Protein-energy insufficiency

Protein-energy deficiency, or protein-caloric insufficiency, is an energy deficit due to chronic deficiency of all macronutrients. It usually includes deficiencies and many micronutrients. Protein-energy deficiency can be sudden and total (fasting) or gradual. The severity varies from subclinical manifestations to apparent cachexia (with edema, hair loss and skin atrophy), multiorgan and multisystem insufficiency is observed. For diagnosis, laboratory tests are usually used, including evaluation of serum albumin. Treatment includes correction of fluid and electrolyte deficiencies by intravenous fluids, and then a gradual nutrient replacement orally, if possible.

In developed countries, protein-energy deficiency is a condition common among nursing homes (although they often do not suspect it) and among patients with disorders that reduce appetite or worsen the digestion, absorption and metabolism of nutrients. In developing countries, protein-energy deficiency is typical for children who do not consume enough calories or protein.

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Classification and causes of protein-energy deficiency

Protein-energy deficiency is mild, moderate or severe. The stage is established by determining the difference in the percentage of the actual and calculated (ideal) weight of the patient corresponding to its growth, using international standards (norm, 90-110%, light protein-energy insufficiency, 85-90%, moderate, 75-85%, heavy , less than 75%).

Protein-energy deficiency can be primary or secondary. Primary protein-energy deficiency is due to inadequate intake of nutrients, and secondary protein-energy deficiency is the result of various disorders or medications that interfere with the use of nutrients.

[4], [5], [6], [7], [8],

Symptoms of protein-energy deficiency

Symptoms of moderate protein-energy deficiency can be general (systemic) or affect certain organs and systems. Apathy and irritability are characteristic. The patient is weakened, working capacity is reduced. Cognitive abilities, and sometimes consciousness, are disrupted. Develop a temporary deficit of lactose and achlorhydria. Diarrhea is common, and they are aggravated by a deficiency of intestinal disaccharidases, especially lactases. Gonads are atrophic. Pan can cause amenorrhea in women and loss of libido in men and women.

Loss of fat and muscle mass is a common manifestation for all forms of PEN. In adult volunteers who were fasting for 30-40 days, weight loss was evident (25% of initial weight). If fasting is more drier, then weight loss can reach 50% in adults and, probably, more in children.

Cachexia in adults is most evident in areas where normally visible fat deposits are present. Muscles decrease in volume, and bones considerably protrude. The skin becomes thin, dry, inelastic, pale and cold. The hair is dry and falls out easily, becoming rare. Weakened wound healing. In elderly patients, the risk of fractures of the hip, pressure sores, trophic ulcers increases.

In acute or chronic severe protein-energy deficiency, the size of the heart and cardiac output decrease; the pulse slows down, blood pressure decreases. The intensity of breathing and the vital capacity of the lungs are reduced. The temperature of the body falls, sometimes leading to death. Swelling, anemia, jaundice and petechiae can develop. Hepatic, renal, or heart failure may occur.

Cellular immunity is weakened, and susceptibility to infections increases. Bacterial infections (eg, pneumonia, gastroenteritis, otitis media, urogenital tract infections, sepsis) are characteristic of all forms of protein-energy deficiency. Infections lead to activation of the production of cytokines, which aggravate anorexia, which leads to an even greater loss of muscle mass and a significant decrease in the serum albumin level.

In infants, marasmus causes hunger, weight loss, growth retardation, loss of subcutaneous fat and muscle mass. Ribs and facial bones protrude. Flabby, thin, "dangling" skin hangs folds.

Kwashiorkor is characterized by peripheral edema. The stomach protrudes, but there is no ascites. Skin is dry, thin and wrinkled; it becomes hyperpigmented, cracks, and then develops its hypopigmentation, looseness and atrophy. The skin of various areas of the body can be affected at different times. Hair becomes thin, brown or gray. Hair on the head easily falls out, eventually becoming rare, but the hair of the eyelashes can even grow excessively. The alternation of malnutrition and adequate nutrition leads to the fact that the hair has the appearance of a "striped flag". Sick children can be apathetic, but become irritable if they are trying to stir.

Complete starvation is fatal if it lasts longer than 8-12 weeks. Thus, the symptoms typical for protein-energy deficiency do not have time to develop.

Primary protein-energy insufficiency

Across the world, primary protein-energy deficiency occurs mainly in children and the elderly, that is, in those who have limited opportunities to obtain food, although the most common cause in old age is depression. This can also be a consequence of fasting, medical starvation or anorexia. Also, the reason may be poor (cruel) treatment of children or the elderly.

