STUDY - Technical - New Dacian's Medicine
Parenteral
and Enteral Nutritional Therapy (3)
Translation Draft
I ended up in my posts at the need for protein and amino acids.
I ended up in my posts at the need for protein and amino acids.
The 0.8 g/kg/day of
protein is suitable for patients not subject to stress (e.g.
those with esophageal strictures). When catabolic increases
exist, up to 1.5 g/kg/day are required to induce nitrogen
balance positivity and restore body mass.
Some studies suggest that the nitrogen balance can be improved by administration of human growth hormone, but it is not clear whether it stimulates muscle growth or improves tissue healing. In the case of a stabilized patient, the energy and protein support is determined by the formula: Protein balance = protein intake - protein losses, where protein losses represent the urea nitrogen in the urine from 24 hours (g) x 6.25 (also counts scarring, restoration of normal body composition, resumption of growth in length). In cases where there are disturbances in the use of proteins (hepatic or renal failure), nitrogenemia or amino acids may occur in abnormal plasma concentrations.
The benefit of special enteral or parenteral solutions, which correct these changes, is not known in hepatic encephalopathy. Certain amino acids or some peptides that are not normally essential in very seriously ill patients, where the endogenous pathways that produce or store them are blocked. This is the case with glutamine, aginin and methionine metabolism products. Glutamine, an important "fuel" for enterocytes and lymphocytes, is insoluble and is missing from many parenteral use solutions, in enteral solutions being present only in low concentrations. Glutamine-containing soluble dipeptides are being investigated.
The related nuleotides and metabolic products have beneficial effects on the immune system, small intestine growth, lipid metabolism and liver function. The nuleotides can be synthesized de novo in all cells only in small amounts, so the body depends on the nutreotides in the diet or the storage pathways that recycle the nucleotides resulting from the turnover of purine and pyrimidine. Nutritionally deficient patients benefit from the intake of formulae enriched by the eulled.
In general, amino acids are administered parenterally systemically and rarely through the physiological pathway of the portal vein. Under these conditions, methionine, the only sulfur amino acid in parenteral solutions, is more transaminaseed in peripheral tissues than transsulphurized in the liver. It follows that products such as carnitine, taurine and glucation become relatively deficient. Preliminary studies have indicated that the addition of an intermediate compound, S-adenozil methionine, to parenteral solutions leads to a decrease in cholestasis.
It's the turn of the need for minerals and vitamins. It may be higher in parenteral nutrition than in enteral nutrition, for several reasons: firstly, these substances are released into the systemic circulation and not into the portal circulation, short-circuiting the liver and being eliminated urinaryly; secondly, many patients with intestinal disorders lose enteral sodium, potassium, chlorine and bicarbonate, have malabsorption for bivalent cations, cobalamin and fat-soluble vitamins. Exposure to oxygen and light of infusion solutions can help destroy vitamins (especially vitamin A) and nutrients can adhere to tubes and bags. The glucose content is gradually increased as the patient proves tolerance to large amounts of glucose.
From the point of view of parenteral nutrition and the technique of infusion and monitoring of the patient, partial and short-term parenteral nutrition can be done through peripheral veins, provided that most energy needs are provided by isotone lipid solutions (instead, total long-term parenteral nutrition should be done through a central vein, as it involves the administration of hypertone glucose that must be rapidly diluted in a considerable blood flow).
Central catheters with peripheral insertion are the cheap option for short-term parenteral nutrition. In one study, the number of catheter infections was the same as with peripheral and central insertion catheters. Catheters with a subcutaneous orifice or tunneling require intraoperative insertion and are stable in long-term use. Central catheters should be changed at the clinically established indication (routine change is expensive and risky). chlorhexedin solution is a better local antiseptic than alcohol or iodophor.
Although transparent dressing is useful for fixing the catheter and allows easy observation of the skin, the incidence of infections due to catheterization is higher than with the use of dry textile dressings (new transparent dressings that do not absorb moisture are under observation). The catheters in silastic or polyurethane associate fewer complications than those of vinyl polychloride. Several types of needle-free systems use central valves (the contamination rate of these installations is not yet known).
