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Medical nutrition for lung diseases
Nutritional support for lung diseases is a relatively new frontier in dietetics, in particular gerontology. It is known that many older patients suffering from chronic lung diseases have protein-energy deficiency, which negatively affects the structure and function of the respiratory muscles, gas exchange, cardiovascular and nervous system, the nature of the immune defense of the body. The adverse effects of malnutrition on the architecture of the lungs and its restoration after injury, on the production of surfactant, as well as on the possibility of implementing other metabolic processes are less studied.
In healthy people and in patients with emphysema, there is a direct correlation between body weight and diaphragm mass. In addition, in patients with protein-energy deficiency, a decrease in the force of the respiratory muscles is observed at the height of the maximum inspiratory and respiratory pressure.
A number of studies examining the influence of nutritional status on lung gas exchange and metabolic rate have shown that an adequate intake of calories is necessary to maintain normal gas exchange and optimal metabolic rate.
Experiments on old animals have demonstrated that an insufficient amount of proteins and calories leads to a decrease in T-lymphocyte-dependent function of alveolar macrophages, despite their continuing neutrophil-dependent function. Thus, along with general susceptibility to infectious diseases in malnourished patients, the development of local immunity of the mucous membrane of the lungs is possible.
Experimental data also indicate that adequate nutrition may play an important role in the production of surfactant and the restoration of normal lung architectonics when they are damaged, but the clinical significance of these observations is still not completely clear.
Depending on the nature of the pathological process, all lung diseases are divided into acute and chronic. This explains the differences in nutritional care (its potential benefits, adverse effects and clinical priorities).
Chronic pulmonary diseases
Most chronic lung diseases are pathophysiologically represented by the formation of obstructive or restrictive damage in the mechanics of external respiration (alone or in combination).
In the structure of chronic lung diseases the most common are chronic obstructive pulmonary diseases (COPD), which occur in more than 14% of men and 8% of women of older age. The concept of COPD include: emphysema, chronic bronchitis and bronchial asthma.
Protein-energy deficiency among patients with chronic lung diseases
Among patients with chronic obstructive pulmonary diseases, protein-energy deficiency is extremely common. According to various studies, this syndrome is observed in 19-25% of cases, which negatively affects the survival of these patients. With progressive weight loss in this group of patients, the mortality was significantly (2 times) higher compared with those patients who did not have weight loss.
In a retrospective analysis, it was reasonably shown that older patients, who had less than 90% of their ideal body weight at the beginning of the study, generally had a greater mortality rate within 5 years, even after eliminating complications associated with lung dysfunction. This effect was observed in patients with moderate obstruction (forced expiratory volume more than 46% required) and those who had severe obstruction (forced expiratory volume less than 35% required), and, therefore, did not depend on lung function. Thus, the progress in the treatment of COPD did not change the unfavorable prognosis of these patients, if they had a concomitant protein-energy deficiency. Interestingly, patients with chronic obstructive pulmonary diseases and protein-energy deficiency have a more pronounced respiratory failure and the absence of the classic symptoms of chronic bronchitis.
Possible pathophysiological mechanisms of protein-energy deficiency in patients with chronic lung disease:
- deterioration of the gastrointestinal tract;
- inadequate nutrition;
- impaired adaptive mechanism to reduce oxygen consumption (in the interests of reducing the work of the respiratory muscles);
- altered pulmonary and cardiovascular hemodynamics, limiting the supply of nutrients to other tissues;
- antioxidant disorders;
- a state of increased metabolism.
Malnutrition, protein deficiency in the diet in patients with chronic obstructive pulmonary diseases is explained by a decrease in food intake and an increase in energy consumption secondary to high respiratory rate, which increases the resistive load and decreases the efficiency of the respiratory muscles. Along with this, inadequate intake of calories and protein can occur with stress, surgery, or the addition of an infection, when the need for energy increases. Thus, stepwise progressive deterioration of lung function and nutritional status may occur.
