osmolality and pH. This is in contrast with a TNA that is hypertonic and has a lower pH. The current CDC recommendation is that a lipid emulsion hung alone should not infuse for more than 12 hours after spiking the container.
Assessing the quantitative needs of patients receiving PN is important. Overfeeding macronutrients or micronutrients can lead to complications, while underfeeding can be associated with malnutrition or micronutrient deficiency.
Assessment of nutritional status has historically been performed based on a combination of physical examination characteristics, biochemical parameters, and immunological markers. Immunological markers include total lymphocyte counts and anergy screening. In parenterally fed patients with a tendency to hyperglycaemia, an increase in the lipid-glucose ratio should be considered. In certain situations i. The recommended daily dose for parenteral lipids in adults is 0.
There is little evidence at this time that the choice of different available lipid emulsions affects clinical endpoints. In bestimmten Situationen z. The infusion of lipid emulsions allows for high energy supply with iso-osmolar solutions. In addition, an adequate proportion of the energy intake as lipids facilitates the prevention of high glucose infusion rates and can, therefore, contribute to the prevention of hyperglycaemia and hepatic steatosis. Lipid emulsions are also indispensable for supplying the requirements of essential fatty acids.
The quantitatively dominant lipids in enteral and parenteral nutrition are triglycerides triacylglycerols, neutral lipids; gylcerol esterified with three fatty acids. The physical, chemical and metabolic properties of triglycerides are determined by their fatty acid contents.
Saturated, monounsaturated and polyunsaturated fatty acids differ in their metabolic and physiological properties. While saturated fatty acids serve primarily as an energy source, polyunsaturated fatty acids play an important role as components of structural lipids, for example in biological membranes.
For healthy adults the recommended dietary intake of linoleic acid is 2. They also modify gene expression by binding to nuclear receptors like PPAR. Certain polyunsaturated fatty acids dihomo-gamma-linolenic acid, n-6; arachidonic acid, n-6; eicosapentaenoic acid, n-3 serve as precursors in the synthesis of eicosanoids.
The n-6 fatty acid arachidonic acid is a precursor of pro-inflammatory mediators such as leukotrienes of the n-4 series , and of prostaglandins and thromboxanes of the n-2 series, which increase the vascular tone and promote platelet aggregation. In contrast, prostaglandins and thromboxanes of the n-3 series and leukotrienes of the n-5 series, formed from the n-3 fatty acid eicosapentaenoic acid, have many antagonistic effects such as a reduction in platelet aggregation and vascular tone as well as anti-inflammatory effects.
More recently novel lipid mediators derived from poly-unsaturated fatty acids with pro-resolving activities on inflammatory processes have been identified. They were identified in exsudates from resolving inflammation and comprise the lipoxins, resolvins, and protectins for review see [ 2 ], [ 3 ]. They are highly stereospecific and act in the pico- to nanomolar range [ 5 ], [ 6 ]. They affect PMN recruitment and trafficking, expression of pro-inflammatory genes, reduce leukocyte-mediated tissue injury, and take part in chemokine removal.
Lipoxins are derived from AA and are generated through different biosynthetic pathways. Alternatively, these lipoxins can also be generated from LTA4 by platelet LO, most preferably under conditions of hypoxia and diminished platelet glutathione content. In addition, lipoxins can be generated from HETE stored in membrane inositol-containing lipids.
Upon release, HETE instead of AA is processed by neighbouring leukocytes resulting in decreased leukotriene and increased lipoxin formation.
On the other hand, they increase monocyte recruitment and uptake of apoptotic PMNs by macrophages [ 9 ]. Alternatively, resolvin E1 RvE1 can be synthesized independent from aspirin by cytochrome P monooxygenase [ 10 ].
RvE1 dramatically reduced neutrophil infiltration in zymosan-induced peritonitis in mice that was BLT1-dependent at low but independent at high RvE1 concentrations [ 12 ]. Furthermore, RvE1 blocked PMN superoxide generation [ 13 ] and reduced the expression of proinflammatory genes.