Complications that occur can be mechanical, metabolic or infectious. In case of mechanical complications, the insertion of the catheter into the central veins will be done only by experienced personnel and under perfect asepsis conditions. Major mechanical complications include pneumothorax, hemothorax by damage to the subclavian artery or vein, damage to the brachial plexus, catheter malposition in a central vein, azigos vein or right ventricle. The correct positioning of the catheter should be confirmed radiologically before the start of the infusion of hypertone solutions.
The catheters may exit the vein after proper installation, break the vessel or detach and produce intracardiac embolisms or in the pulmonary artery. Catheter thrombosis may occur, especially if it is used for blood collection. The catheter thrombosis of the central veins is usually accompanied by infections. Sometimes it is effective to unlock the catheter by using urokinase. The addition of low doses of heparin (1,000 units/l) to eliminate thrombosis is controversial (no study has shown potential benefits, and heparin may contribute to bone demineralization which is a particular problem of long-term parenteral nutrition).
For metabolic complications, fluid overload causes congestive heart failure, especially in elderly and debilitated patients. Glucose in too large quantities produces osmotic diuresis and, by stimulating insulin, produces the massive intracellular passage of phosphorus and potassium into the extracellular space. Such transfer is more likely in casec patients, who have total phosphorus and potassium doutination in the body (decrease in plasma levels of the two elements produces arrhythmias, cardiopulmonary dysfunction and neurological symptoms).
To avoid them, parenteral nutrition should be progressively established and closely monitored. The amount of glucose is gradually increased as patients develop tolerance to glucose loading. Late metabolic complications consist of cholestatic liver damage with thick bile syndrome and formation of gallstones. The exact cause of liver damage is unknown, but it appears that the disorder of the metabolism of sulphide amino acids plays an important role. Cholestasis is likely associated with lack of enteral stimulation and is unlikely to occur in the presence of minimal enteral intake.
Parenteral nutrition induces hypercalciuria, which can lead to negative calcium balance in the body and osteopenia. Hypercalciuria appears to be caused by several factors, including the effects of amino acid infusion and the fixed acid load of the bisulphite preservative. In the past, protein hydrolysated solutions produced aluminium contamination, with damage to bone mineralization (aluminum may still exist as an additive in some infusion solutions, such as calcium gluconate). As soon as the patient undergoes long-term parenteral nutrition passes from the catabolic to the anabolic phase, supplementation with essential fatty acids, minerals, vitamins is necessary to prevent possible deficiencies.
In the case of infectious "problems", infection of venous approach paths rarely occurs within the first 72 hours, usually fever occurring during this period due to an infection located elsewhere in the body or other cause. Infection of the venous approach is likely when the fever decreases, reducing the rate of infusion of solutions. Positive cultures in the central lines suggest catheter septicaemia, especially when another source of infection cannot be identified in the body and if the microbe highlighted is staphylococcus or Candida. If mycotic infection can be resolved by the body's own resources (after removal of the catheter), bacterial infections or more aggressive fungi require antibiotic therapy.
Catheter sepsis is more likely to occur when triple lumen venous catheters are used (single lumen catheters are used exclusively for parenteral nutrition, central catheters with peripheral insertion and tunneled catheters have an equal incidence of catheter septicaemia). When antibiotic prophylaxis is not indicated, recurrent catheter septicaemia can be avoided by stationing minimal amounts of antibiotics in the lumen of the catheter with a "dop" of heparin or by a "sleeve" at the insertion of the catheter.
Let me present some elements about enteral nutrition in reference to tube placement and patient monitoring. Patients receiving enteral nutrition are at risk for some of the metabolic complications referred to in parenteral nutrition, the monitoring should be identical. Since small diameter tubes can be easily moved from the location, the position of the tube should be tested by aspiration of the digestive fluid and determination of the pH of the intestinal fluid (less than 4 in the stomach and greater than 6 in the jejun). Complications that may occur are represented by suction and diarrhea.
In the case of aspiration, debilitated patients with unsatisfactory gastric discharge and impaired swallowing and cough mechanisms are at risk of suction. In patients connected to the ventilation system, tracheal suction induces coughing and causes gastric regurgitation, in this case the endotracheal balloon probe and tracheostomy sleeve rarely preventing pulmonary aspiration of regurgitated fluid. In these conditions, it is safer to use a wide tube, allowing accurate verification of the residual gastric contents and, if necessary, its discharge before suctioning the trachea or using jejunal nutrition.