The research results showed that the real energy need in patients with chronic obstructive pulmonary diseases with and without loss of weight significantly exceeds the value that is calculated using the Harris-Benedict equation. Although these patients have an increased metabolism, they do not have an increased catabolism, which is observed in a state of stress with a predominance of fat oxidation. Increased energy needs may be associated with increased oxygen consumption by the respiratory muscles. A higher level of energy consumption by the respiratory muscles in patients with COPD compared with healthy people may maintain hypermetabolism and lead to progressive weight loss if the consumption of calories exceeds their consumption.
Most studies demonstrate adequate intake of calories, the need for which in patients with COPD was calculated or measured for dormancy. However, they did not take into account the required number of calories and protein for active physical activity or intercurrent disease, in order to assess their real adequacy for a given patient.
An attempt to increase the introduction of calories and protein above the usual (initial) level may be difficult in these patients due to respiratory and gastrointestinal disorders (for example, anorexia, early satiety, shortness of breath, weakness, bloating, constipation, dental problems). Some of these symptoms (bloating, early satiety, anorexia) may be associated with flattening of the diaphragmatic muscle and its effect on the abdominal cavity. In patients with COPD who are in a state of hypoxia, shortness of breath during eating may increase, which further limits the amount of food ingested. Smaller and more frequent meals may to some extent alleviate some of these conditions.
Studies in which patients with malnutrition and COPD were prescribed a therapeutic diet enriched with a specialized food product with a mixture of protein composite dry (SBKS) Diso® Nutrinor, containing 40 g of protein per 100 g of product, showed the effectiveness of this method of enriching dietary protein meals and increasing the nutritional value of diets without increasing the amount of food consumed.
It has been shown that patients with COPD and low body mass have the same energy requirement as patients with normal body weight. But in the first group there is a lower calorie intake relative to the energy requirement measured by them.
Medical nutrition in COPD
In COPD, emphasis is placed on maintaining the strength of the respiratory muscles, especially the diaphragm, their mass, as well as the ability to optimize the overall functioning of the patient.
A number of studies have shown that admission of additional calories and protein to patients for more than 16 days leads to a significant increase in body weight and an improvement in the maximum respiratory pressure compared with people of the same age without lung pathology.
With longer follow-up of patients with COPD, after 3 months of dieting with an increased amount of protein (including 36 g of a mixture of protein composite dry in the treatment ration), an increase in their body weight and other anthropometric data was observed, an increase in the strength of the respiratory muscles, improvement in overall health was observed and portability of 6-minute pedestrian distances, as well as a decrease in the degree of dyspnea. With a longer duration of observance of the high protein diet, along with an increase in the muscle mass of the patients, there was a further improvement in the functions of the respiratory muscles.
Interestingly, patients with initially lower body mass and lower calorie intake benefit greatly from eating a specialized protein food mixture of a protein composite dry, especially if it lasts for a long time, while they have a significant weight gain. Therefore, the likelihood of improving the function of the respiratory muscles may be related to the degree of weight gain and, possibly, the severity of initial deficiencies.
The problem of adequate caloric intake in this category of patients may be due to diet-induced thermogenesis: it has been shown that patients with reduced nutrition combined with COPD have a greater increase in oxygen consumption alone after eating than patients who do not suffer from this disease.
There are no long-term studies that consider nutritional support as a criterion for improving the overall prognosis in elderly patients with COPD. If survival is associated with an increase in body weight and it is an independent variable, and the inclusion in the medical ration of a mixture of protein composite dry can improve and maintain body weight, then it is expected that survival is associated with the optimization of nutrition in this group of patients. It is unclear what potential effect on the function of the respiratory organs could lead to an improvement in clinical results: immunocompetent, improvement of gas exchange, effect on reparative processes in the lung or the production of surfactant. Despite the heterogeneous results of short-term studies, today it is quite obvious the clinical validity of the use of SBCS specialized food products in patients with COPD.
Diet vector
Since patients with COPD have limited respiratory reserve, it is likely that a diet high in carbohydrates would be undesirable for the respiratory system. A high-fat diet is more beneficial. The study showed that a 5-day low-carbohydrate diet in patients with COPD and hypercapnia (calories from carbohydrates were 28%, due to fats - 55%) leads to a significantly lower production of CO2 and an arterial partial pressure of CO2 than the 5-day high carbohydrate diet (calories from carbohydrates - 74%, from fat - 9.4%). A significant functional parameter was evaluated (a 12-minute walk), and it was found that a large amount of carbohydrates reduces the distance traveled by patients with COPD, which was compared with placebo.
