Severe Protein Calorie Malnutrition Icd 10 Caloric-protein malnutrition (DCP), formerly called protein-calorie malnutrition, is an energy deficiency caused by the deficiency of all macronutrients. It is usually accompanied by deficiencies of many micronutrients. DCP can be sudden and complete (starvation) or gradual.
The severity ranges from subclinical deficiencies to evident wasting (with edema, alopecia, and skin atrophy) and starvation. It frequently affects various organ systems. For diagnosis, laboratory tests are usually performed, including measurement of serum albumin. Treatment consists of correcting fluid and electrolyte deficits with IV solutions and then gradually replacing the nutrients with VO whenever possible.
In industrialized countries, FAD is common in institutionalized older adults (although sometimes not suspected) and in patients with disorders that decrease appetite or alter digestion, absorption, or metabolism. In developing countries, FAD affects children who do not consume enough calories or protein.
Caloric-protein malnutrition is classified as mild, moderate, or severe. The grade is determined by calculating weight as a percentage of the desired weight for height or height according to international criteria (normal, 90 to 110%; mild, 85 to 90%; moderate, 75 to 85%; severe, <75% ).
DCP can be
Primary: caused by inadequate nutrient intake
Secondary: the result of diseases or the use of drugs that interfere with the use of nutrients.
Throughout the world, FAD affects mainly children and older adults who do not have access to nutrients, although a frequent cause in this latter group is depression. DCP can also be the result of fasting or anorexia nervosa. Abuse can also be a cause in these age groups. In children, primary chronic DCP has two common forms: marasmus and kwashiorkor. How it occurs depends on the balance between non-protein and protein-energy sources. Starvation is an acute and severe form of primary DCP.
In children, chronic primary DCP has two common forms: marasmus and kwashiorkor.
The form depends on the balance of nonprotein and protein sources of energy. Starvation is an acute severe form of primary PEU.
Marasmus (also called the dry form of DCP) causes weight loss and depletion of fat and muscle mass. Marasmus is the most common cause of DCP in children in industrialized countries.
Kwashiorkor (also called the edematous or wet form of FAD) is a risk seen after early abandonment of breastfeeding, which usually occurs when a younger sibling is born who displaces the other from the breast. Children with kwashiorkor tend to be older than those affected by marasmus.
Kwashiorkor may also be the result of an acute illness, often gastroenteritis or other infection (probably in these cases secondary to cytokine release) in a child who already has DCP. A diet that is poorer in protein than in calories is more likely to cause kwashiorkor than marasmus. Kwashiorkor is less common than marasmus and tends to be limited to specific regions of the globe, such as rural Africa, the Caribbean, and the Pacific islands. In these areas, indigenous foods (eg, sweet potato, cassava, sweet potatoes, green bananas) are low in protein and rich in carbohydrates. In kwashiorkor, cell membranes allow fluids to leak, causing intravascular fluid and protein to be lost; consequently, peripheral edema appears.
In both marasmus and kwashiorkor, cell-mediated immunity is impaired, thereby increasing the predisposition to infection. Bacterial infections (eg, pneumonia, gastroenteritis, otitis media, urinary tract infections, and sepsis) are common. Infections cause cytokine release, which in turn leads to anorexia, worsen muscle loss, and causes a marked decrease in serum albumin levels.
Starvation is the total lack of nutrients. Sometimes it is voluntary (as in the case of fasting or anorexia nervosa), although it may be secondary to external factors (eg, during famines or exposure to nature).
Disorders that affect gastrointestinal function: These disorders may interfere with digestion (eg, pancreatic insufficiency), absorption (eg, enteritis and enteropathies), or lymphatic nutrient transport (eg, retroperitoneal fibrosis). and Milroy’s disease).
Consumptive disorders: in this type of disorder (eg AIDS, cancer, and COPD) and in kidney failure, catabolism causes an excess of cytokines, which in turn causes malnutrition by mechanisms such as anorexia and cachexia (loss of muscle mass and fat). End-stage heart failure can lead to cardiac cachexia, which is a severe form of malnutrition; mortality is particularly high. Factors contributing to cardiac cachexia are passive liver congestion (which causes anorexia), edema in the gastrointestinal tract (which affects absorption), and, in advanced disease, increased oxygen requirements due to anaerobic metabolism. Consumptive disorders can decrease appetite or alter nutrient metabolism.