Although the stomach retains its normal motility and is able to fragment food and then propel it into the duodenum, constant administration of fluids from enteral solutions is preferred, as this is better tolerated by patients than intermittent gastric bolus. Continuous infusion can be achieved with the help of a special pump, especially in the case of tubes with fine lumen that have a greater possibility of obstruction.
If long-term enteral feeding is expected, most patients prefer endoscopically placed, radiological or surgical gastric tube. In the ambulatory, the gastrostoma tube can be used in a "button" on the skin. The naso-jejunal tube reduces the risk of suction. However, the fluoroscopic placement of these tubes through the pilor takes time and often followed by its return to the stomach. Safer is the percutaneous gastro-jejunal placement under radiological control.
Enteral nutrition often causes diarrhea, especially if intestinal functions are compromised by intestinal disorders or by taking medication. Diarrhea can be controlled by continuous feeding in small amounts, by adding hydrofile mucilages (psyllium) by anticholinergic medication. Diarrhea stimulated by enteral nutrition does not necessarily involve malabsorption of nutritional compounds (other than water and electrolytes). Moreover, because they have trophic effects on the mucosa and stimulate the intestinal immunological barrier, it is not recommended to stop enteral nutrition in the presence of diarrhea, even when parenteral intake of loss replacement is necessary.
I'll finish by inserting some elements about the cost of nutritional therapy. Approximately 25% of patients admitted to chronic hospitals have central catheters fitted and 25-30% of these catheters are used for parenteral nutrition. The incidence of catheter infections reflects the quality of the medical act and the conditions offered and ranges from 2 to 30% of catheters/day, depending on the type of patient. In critically ill patients, catheter infection is associated with a mortality of 35%, with an estimated cost of EUR 30,000/ survivor.
Most complications stem from faulty insertion and catheter tracking than from plant failures. In the special wards of large hospitals where the insertion and follow-up of catheterization lines is carried out by specially trained teams, complications have been reduced by 80%, with a significant impact on the recovery of patients and costs. The change of optics on nutritional support in hospitalized patients, with an emphasis on enteral nutrition, promises a significant decrease in costs. Parenteral nutrition at home is twice as cheap as in the hospital, and the cost of enteral nutrition at home represents one-tenth of the intrahospital cost.
That's enough for today and for this series of posts about parenteral and enteral nutritional therapy. Next time I'll tackle the deficiency and excess vitamins...
Some studies suggest that the nitrogen balance can be improved by administration of human growth hormone, but it is not clear whether it stimulates muscle growth or improves tissue healing. In the case of a stabilized patient, the energy and protein support is determined by the formula: Protein balance = protein intake - protein losses, where protein losses represent the urea nitrogen in the urine from 24 hours (g) x 6.25 (also counts scarring, restoration of normal body composition, resumption of growth in length). In cases where there are disturbances in the use of proteins (hepatic or renal failure), nitrogenemia or amino acids may occur in abnormal plasma concentrations.
The benefit of special enteral or parenteral solutions, which correct these changes, is not known in hepatic encephalopathy. Certain amino acids or some peptides that are not normally essential in very seriously ill patients, where the endogenous pathways that produce or store them are blocked. This is the case with glutamine, aginin and methionine metabolism products. Glutamine, an important "fuel" for enterocytes and lymphocytes, is insoluble and is missing from many parenteral use solutions, in enteral solutions being present only in low concentrations. Glutamine-containing soluble dipeptides are being investigated.
The related nuleotides and metabolic products have beneficial effects on the immune system, small intestine growth, lipid metabolism and liver function. The nuleotides can be synthesized de novo in all cells only in small amounts, so the body depends on the nutreotides in the diet or the storage pathways that recycle the nucleotides resulting from the turnover of purine and pyrimidine. Nutritionally deficient patients benefit from the intake of formulae enriched by the eulled.
In general, amino acids are administered parenterally systemically and rarely through the physiological pathway of the portal vein. Under these conditions, methionine, the only sulfur amino acid in parenteral solutions, is more transaminaseed in peripheral tissues than transsulphurized in the liver. It follows that products such as carnitine, taurine and glucation become relatively deficient. Preliminary studies have indicated that the addition of an intermediate compound, S-adenozil methionine, to parenteral solutions leads to a decrease in cholestasis.