Macro and micronutrient metabolism disorders
Electrolyte deficiency such as hypophosphatemia, hypokalemia and hypocalcemia can adversely affect the function of the respiratory muscles. An improvement in the contractile function of the diaphragm after replenishing phosphorus deficiency in patients with acute respiratory failure and hypophosphatemia was shown. This observation is especially appropriate for elderly patients with COPD who require artificial ventilation of the lungs, as they usually occur intracellular shifts after correction of respiratory acidosis. Clinical manifestations of hypophosphatemia result from the depletion of intracellular phosphorus reserves, which, as a rule, is accompanied by chronic hypophosphatemia.
It has been reported that a sharp decrease in serum calcium levels may also decrease the maximum contraction of the diaphragm.
A case of hypokalemic respiratory arrest has been described, i.e. there has been hypokalemic paralysis of the respiratory muscles.
The significant interest of researchers is magnesium. It is established that it activates adenylate cyclase, catalyzing the formation of cAMP, inhibits mast cell degranulation and provides relaxation of bronchial smooth muscle. In patients with hypomagnesemia, obstructive respiratory dysfunction and bronchial hypersensitivity to histamine were detected, which were fully or partially corrected by prescription of magnesium preparations. Magnesium salts after intravenous administration have a bronchodilator effect, relieving asthma attacks, as well as asthmatic status, increase the force of contraction of the respiratory muscles and reduce pulmonary hypertension in patients with bronchial asthma and other obstructive pulmonary diseases. Thus, clinical and experimental observations indicate the involvement of magnesium ions in the regulation of bronchial patency, pressure in the pulmonary artery and contractility of the respiratory muscles. Replenishing electrolytes may ultimately be more important than protein anabolism and lead to a dramatic improvement in the strength of the respiratory muscles.
The role of trace elements and vitamins
Increased attention to the relationship between trace elements, vitamins and respiratory diseases. The dependence of respiratory symptoms of bronchitis with the level of vitamin C, zinc, copper, and nicotinic acid in blood serum was found.
Vitamin C is an antioxidant, and copper is an important cofactor for the lysyl oxidase enzyme, which is involved in the synthesis of elastic fibers and glycosaminoglycans that make up the structural component of the framework (basal tone) of the bronchi. Severe copper deficiency can lead to a decrease in the elasticity of the bronchi.
In artificially induced copper-deficient states in mammals, the development of primary emphysema was observed as a result of a sharp decrease in elastin in the lungs. The cause of the irreversible defect in the lung tissue is the inactivation of the copper-containing lysyl oxidase enzyme, superoxide dismutase depression and the associated intensification of lipid peroxidation.
Selective zinc deficiency leads to thymic hypoplasia, a decrease in the activity of thyroid hormones and contributes to T-cell lymphocytosis. It is believed that the change in the microelement composition of the blood is one of the reasons for the formation of secondary immunodeficiency states in diseases of the respiratory system.
Noteworthy data on the ability of trace elements to control the activity of lipid peroxidation and antioxidant defense system. It is known that copper, zinc and manganese are part of superoxide dismutase, selenglutation peroxidase. These enzymes are components of the intracellular antioxidant system. Ceruloplasmin, one of the main extracellular antioxidants, is in the class of copper-containing proteins. Zinc, which forms chemical bonds with sulfhydryl groups of proteins, phosphate residues of phospholipids and carboxyl groups of sialic acids, has a membrane stabilizing effect. A deficiency of copper and zinc leads to an accumulation of free radicals in the tissues. An excess of ionized iron has a pro-oxidant effect.
In studies performed in recent years, it has been established that elderly patients with COPD, and especially elderly people, have a deficiency of selenium associated with depression of the intracellular antioxidant glutathione peroxidase. Supplements of sodium selenite in a daily dose of 100 µg for 14 days increase the activity of this enzyme and significantly reduce the clinical manifestations of bronchial obstruction.