Conditions that can increase metabolic demands: infections, hyperthyroidism, pheochromocytoma, and other endocrine disorders, burns, traumatisms, surgeries, and other critical diseases.
The initial metabolic response is a decrease in metabolic rate. To provide energy, the body first breaks down brown fat. However, later, when these tissues lose their reserves, the body can use protein for energy, leading to a negative nitrogen balance. The viscera and muscles are degraded, and weight is lost. This loss of organ weight is most marked in the liver and intestine, in the heart and kidneys, and least in the nervous system.
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Symptoms of moderate DCP can be general or affect specific organ systems. Apathy and irritability are common. The patient presents weakness and decreased ability to work. The cognitive state and sometimes consciousness are altered. A temporary deficiency of lactose and achlorhydria develops. Diarrhea is frequent and can be aggravated by a deficiency of intestinal disaccharidases, especially lactase. There is atrophy of the gonadal tissue. DCP can cause amenorrhea and loss of libido in men and women.
Fat and muscle loss is a common feature in all forms of DCP. In adult female volunteers who fasted for 30 to 40 days, weight loss was considerable (25% of initial weight). If starvation is longer, weight loss can be as high as 50% in adults and perhaps even more in children.
In adults, cachexia is most evident in areas where, under normal conditions, there are fatty deposits. The muscles shrink and the bones bulge. The skin becomes thin, dry, pale, cold, and loses elasticity. The hair is dry and falls out easily, so it is usually sparse. Wound healing is disturbed. In older adults, the risk of hip fracture and pressure ulcers increases.
In cases of acute or severe chronic DCP, the size of the heart and cardiac output decrease; the pulse slows down and lowers blood pressure. The respiratory rate and vital capacity are also reduced. There is a drop in body temperature, which sometimes leads to death. There may be edema, anemia, jaundice, and petechiae. Liver, kidney, or heart failure may occur.
In infants, marasmus causes hunger, weight loss, stunted growth, and loss of subcutaneous fat and muscle mass. The ribs and bones of the face become prominent. The skin is loose and hangs in folds.
Kwashiorkor is characterized by the presence of peripheral and periorbital edema due to a decrease in serum albumin. The abdomen protrudes from weak abdominal muscles, the intestine is distended, the liver is enlarged, and there is ascites. The skin is dry, fine, and wrinkled; there may be hyperpigmentation, and fissures are observed. Later, it can hypopigmented and become friable and atrophic. There may be skin involvement in different parts of the body at different times. The hair is fine, reddish-brown, or grayish in color. Scalp hair falls out very easily and becomes thin over time, although lashes can grow too long. Alternating malnutrition episodes with other properly nourished episodes can give hair a “striped flag” appearance. Affected children may be apathetic, but irritable if taken care of.
Absolute starvation is fatal in 8 to 12 weeks. Therefore, some of the symptoms of DCP do not have time to develop.
Diagnosis is usually based on anamnesis
To establish severity: body mass index (BMI), serum albumin, total lymphocyte count, CD4 + count, serum transferrin
To diagnose complications and consequences: complete blood count, electrolytes, blood urea nitrogen, blood glucose, blood glucose, magnesium, phosphatemia
Diagnosis of protein-calorie malnutrition can be based on anamnesis when dietary intake is markedly inadequate. It is necessary to identify the cause of this inappropriate diet, especially in children. In these and adolescents, the possibility of mistreatment and anorexia nervosa should be considered.
The physical examination may include determination of weight and height, an inspection of body fat distribution, and anthropometric measurements of lean body mass. The body mass index (BMI = weight [kg] / height [m] 2) is calculated to determine severity. The findings usually confirm the diagnosis.