It's the turn of the need for minerals and vitamins. It may be higher in parenteral nutrition than in enteral nutrition, for several reasons: firstly, these substances are released into the systemic circulation and not into the portal circulation, short-circuiting the liver and being eliminated urinaryly; secondly, many patients with intestinal disorders lose enteral sodium, potassium, chlorine and bicarbonate, have malabsorption for bivalent cations, cobalamin and fat-soluble vitamins. Exposure to oxygen and light of infusion solutions can help destroy vitamins (especially vitamin A) and nutrients can adhere to tubes and bags. The glucose content is gradually increased as the patient proves tolerance to large amounts of glucose.
From the point of view of parenteral nutrition and the technique of infusion and monitoring of the patient, partial and short-term parenteral nutrition can be done through peripheral veins, provided that most energy needs are provided by isotone lipid solutions (instead, total long-term parenteral nutrition should be done through a central vein, as it involves the administration of hypertone glucose that must be rapidly diluted in a considerable blood flow).
Central catheters with peripheral insertion are the cheap option for short-term parenteral nutrition. In one study, the number of catheter infections was the same as with peripheral and central insertion catheters. Catheters with a subcutaneous orifice or tunneling require intraoperative insertion and are stable in long-term use. Central catheters should be changed at the clinically established indication (routine change is expensive and risky). chlorhexedin solution is a better local antiseptic than alcohol or iodophor.
Although transparent dressing is useful for fixing the catheter and allows easy observation of the skin, the incidence of infections due to catheterization is higher than with the use of dry textile dressings (new transparent dressings that do not absorb moisture are under observation). The catheters in silastic or polyurethane associate fewer complications than those of vinyl polychloride. Several types of needle-free systems use central valves (the contamination rate of these installations is not yet known).
Complications that occur can be mechanical, metabolic or infectious. In case of mechanical complications, the insertion of the catheter into the central veins will be done only by experienced personnel and under perfect asepsis conditions. Major mechanical complications include pneumothorax, hemothorax by damage to the subclavian artery or vein, damage to the brachial plexus, catheter malposition in a central vein, azigos vein or right ventricle. The correct positioning of the catheter should be confirmed radiologically before the start of the infusion of hypertone solutions.
The catheters may exit the vein after proper installation, break the vessel or detach and produce intracardiac embolisms or in the pulmonary artery. Catheter thrombosis may occur, especially if it is used for blood collection. The catheter thrombosis of the central veins is usually accompanied by infections. Sometimes it is effective to unlock the catheter by using urokinase. The addition of low doses of heparin (1,000 units/l) to eliminate thrombosis is controversial (no study has shown potential benefits, and heparin may contribute to bone demineralization which is a particular problem of long-term parenteral nutrition).
For metabolic complications, fluid overload causes congestive heart failure, especially in elderly and debilitated patients. Glucose in too large quantities produces osmotic diuresis and, by stimulating insulin, produces the massive intracellular passage of phosphorus and potassium into the extracellular space. Such transfer is more likely in casec patients, who have total phosphorus and potassium doutination in the body (decrease in plasma levels of the two elements produces arrhythmias, cardiopulmonary dysfunction and neurological symptoms).
To avoid them, parenteral nutrition should be progressively established and closely monitored. The amount of glucose is gradually increased as patients develop tolerance to glucose loading. Late metabolic complications consist of cholestatic liver damage with thick bile syndrome and formation of gallstones. The exact cause of liver damage is unknown, but it appears that the disorder of the metabolism of sulphide amino acids plays an important role. Cholestasis is likely associated with lack of enteral stimulation and is unlikely to occur in the presence of minimal enteral intake.
Parenteral nutrition induces hypercalciuria, which can lead to negative calcium balance in the body and osteopenia. Hypercalciuria appears to be caused by several factors, including the effects of amino acid infusion and the fixed acid load of the bisulphite preservative. In the past, protein hydrolysated solutions produced aluminium contamination, with damage to bone mineralization (aluminum may still exist as an additive in some infusion solutions, such as calcium gluconate). As soon as the patient undergoes long-term parenteral nutrition passes from the catabolic to the anabolic phase, supplementation with essential fatty acids, minerals, vitamins is necessary to prevent possible deficiencies.