Diet therapy focus
Chronic lung diseases can be associated with the damaging effects of free radicals when the natural antioxidant defense system of the lung is suppressed (for example, by smoking, severe vascular disorders in old age) or insufficient (α-antitrypsin deficiency). Dietary micronutrient deficiencies can also increase susceptibility to damage by free radicals and may be one of the factors that leads to excessive activation of lipid peroxidation.
Diet therapy in COPD is aimed at reducing intoxication and increasing the body's defenses, improving the regeneration of the respiratory tract epithelium, reducing exudation in the bronchi. In addition, the diet provides for the replacement of significant losses of proteins, vitamins and mineral salts, sparing the activity of the cardiovascular system, stimulation of gastric secretion, blood formation.
High Protein Diet (VBD)
Patients with chronic obstructive pulmonary diseases are advised to prescribe a high-protein diet (IAP) of high energy value (2080–2690 kcal), with an increased content of full-fledged proteins - 110–120 g (of which at least 60% are of animal origin), with a fat quota of 80–90 g and the carbohydrate content within the physiological norm is 250–350 g (with an exacerbation, the amount of carbohydrates is reduced to 200–250 g).
If a high-protein diet is observed, an increase in foods rich in vitamins A, C, B group (decoctions of wheat bran and rosehip, liver, yeast, fresh fruits and vegetables, their juices), as well as calcium, phosphorus, copper and zinc salts is envisaged. Improving appetite contributes to the inclusion of vegetables, fruits, berries and juices from them, meat and fish broths.
Limiting salt to 6 g / day has an anti-inflammatory effect, reduces exudation, fluid retention in the body and thereby prevents the development of circulatory failure during the formation of pulmonary heart. The diet provides for the restriction of free fluid, which helps to reduce the amount of secreted sputum and ensure a gentle regimen for the cardiovascular system.
In accordance with the norms of medical nutrition, approved by the Order of the Ministry of Health of Russia dated June 21, 2013 No. 395n “On approval of norms of therapeutic nutrition”, a patient with COPD, while observing a high protein diet, should receive daily 36 g of a specialized food product of a mixture of protein composite dry. For example, with the use of Diso® Nutrinor, the patient's diet is enriched with 14.4 g of high-quality, high-grade and easily digestible protein.
Diet therapy in bronchial asthma
If there are no indications of intolerance to certain products, physiologically good nutrition is recommended for patients with bronchial asthma, but with a restriction of strong meat and fish broths, salt, spicy and salty foods, spices, seasonings and products containing easily digestible carbohydrates (sugar, honey, chocolate and others). It is known that at least some of the patients with bronchial asthma are sodium-sensitive. Food supplements of table salt lead to a worsening of bronchial patency and an increase in nonspecific bronchial hyperreactivity.
Since the pathophysiology of asthma plays a central role in the inflammatory process in the respiratory mucosa, bronchial hyperreactivity can be reduced by supplementing the diet with nutritional supplements that contain essential ω-3 fatty acids (eg, eiconol oil, cod liver oil), which can have a modulating effect on cytokines.
Fish oil effect
Numerous trials have demonstrated the anti-inflammatory effect of fish oil in bronchial asthma. Studies have shown that there is a significant decrease in the severity of late allergic reaction due to the replacement of arachidonic acid in cell membranes with ω-3-polyunsaturated fatty acids, which inhibit the production of lipid mediators of inflammation (5-lipoxygenase and cyclooxygenase) and reduce the tissue response to cytokines. This leads to qualitative changes in the course of the disease: severe asthma attacks occur less frequently, the dosage of drugs decreases.