In children, chronic primary protein-energy deficiency has three forms: marasmus, kwashiorkor and a form that has characteristic features of both (marasmic kwashiorkor). The form of protein-energy deficiency depends on the ratio in the diet of non-protein and protein sources of energy. Fasting is an acute severe form of primary protein-energy deficiency.

Marasmus (also called dry form of protein-energy deficiency) causes weight loss and muscle and fat loss. In developing countries, insanity is the most common form of protein-energy deficiency in children.

Kwashiorkor (also called wet, puffy or swollen form) is associated with the premature withdrawal of the older baby from the breast, which usually occurs when a young child is born, "pushing" the older child from the chest. Thus, children with a kwashiorkor are usually older than with marasmus. Kwashiorkor can also result from an acute illness, often a gastroenteritis or other infection (probably secondary, due to the production of cytokines) in children who already have protein-energy deficiency. A diet that is more protein deficient than energy can be more likely to cause a kwashiorkor than marasmus. Less often than marasmus, kwashiorkor tends to be limited to certain regions of the world, such as the rural regions of Africa, the Caribbean and Pacific Islands. In these areas, staple foods (for example, cassava, sweet potatoes, green bananas) are poor in proteins and are rich in carbohydrates. With kwashiorkor, the permeability of cell membranes increases, causing the intravascular fluid and protein to be transudated, leading to peripheral edema.

Marasmatic kwashiorkor is characterized by total features of marasmus and kwashiorkor. The affected children are swollen and have more fat in the body than in the case of marasmus.

Fasting is complete insufficiency of nutrients. Sometimes fasting is voluntary (as in the period of religious fasting or with neurogenic anorexia), but usually it is due to external factors (eg, spontaneous circumstances, being in the desert).

Secondary protein-energy insufficiency

This type is usually the result of disorders that affect the function of the GI tract, cachectic disorders and conditions that increase metabolic needs (eg, infections, hyperthyroidism, Addison's disease, pheochromocytoma, other endocrine disorders, burns, trauma, surgery). With cachectic disorders (eg, AIDS, cancer) and kidney failure, catabolic processes lead to the formation of an excess of cytokines, which in turn leads to malnutrition. Heart failure of the terminal stage can cause cardiac cachexia - a severe form of malnutrition, mortality from which is particularly high. Cachectic disorders can reduce appetite or worsen the metabolism of nutrients. Disorders that affect GI function can disrupt digestion (eg, pancreatic insufficiency), absorption (eg, enteritis, enteropathy) or lymphatic transport of nutrients (eg, retroperitoneal fibrosis, Milroy's disease).

Pathophysiology

The initial metabolic reaction is a decrease in the intensity of metabolism. To provide energy, the body first "splits" fat tissue. However, then the internal organs and muscles also begin to break down, and their mass decreases. Liver and intestines lose weight most of all, the heart and kidneys occupy an intermediate position, and the nervous system loses the least weight.

Diagnosis of protein-energy deficiency

The diagnosis is based on the medical history, when clearly inadequate food intake is established. The reason for inadequate nutrition should be identified, especially in children. Children and adolescents must always bear in mind the possibility of ill-treatment and anorexia nervosa.

The objective survey data can usually confirm the diagnosis. Laboratory studies are needed to identify the cause of secondary protein-energy deficiency. Measurement of plasma albumin level, total lymphocyte count, CD4 ⁺ T-lymphocytes, and reaction to skin antigens help determine the severity of protein-energy deficiency or confirm the diagnosis in borderline states. Conducting a measurement of the level of the C-reactive protein or the soluble interleukin-2 receptor can help determine the cause of malnutrition with its ambiguity and confirm a disruption in the production of cytokines. Many additional indicators may differ from normal values: for example, reduced levels of hormones, vitamins, lipids, cholesterol, prealbumin, insulin-like growth factor-1, fibronectin and retinol-binding protein are characteristic. Levels of creatinine and methyl-histidine in urine can be used as criteria for assessing the degree of loss of muscle mass. As protein catabolism slows down, the level of urea in the urine also decreases. These data are rarely taken into account when choosing treatment tactics.

With the help of other laboratory tests, it is possible to identify concomitant abnormalities that require treatment. Serum electrolyte levels, urea and creatinine levels, BUN, glucose, possibly Ca, Mg, phosphate and Na should be determined. Blood glucose and electrolyte levels (especially K, Ca, Mg, phosphate, sometimes Na) are usually low. Indicators of urea and creatinine, BUN in most cases remain at low values, until the development of renal failure. It is possible to detect metabolic acidosis. A general blood test is performed; usually there is normocytic anemia (mainly due to protein deficiency) or microcytic anemia (due to simultaneous iron deficiency).