In the case of infectious "problems", infection of venous approach paths rarely occurs within the first 72 hours, usually fever occurring during this period due to an infection located elsewhere in the body or other cause. Infection of the venous approach is likely when the fever decreases, reducing the rate of infusion of solutions. Positive cultures in the central lines suggest catheter septicaemia, especially when another source of infection cannot be identified in the body and if the microbe highlighted is staphylococcus or Candida. If mycotic infection can be resolved by the body's own resources (after removal of the catheter), bacterial infections or more aggressive fungi require antibiotic therapy.
Catheter sepsis is more likely to occur when triple lumen venous catheters are used (single lumen catheters are used exclusively for parenteral nutrition, central catheters with peripheral insertion and tunneled catheters have an equal incidence of catheter septicaemia). When antibiotic prophylaxis is not indicated, recurrent catheter septicaemia can be avoided by stationing minimal amounts of antibiotics in the lumen of the catheter with a "dop" of heparin or by a "sleeve" at the insertion of the catheter.
Let me present some elements about enteral nutrition in reference to tube placement and patient monitoring. Patients receiving enteral nutrition are at risk for some of the metabolic complications referred to in parenteral nutrition, the monitoring should be identical. Since small diameter tubes can be easily moved from the location, the position of the tube should be tested by aspiration of the digestive fluid and determination of the pH of the intestinal fluid (less than 4 in the stomach and greater than 6 in the jejun). Complications that may occur are represented by suction and diarrhea.
In the case of aspiration, debilitated patients with unsatisfactory gastric discharge and impaired swallowing and cough mechanisms are at risk of suction. In patients connected to the ventilation system, tracheal suction induces coughing and causes gastric regurgitation, in this case the endotracheal balloon probe and tracheostomy sleeve rarely preventing pulmonary aspiration of regurgitated fluid. In these conditions, it is safer to use a wide tube, allowing accurate verification of the residual gastric contents and, if necessary, its discharge before suctioning the trachea or using jejunal nutrition.
Although the stomach retains its normal motility and is able to fragment food and then propel it into the duodenum, constant administration of fluids from enteral solutions is preferred, as this is better tolerated by patients than intermittent gastric bolus. Continuous infusion can be achieved with the help of a special pump, especially in the case of tubes with fine lumen that have a greater possibility of obstruction.
If long-term enteral feeding is expected, most patients prefer endoscopically placed, radiological or surgical gastric tube. In the ambulatory, the gastrostoma tube can be used in a "button" on the skin. The naso-jejunal tube reduces the risk of suction. However, the fluoroscopic placement of these tubes through the pilor takes time and often followed by its return to the stomach. Safer is the percutaneous gastro-jejunal placement under radiological control.
Enteral nutrition often causes diarrhea, especially if intestinal functions are compromised by intestinal disorders or by taking medication. Diarrhea can be controlled by continuous feeding in small amounts, by adding hydrofile mucilages (psyllium) by anticholinergic medication. Diarrhea stimulated by enteral nutrition does not necessarily involve malabsorption of nutritional compounds (other than water and electrolytes). Moreover, because they have trophic effects on the mucosa and stimulate the intestinal immunological barrier, it is not recommended to stop enteral nutrition in the presence of diarrhea, even when parenteral intake of loss replacement is necessary.
I'll finish by inserting some elements about the cost of nutritional therapy. Approximately 25% of patients admitted to chronic hospitals have central catheters fitted and 25-30% of these catheters are used for parenteral nutrition. The incidence of catheter infections reflects the quality of the medical act and the conditions offered and ranges from 2 to 30% of catheters/day, depending on the type of patient. In critically ill patients, catheter infection is associated with a mortality of 35%, with an estimated cost of EUR 30,000/ survivor.
Most complications stem from faulty insertion and catheter tracking than from plant failures. In the special wards of large hospitals where the insertion and follow-up of catheterization lines is carried out by specially trained teams, complications have been reduced by 80%, with a significant impact on the recovery of patients and costs. The change of optics on nutritional support in hospitalized patients, with an emphasis on enteral nutrition, promises a significant decrease in costs. Parenteral nutrition at home is twice as cheap as in the hospital, and the cost of enteral nutrition at home represents one-tenth of the intrahospital cost.
That's enough for today and for this series of posts about parenteral and enteral nutritional therapy. Next time I'll tackle the deficiency and excess vitamins...
Love, Understanding and
Gratitude!!!
Dorin, Merticaru