The increase in asthma prevalence over the past two decades has been associated with a decrease in animal fat consumption and an increase in the use of margarine and vegetable oils containing ω-6-polyunsaturated fatty acids, which can increase the production and activity of pro-inflammatory cytokines of type IL-1, IL-6. The production of IL-1 and IL-6 induced by TNF-α is associated with the supply of linoleic acid with food. In addition, linoleic acid is a precursor of arachidonic acid, which turns into prostaglandin E2, which, in turn, affects T-lymphocytes, reducing the formation of g-interferon, without affecting the synthesis of interleukin-4 (IL-4). This can lead to the development of allergic sensitization, since IL-4 promotes the synthesis of IgE, whereas g-interferon produces the opposite effect. The adverse effect of diet can be mediated through an increase in prostaglandin E2 synthesis, which, in turn, can enhance the production of IgE, while w-3-polyunsaturated fatty acids inhibit the formation of prostaglandin E2.
Nutritional nuances
Epidemiological data suggest that reduced intake of dietary magnesium is associated with impaired lung function, increased bronchial reactivity and shortness of breath, as was mentioned earlier in the article. The intake of increased amounts of magnesium from food helps to improve the general condition of the patient with bronchial asthma.
A decrease in the intake of vitamin C and manganese with food is accompanied by a more than fivefold increase in the risk of impaired bronchial reactivity. Thus, the antioxidant diet and biologically active additives (BAA) with an antioxidant effect can have a modulating effect on the incidence of asthma and the course of the disease.
Well-relieved diet therapy in patients no older than old, which should be carried out in a hospital with the obligatory consent of the patient. The duration of the unloading period usually does not exceed 2-3 weeks. The recovery period for the duration corresponds to the discharge period.
Bronchial asthma and food allergies
Among patients with bronchial asthma, there is a group of patients with endogenous asthma who develop sensitization to food allergens. In particular, 6% of asthmatics who report isolated food allergies have true food allergies to one or more products.
Food and additional food triggers play an important role in approximately 5–8% of all cases of bronchial asthma. The involvement of respiratory symptoms in food allergies reaches 40%. A reliable diagnosis can only be established with a combination of research methods used for food allergies and asthma. As a rule, type 1 immune reactions are involved in the formation of bronchial obstruction, with the involvement of IgE antibodies in the pathological process. In the next 1-2 days, the late phase of the allergic reaction develops, in which cell infiltration of lymphocytes and monocytes dominates, which corresponds to the picture of chronic inflammation.
When the allergen is reintroduced with food, mononuclear cells secrete a cytokine (histamine-producing factor), which interacts with IgE on the membranes of mast cells and basophils, while increasing their release of inflammatory mediators. Active cytokine production, thus, correlates with increased bronchial reactivity in patients with bronchial asthma.
In therapy, in addition to the usual basic therapy of bronchial asthma, the normalization of the intestinal mucosa is of great importance. The use of antihistamines can only be effective for blocking the early phase of an allergic reaction, while manifestations of the late phase, including cell infiltration, can be more successfully inhibited by corticosteroid drugs.
Dietary recommendations are to use a diet with the exception of foods that are causative allergens.
Other chronic lung diseases
The nutritional effects of other chronic lung diseases are not well understood. However, since most of them have respiratory stress in respiratory mechanics, those recommendations that are designed to improve the function of respiratory muscles in COPD should also be important.
Medical nutrition in Heiner syndrome
Heiner syndrome is a chronic recurrent lung disease characterized by chronic rhinitis, pulmonary infiltrates and the development of pulmonary hemosiderosis, gastrointestinal bleeding, iron deficiency anemia. This form of pulmonary hemosiderosis most often accompanies acquired intolerance to cow's milk, but may also be accompanied by intolerance to eggs and pork.
Characteristic manifestations of this disease are peripheral blood eosinophilia and the formation of precipitates in the blood serum to bovine milk. However, immunological mechanisms are still not fully understood. This is not an IgE-mediated immune response.
Diet therapy - the rejection of the causative allergen (cow's milk, eggs, pork).
Acute lung diseases
In acute lung diseases accompanied by hypercatabolism, the main purpose of nutritional support is to provide for the increased needs of the body and prevent protein breakdown.
Acute lung diseases can be represented in a wide range: from a local lung infection (pneumonia) to widespread alveolar damage, such as, for example, respiratory distress syndrome observed in the elderly.