Indicators used to assess the severity of protein-energy deficiency

Index	Norm	Lightweight	Moderate	Heavy
Normal weight (%)	90-110	85-90	75-85	<75
Body mass index (BMI)	19-24	18-18.9	16-17.9	<16
Whey protein (g / dL)	3.5-5.0	3.1-3.4	2.4-3.0	<2.4
Serum transferrin (mg / dL)	220-400	201-219	150-200	<150
The total number of lymphocytes (in mm 3 )	2000-3500	1501-1999	800-1500	<800
Hypersensitivity index of delayed type	2	2	1	0

In the elderly, a BMI <21 may increase the risk of death.

The delayed-type hypersensitivity index shows the amount of hardening detected by the skin test, using a common antigen obtained from Candida sp. Or Trichophyton sp. The degree of induration is 0 - <0.5 cm, 1 - 0.5-0.9 cm, 2 -> 1.0 cm.

We also take an analysis of the culture of feces on eggs of worms and parasites if the diarrhea is severe and does not respond to treatment. Urine analysis is sometimes performed, bacteriological examination of urine, bacteriological tests of blood, tuberculin test and chest X-ray for the diagnosis of hidden infections, because people with protein-energy deficiency can have a slow reaction to infection.

[9], [10], [11]

Prophylaxis and treatment of protein-energy deficiency

Worldwide, the most important strategy for preventing protein-energy deficiency is to reduce poverty, improve knowledge about the correctness of nutrition and the level of medical care.

Light or moderate protein-energy deficiency, including short-term fasting, is treated by using a balanced diet, preferably orally. Liquid oral nutritional supplements (usually without lactose) can be used if solid food can not be adequately digested. Diarrhea often complicates oral feeding, because fasting increases the sensitivity of the gastrointestinal tract and the entry of bacteria into Peyer's plaques, contributing to infectious diarrhea. If diarrhea persists (presumably due to a lack of tolerance to lactose), mixtures are made based on yogurt, and not on milk, because people with a lack of lactose tolerance can tolerate yogurt and other sour-milk products. Patients also need the appointment of multivitamin supplements.

Severe protein-energy deficiency or long-term fasting requires treatment under stationary conditions with a controlled diet. The main priorities are correction of violations of water and electrolyte balance and treatment of infections. The next step is filling macronutrients orally or, if necessary, through a probe: nasogastric (usually) or gastric. Parenteral nutrition is prescribed in the event of severe malabsorption.

To correct specific deficiencies of nutrients, which may manifest in weight gain, another treatment may be needed. To avoid micronutrient deficiency, patients should continue to take micronutrients at doses approximately 2 times the recommended daily dose (RDA), before recovery.

Children

It is necessary to treat the underlying pathological condition of the disorder. In children with diarrhea, feeding can be delayed for 24-48 hours to avoid aggravation of diarrhea. Feeding is often done (6-12 times / day), but in order to avoid damage to the already limited ability of the intestine to suck in small amounts (<100 ml). During the first week, infant formulas are usually given in progressively increasing amounts; after a week, you can give full quantities at a rate of 175 kcal / kg and 4 g protein / kg. Double doses of micronutrients that exceed the recommendations of the RDA are mandatory, for which the use of commercial multivitamin supplements is recommended. After 4 weeks, the milk formula can be replaced with whole milk, fish oil and solid foods, including eggs, fruits, meat and yeast.

The distribution of the energy value of macronutrients should be approximately: 16% protein, 50% fat and 34% carbohydrates. As an example, we give a combination of skimmed powdered cow milk (110 g), sucrose (100 g), vegetable oil (70 g) and water (900 ml). Many other milk formulas can also be used (for example, whole fat fresh milk plus corn oil and maltodextrin). Dry milk used in milk mixtures is diluted with water.

Usually, additives are added to the milk mixtures: Md 0.4 meq / kg / day intramuscularly for 7 days; B group vitamins in double RDA are given parenterally for the first 3 days, usually with vitamin A, phosphorus, zinc, manganese, copper, iodine, fluoride, molybdenum and selenium. Since absorption of food iron in children with protein-energy deficiency is difficult, it is prescribed in supplements orally or intramuscularly. Parents are instructed about the nutritional needs.