Laboratory tests are necessary if the diet data does not clearly indicate inadequate caloric intake. Measurement of serum albumin, total lymphocyte count, CD4 + T lymphocyte count, transferrin, and response to skin antigens can help determine the severity of FAD (see Table Frequently Used Values to Measure the severity of protein-calorie malnutrition) or confirm the diagnosis in cases that raise doubts.
There are many other laboratory tests that can give abnormal results: decreased levels of some hormones, vitamins, lipids, cholesterol, prealbumin, insulin-like growth factor-1, fibronectin, and retinol-binding protein. It is possible to use the levels of urinary creatine and methylhistidine to calculate the degree of loss of muscle mass. Because protein catabolism slows, urine urea concentrations also increase. These data rarely modify the treatment.
Laboratory tests are necessary to identify the causes when secondary DCP is suspected. C-reactive protein or interleukin-2 receptor levels should be determined when the cause of malnutrition is unknown; These determinations allow establishing if there is an excess of cytokines. Thyroid function tests may also be done.
Abnormalities can be detected with other laboratory tests, which may require treatment. Serum levels of electrolytes, blood urea nitrogen, glucose, and perhaps calcium, magnesium, and phosphate levels should be measured. Blood glucose levels, electrolytes (especially potassium and sometimes sodium), and phosphate, calcium, and magnesium are usually low. Ureic nitrogen is usually low unless there is kidney failure. There may be metabolic acidosis. A complete blood count is requested, in which normocytic anemia (generally secondary to protein deficiency) or microcytic anemia (due to iron deficiency) can be detected.
Samples should be obtained for stool culture and to check for the presence of parasites and eggs if the diarrhea is severe or does not resolve with treatment. Sometimes urinalysis, urine culture, blood culture, tuberculin test, and chest x-ray are done to diagnose occult infections, as individuals with DCP may have a decreased response to infections.
In children, mortality varies between 5 and 40%. Mortality is lower in children with mild CPD and in those receiving intensive care. The cause of death during the first days of treatment is usually electrolyte deficiency, sepsis, hypothermia, or heart failure. Signs of poor prognosis are impaired consciousness, jaundice, petechiae, hyponatremia, and persistent diarrhea. The resolution of apathy, edema, and anorexia are favorable signs. Recovery is faster in cases of kwashiorkor than marasmus.
The long-term effects of DCP have not been verified in detail. Some children develop chronic malabsorption and pancreatic insufficiency. Very young children can develop mild intellectual disabilities, which can persist until at least school age. There may be permanent cognitive changes, depending on the duration, severity, and age of onset of FAD.
In adults, DCP can cause morbidity and mortality (eg, progressive weight loss increases mortality by 10% in older adults living in nursing homes). In older adults, DCP increases the risk of morbidity and mortality due to surgery, infections, or other disorders.
Except when organ failure occurs, treatment is almost always effective.
In general, enteral feeding
Avoiding lactose is likely to be helpful (eg, persistent diarrhea suggests lactose intolerance)
Supportive treatment (eg, environmental modifications, feeding assistance, orexigenic drugs)
In children, delay feeding for 24 to 48 hours
Globally, the most important prevention strategy is to reduce poverty and improve nutrition education and public health measures.
Mild to moderate calorie-protein malnutrition, including a short total fast, can be treated with a balanced diet, preferably orally. Oral liquid food supplements (generally lactose-free) may be used when solid foods are not well tolerated. Diarrhea often complicates oral feeding because starvation causes the digestive tract to move bacteria to Peyer’s patches, facilitating infectious diarrhea. If diarrhea persists (which suggests lactose intolerance), formulas based on yogurt (not milk) are indicated, because people with lactose intolerance can tolerate it. Patients should also receive multivitamin supplements.
Patients with severe DCP or prolonged starvation require hospital treatment and a controlled diet. The priority is to correct the hydro-electrolyte abnormalities and treat infections. A recent study suggests that children may benefit from antibiotic prophylaxis. The next priority is to administer macronutrients orally or, if necessary (eg, when there are swallowing disorders), using a feeding tube, a nasogastric tube (most commonly), or a gastrostomy tube (enteral nutrition ). Parenteral nutrition is indicated when malabsorption is severe.