Most respiratory diseases are accompanied by such common complaints as lack of appetite, fatigue, and general malaise. When these symptoms are combined with coughing, shortness of breath and / or suffocation, the ingestion through the mouth in most cases becomes impossible: the patient needs tracheal intubation and mechanical ventilation. It is often difficult to estimate the expected duration of reduced food intake through the mouth. If this develops a negative nitrogenous balance, then as a result it can weaken the force of contraction of the diaphragm, decrease the volume of respiratory movements and change the state of the immune system, which may threaten the recovery of the body.
Clinical priorities
In severe lung disease (for example, in lobar pneumonia), the degree of metabolic stress and nutrient intake requirements are similar to those observed in sepsis, multitrauma, severe injuries or burns. The negative nitrogenous balance occurs, as a rule, in the hypercatabolism phase. The metabolism of carbohydrates changes. Hyperglycemia may occur due to increased glucose metabolism. Due to relative insulin resistance, increased gluconeogenesis in the liver and an excess of contrainsular (catabolic) hormones (glucagon, adrenaline and cortisol), lipid oxidation is predominant, which can be the main source of calories in a stressed patient.
However, in a state of shock and polysystem organ failure, poor utilization of lipids can occur, leading to their accumulation in the body. In order to maintain a constant supply of glucose to the brain and other glucose-dependent tissues, gluconeogenesis is intensified, muscular proteolysis develops (muscle proteins are the source of amino acids for gluconeogenesis), which leads to a negative nitrogen balance.
In this case, energy needs can be measured using indirect calorimetry at the patient’s bedside or estimated using the Harris-Benedict equation.
Energy control
An accurate assessment of the energy need in patients with acute lung disease is particularly important. Excessive parenteral and enteral nutrition can lead to fluid overload, impaired glucose tolerance, and fatty liver dystrophy. Excessive enteral nutrition can cause diarrhea. On the other hand, underestimation of the need for calories leads to malnutrition and a negative nitrogen balance with a decrease in muscle mass. At the same time, there is a negative effect on pulmonary mechanics, the volume of respiratory movements is reduced, the function of the diaphragm and immune mechanisms of lung protection are disturbed, thus increasing the need for artificial ventilation of the lungs.
Adequate nutritional support is important in canceling mechanical ventilation in patients with respiratory failure. Its goal should be to achieve an equilibrium of metabolic processes in acute lung diseases, and not just an increase in body weight.
Artificial nutrition
Despite clinical doubts, several strategies have been developed for the organization of artificial feeding of patients with acute lung injury. The main problems are the choice of substrates that meet the patient’s clinical conditions and the optimal way to administer them.
Artificial nutrition can be carried out using proteins, carbohydrates or fats. Consider the merits of these substrates in terms of their connection with lung diseases.
Most patients with acute respiratory failure who need mechanical ventilation are in a state of hypercatabolism with the breakdown of endogenous protein. In addition, under conditions of limited glucose supply, the need for glucose-dependent tissues (brain, erythrocytes and healing wounds) is satisfied by gluconeogenesis from amino acids. The suppression of gluconeogenesis in order to save protein in starving patients is performed by administering 100 g of glucose per day.
In patients with multitrauma or sepsis, theoretically, 600 g or more of glucose per day may be required. Intravenous fat emulsions will help save proteins if they are used together with carbohydrates (at least 500 kcal / day due to carbohydrates). The intake of proteins from the outside can also restore their endogenous reserves. Being a substrate for gluconeogenesis, it will limit proteolysis. Given the priority role of proteins in normal physiology and cell functions, saving it is an integral part of recovery for any damage.
However, it must be remembered that a protein supplement can increase oxygen consumption (the thermal effect of proteins), minute ventilation of the lungs and hypoxemia. A clinically high protein diet could lead to an increase in shortness of breath in patients with an already increased volume of respiratory movements and / or with a limited respiratory reserve.
Glucose control
The appropriate mixture of delivered substrates (proteins, carbohydrates or fats) depends on the clinical condition and the goals to be achieved. In patients with acute or chronic respiratory failure, with a limited respiratory reserve, carbohydrates place greater demands on the respiratory system than other substrates, due to the relatively higher carbon dioxide production during their oxidation. One molecule of carbon dioxide is produced for each molecule of oxidized glucose, making the respiratory coefficient equal to 1.