In adults

It is necessary to eliminate the disorders associated with protein-energy deficiency. For example, if AIDS or cancer leads to excessive production of cytokines, megestrol acetate or hydroxyprogesterone can improve food intake. However, since these drugs dramatically decrease the production of testosterone in men (possibly causing loss of muscle mass), it is necessary to simultaneously use testosterone. Since these drugs can cause a decrease in adrenal function, they should be used only briefly (<3 months). In patients with functional limitations, the key points of treatment are food delivery and feeding assistance.

Medicines that stimulate appetite (cannabis extract - dronabinol) should be given to patients with anorexia, when none of the causes of their disease are found out, or to patients on the slope of life when anorexia worsens the quality of their life. Anabolic steroids have some positive effects (for example, an increase in muscle mass, possibly functional improvement) in patients with cachexia due to renal insufficiency and, possibly, in elderly patients.

Principles of correction of protein-energy deficiency in adults in general are similar to those in children. For most adults, feeding should not be delayed; recommended small amounts of food with frequent intake. It is possible to use commercial milk formula for oral feeding. Nutrients are given at the rate of 60 kcal / kg and 1.2-2 g protein / kg. If liquid oral supplements are used with solid foods, they should be taken at least 1 hour before it is taken so that the amount of solid food eaten does not decrease.

Treatment of patients with protein-energy deficiency placed in a nursing home requires a variety of conditions, including changes in the environment (for example, making the dining area more attractive); assistance in feeding; changes in diet (for example, increased nutrition and high-calorie supplements between meals); treatment of depression and other underlying disorders; use of appetite stimulants, anabolic steroids or a combination thereof. For patients with severe dysphagia, prolonged use of gastrostomy for feeding is indispensable; although its use in patients with dementia is debatable. A tangible benefit is caused by the rejection of tasteless diets (for example, low-salt, diabetic, low-cholesterol), since these diets reduce food intake and can cause severe protein-energy deficiency.

Complications of treatment of protein-energy deficiency

Treatment of protein-energy deficiency can cause complications (re-feeding syndrome), including fluid overload, electrolyte deficiencies, hyperglycemia, cardiac arrhythmias and diarrhea. Diarrhea is usually mild and passes alone; However, diarrhea in patients with severe PEN sometimes causes severe dehydration or death. Such causes of diarrhea, such as sorbitol, used for feeding through a probe, or Clostridium difficile, if a patient is receiving antibiotic therapy, can be eliminated by special interventions. Osmotic diarrhea due to the consumption of excess calories is rarely observed in adults and can be considered as a cause only when other causes of protein-energy insufficiency have been ruled out.

Since protein-energy deficiency can worsen cardiac and renal functions, hydration can cause an increase in the intravascular volume of the fluid. Treatment reduces the concentration of extracellular K and Mg. Reducing K or Mg may cause arrhythmias. The activation of carbohydrate metabolism during treatment stimulates the release of insulin, which leads to the entry of phosphate into the cells. Hypophosphatemia can cause muscle weakness, paresthesia, paralysis, arrhythmias, coma. The levels of phosphate in the blood with parenteral nutrition should be regularly measured.

In the process of treatment, endogenous insulin can become ineffective, which leads to hyperglycemia. A consequence of this can be dehydration and hyperosmolarity. Fatal ventricular arrhythmias may develop, which is characterized by an increase in the QT interval .

[12], [13]

Prognosis of protein-energy deficiency

In children, lethality varies from 5 to 40%. Mortality rates are lower in children with mild protein-energy deficiency and in those who have undergone intensive therapy. Death in the first days of treatment is usually due to a deficiency of electrolytes, sepsis, hypothermia, or heart failure. Disturbance of consciousness, jaundice, petechiae, hyponatremia and persistent diarrhea are sinister prognostic symptoms. Cessation of apathy, edema and anorexia are favorable symptoms. A faster recovery is noted with a kwashiorkor than with marasmus.

To date, it has not been fully established, to which the long-term protein-energy deficiency in children leads. Some children develop chronic malabsorption syndrome and pancreatic insufficiency. Young children may develop moderate oligophrenia, which can persist until school age. Constant cognitive disorders, depending on the duration, severity and age, in which protein-energy deficiency has begun, can be observed.

In adults, protein-energy deficiency can lead to a complicated course and lethality (for example, progressive weight loss increases the mortality by 10% in elderly people in nursing homes). In addition to cases when the deficiency of organs or systems develops, the treatment of protein-energy deficiency is almost always successful. In elderly patients, protein-energy deficiency increases the risk of complications and lethality in surgical interventions, infections or other disorders.