Furthermore, they regulate PMN infiltration into inflamed tissues [ 14 ], [ 15 ], [ 16 ]. Like resolvins, protectins regulate PMN infiltration as demonstrated by reduced peritoneal PMN recruitment in a mouse model [ 6 ].
PD1 exerts its actions also when administered after the initiation of inflammation and was shown to act in an additive fashion together with RvE1. In this context, Lukiw and coworkers demonstrated that protection by NPD1 from oxidative stress-mediated injury mainly occurs through the modulation of apoptotic signaling pathways [ 17 ].
Furthermore, in concert with lipoxins and resolvins, it increases CCR5 expression on apoptotic PMNs thereby promoting removal of CCR5L and termination of the inflammatory reaction [ 20 ]. Endogenous lipid stores are the main energy source for critically ill patients with an inadequate food intake. In such situations, adipose tissue triglycerides are hydrolyzed to release free fatty acids and glycerol into the circulation [ 21 ].
The markedly increased mobilisation of free fatty acids results in a decrease in intracellular triglyceride storage. This increased lipid catabolism is not countered by parenteral administration of carbohydrates.
Usually, the released free fatty acids are rapidly utilised in peripheral tissues. Depending on the overall metabolic situation, there is either ketone body formation or re-esterification and triglyceride formation in the liver, subsequently released into the circulation as very low density lipoproteins VLDL.
The increase in plasma levels of free fatty acids is proportional to the severity of the trauma, and the extent to which the production of free fatty acids surpasses their utilisation. Fat-free parenteral nutrition can result in subnormal serum levels of essential fatty acids within one week IIb.
Administration of lipid emulsions is required within no more than one week after starting PN C. These deficiencies can be corrected by parenteral administration of lipid emulsions [ 23 ].
In infants, not only biochemical but also clinical signs of essential fatty acid deficiency, such as scaly dermatitis, can be seen after just one week of fat-free PN [ 24 ], [ 25 ], [ 26 ]; Ib. In parenterally fed patients with a tendency to hyperglycaemia, an increase in the lipid-glucose ratio should be considered C.
Tappy et al. The low lipid intake was associated with increased blood glucose levels Ia. The typical metabolic changes resulting from the systemic inflammatory reaction is characterized by reduced carbohydrate and increased lipid oxidation. Therefore, an increased exogenous carbohydrate intake enhances the risk of hyperglycaemia. In contrast, a meta-analysis of studies in surgical patients showed no differences in the course of the illness and rate of complications with PN either with or without lipid emulsions administered [ 29 ].
However, both lipid emulsions reduced glucose oxidation as compared to the control group [ 30 ], IIa. In adult patients with gastrointestinal disorders, administration of PN containing soybean oil, which provided either 2. In critically ill patients, an excessive intake of glucose increases hepatic lipogenesis [ 33 ], [ 34 ], [ 35 ], [ 36 ], whereas intravenous lipids reduce the dependency on glucose as an energy source. A case study showed that intravenous lipid administration lowered hepatic steatosis [ 37 ].
The impact of PN with or without lipids on hepatic steatosis was tested in a randomised controlled study on 37 patients 22 men. The patients received their non-protein energy intake either from glucose only or from glucose and a lipid emulsion; a third group received an extremely high amino-acid low-carbohydrate intake [ 39 ].
The accumulation of fat in the liver was associated with raised levels of serum ALT and AST, but no cholestatic changes. Development of cholestatic liver disease associated with PN has been frequently observed in premature infants with septic infections [ 38 ]. Case studies suggest that PN-associated cholestasis in children receiving long-term PN can be improved by reducing or interrupting the parenteral lipid intake [ 40 ].
General conclusions can not be deduced as there were methodological limitations of this study. The occurrence of cholestasis has been associated with increased serum concentrations of phytosterols that are found in vegetable oils and in lipid emulsions [ 42 ], [ 43 ]. In newborn pigs, phytosterols reduced bile flow [ 44 ].
However, it remains controversial whether the increased phytosterol serum levels in cholestatic PN patients are a cause or an effect of cholestasis [ 42 ], [ 43 ]. The infusion of lipid emulsions presents no independent, clinically relevant risk of infection IV. In contrast, a clinical study in newborns found bacterial contamination of the infusion solution to occur after 24 or 48 hours, irrespective of whether mixtures contain lipids or not [ 49 ].