The oxidation of carbohydrates more than the oxidation of fats or proteins, produces CO2 emitted by the lungs. If VCO2 increases, alveolar gas exchange also increases in order to maintain normal PaCO2 in the blood. The increase in alveolar ventilation can occur by increasing the frequency of respiratory movements or minute ventilation of the lungs, which, in turn, increase the work of the respiratory system. Thus, respiratory failure may be exacerbated when large amounts of glucose are given to patients with reduced lung function.
Increase fat quota
In an attempt to provide full parenteral nutrition to patients by first adding fat emulsions and then glucose, constituting 50% of non-protein calories, it was noted that after switching from a source rich in fat to a source with a high content of glucose, CO2 increased by 20%, and minute ventilation - by 26–71%. In patients with hypermetabolism, minute ventilation of the lungs may increase by 121%. This result can be explained by the amount of CO2 released during the production of triglycerides from glucose, which is 30 times more than the amount of CO2 produced during the conversion of dietary fats to endogenous triglycerides.
Thus, for those patients who have a limiting respiratory reserve and the danger of respiratory failure, it seems more appropriate to prescribe a diet with a higher percentage of fat than carbohydrates (more than 50% of non-protein calories, due to lipids), and refrain from overfeeding these patients. Thus, it is possible to avoid an increase in acute respiratory failure or (with the abolition of mechanical ventilation) to facilitate their transition to independent breathing.
As for micronutrients (vitamins, minerals), the majority of ready-made nutritional mixtures provide or can be supplemented in order to provide the recommended dietary requirements for them. These mixtures can also be adjusted to eliminate the existing deficiency or excess fluid and electrolytes and / or for other clinical conditions (hepatic, renal, enteral, cardiac, or pulmonary insufficiency).
The route of administration of artificial nutrition may be parenteral or enteral. If the patient is able to eat independently, the supplementary feeding through the mouth is the predominant way. If the patient is not able to eat, then the choice lies between the enteral and parenteral routes.
Enteral nutrition
This type of supplemental feeding can be performed using a gastric or duodenal probe. Gastric probes are less difficult to set, but are more likely to cause complications such as aspiration and / or hospital pneumonia, despite tracheal intubation.
Paresis of the stomach is common in elderly patients in serious condition, especially in those who need mechanical ventilation. The presence of a probe intersecting the lower esophageal sphincter makes it possible to regurgitate gastric contents and pulmonary aspiration. In addition, the neutralization of the acidic pH of the stomach with enteral nutrition contributes to the overgrowth of bacteria in the stomach and subsequent colonization of the oropharynx. To minimize micro-aspiration, the head of the patient's bed should be raised at least 45 °. Unfortunately, it is difficult to keep this position in the intubated patient, because it requires frequent turning over in order to hold the toilet of the lungs and reduce the risk of formation of pressure sores. In connection with these points, it is preferable to set up food probes intended for insertion into the duodenum.
Parenteral nutrition
Full parenteral nutrition can be performed through the central vein, while allowing for the use of high-osmolar solutions, or through a peripheral vein.
In the peripheral route of administration, a large fluid load may be required to meet the same energy requirements for the central route of administration. Since impaired water metabolism is common for acute lung damage, it is preferable to have limited fluid intake. In patients with respiratory failure, it is more advantageous to introduce a large proportion of fat calories, resulting in a lower respiratory coefficient. This is especially important when attempting to abolish mechanical ventilation.
Research results suggest that, despite an excellent, compact source of calories, the possible effects of lipid emulsions on the regulation of the immune system may be so important in severe, often infected, elderly patients with impaired respiratory function, which may raise the question of whether they should be used in this patient groups.
Some experimental studies have shown that the conversion of linoleic acid to arachidonic acid, a precursor of prostaglandins and leukotrienes, can have a strong influence on the cytokine regulation of the immune response. Linolenic acid may, conversely, reduce the production of prostaglandins and leukotrienes and therefore reduce the inflammatory response. The relationship between diet and the inflammatory response in the body of an elderly patient is, if not in the initial, then not in the final stages of the study.