Although the in vitro multiplication of Candida albicans was similar in all infusion solutions [ 45 ], [ 46 ], in a clinical study contamination in lipid emulsions was higher after 24 hours than after 48 hours [ 49 ]; IIb. A case-control study, however, showed that post-operative infections or febrile episodes associated with the infusion of lipid-based hypnotic propofol were due to insufficient aseptic techniques during the administration of the infusion [ 50 ].
A lower risk of contamination has been reported in complete mixtures used for PN than in the infusion of individual components with added lipid solutions [ 46 ], [ 51 ].
A meta-analysis of studies in surgical patients showed no association of infectious complications with the administration of parenteral lipid emulsions [ 29 ]. A lipid emulsion should usually be provided with PN to prevent depletion of essential fatty acids, lower the risk of hyperglycaemia, and prevent hepatic steatosis.
If PN is indicated, lipid emulsions should commence after hemodynamic stability has been established or achieved. Huschak et al. The recommended daily dose for parenteral lipids in adults is between 0. Fatty acids are oxidised in hepatocytes, myocardium, skeletal muscles, and other tissues.
A lipid supply greater than the maximum rate of lipid oxidation, estimated between 1. Non-utilised lipid particles can be taken up by the mononuclear phagocyte system MPS , and the immune defence might deteriorate, as a result of inadequate chronic activation of the MPS [ 58 ], [ 59 ]. Hypertriglyceridemia induced by lipid infusion can usually be controlled by reducing the dose [ 60 ]; IIb.
During the first days of infusion, plasma triglyceride levels should be monitored so that the dose can be modified, if necessary.
When lipid utilisation is impaired, e. Determination of serum opacity in the supernatant after centrifugation of whole blood is not considered useful. Lipid infusion with PN is not indicated in severe hyperlipidemia e. The administration of TPN must follow strict adherence to aseptic technique, and includes being alert for complications, as many of the patients will have altered defence mechanisms and complex conditions Perry et al. To administer TPN, follow the steps in Checklist TPN requires special IV tubing with a filter.
Generally, new TPN tubing is required every 24 hours to prevent catheter-related bacteremia. Follow agency policy. Use strict aseptic technique with IV changes as patients with high dextrose solutions are at greater risk of developing infections. Start TPN infusion rate as per physician orders.
Prevents medication errors. Discard old supplies as per agency protocol, and perform hand hygiene. These steps prevent the spread of microorganisms. Monitor for signs and symptoms of complications related to TPN. See Table 8. Complete daily assessments and monitoring for patient on TPN as per agency policy. See daily and weekly assessments in Table 8.
Flow rate may be monitored hourly. Document the procedure in the patient chart as per agency policy. Note time when TPN bag is hung, number of bags, and rate of infusion, assessment of CVC site and verification of patency, status of dressing, vital signs and weight, client tolerance to TPN, client response to therapy, and understanding of instructions. Data source: North York Hospital, ; Perry et al. A patient receiving TPN for the past 48 hours has developed malaise and hypotension.
What potential complication are these signs and symptoms related to? Additional Videos Video 8. Video 8. Previous: 8. Skip to content Chapter 8. Intravenous Therapy. Patients with paralyzed or nonfunctional GI tract, or conditions that require bowel rest, such as small bowel obstruction, ulcerative colitis, or pancreatitis.
Describe refeeding syndrome and state one method to reduce the risk of refeeding syndrome. Next: 8. Share This Book Share on Twitter. Rationale and Interventions. CR-BSI, which starts at the hub connection, is the spread of bacteria through the bloodstream. Symptoms include tachycardia, hypotension, elevated or decreased temperature, increased breathing, decreased urine output, and disorientation. Due to poor aseptic technique during insertion, care, or maintenance of central line or peripheral line Interventions: Apply strict aseptic technique during insertion, care, and maintenance.
A pneumothorax occurs when the tip of the catheter enters the pleural space during insertion, causing the lung to collapse.
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