Other treatments may be necessary to correct specific deficiencies, which become apparent as the patient gains weight. To avoid deficiencies, patients should ingest macronutrients at doses double the recommended daily requirements until complete recovery.
Underlying diseases must be treated.
In children with diarrhea, feeding is delayed 24 to 48 hours to avoid worsening diarrhea; During this interval, children require oral or IV rehydration. Meals are administered with some frequency (6 to 12 times / day), although to avoid saturating the limited intestinal absorption capacity, small amounts (<100 mL) are suggested. During the first week, milk formulas with supplements are usually administered in progressively greater amounts; after one week, the recommended amounts of 175 kcal / kg and 4 g of protein / kg can be administered. Twice the RDAs for micronutrients are indicated with commercial multivitamin supplements. After 4 weeks, the whole milk formula can be replaced with cod liver oil and solid foods, including eggs, fruit, meat, and yeast.
The distribution of energy provided by macronutrients should be 16% for proteins, 50% fats and 34% carbohydrates. An example is the combination of skimmed cow’s milk powder (110 g), sucrose (100 g), vegetable oil (70 g) and water (900 mL). Many other formulas can be used (eg, fresh whole milk with corn oil and maltodextrin). Powdered milks are prepared with water.
In general, these supplements should be administered along with the formulas:
0.4 mEq / kg / day magnesium is indicated by IM route, for 7 days.
Vitamin B complex is administered in a dose of twice the RDA, parenterally during the first 3 days, generally with vitamin A, phosphorus, zinc, manganese, copper, iodine, fluorine, molybdenum and selenium.
Because iron absorption is low in children with DCP, it may be necessary to take an iron supplement orally or IM.
Parents should be educated about nutritional requirements.
Underlying diseases must be treated. For example, if AIDS or cancer cause excess cytokine production, megestrol acetate or medroxyprogesterone may improve food intake. However, because these drugs markedly decrease testosterone in men (and may cause loss of muscle mass), testosterone must be replaced. These drugs can cause adrenal insufficiency, so they should be used only for short periods (<3 months).
In patients with functional limitations, the delivery of meals to the home and assistance in feeding are essential.
An orexygen drug such as dronabinol, an extract from cannabis, should be indicated in patients with anorexia when the cause is not detected or in terminally ill patients when anorexia affects their quality of life. Anabolic steroids (eg, testosterone enanthate, nandrolone) or growth hormone may benefit patients with cachexia from kidney failure and, perhaps, older adults (due to increased muscle mass or improvement in muscle mass). its function).
The correction of DCP in adults is usually similar to that of children; the food is offered in small quantities. However, in most adults, feeding should not be delayed. A commercial formula for oral feeding may be indicated. A nutritional supplement with 60 kcal/kg and 1.2 to 2 g of protein/kg is administered. If liquid supplements are administered orally together with solid foods, they should be done at least 1 hour before meals, so that the amount of food eaten at mealtime does not decrease.
The treatment of older adults with institutionalized FADs requires multiple interventions:
Environmental measures (eg, make the dining room more attractive)
Assistance with feeding
Diet modifications (eg, use of appetite stimulants and calorie supplements between meals)
Treatment of depression and other underlying illnesses
Use of orexigenic drugs, anabolic steroids or both
For patients with severe dysphagia, the use of a gastrostomy feeding tube is essential; its use in patients with dementia is controversial. More and more evidence supports avoiding non-palatable therapeutic diets (eg, with low salt and cholesterol content) in institutionalized patients because these reduce food intake and can cause severe DCP.
Treatment of DCP can cause complications (refeeding syndrome), including fluid overload, electrolyte deficiency, hyperglycemia, cardiac arrhythmias, and diarrhea. Diarrhea is usually mild and resolves; however, in patients with severe DCP it causes severe dehydration and can lead to death. The causes of diarrhea (eg, sorbitol used as an elixir in feeding tubes, Clostridium difficile if the patient received antibiotics) can be corrected. Osmotic diarrhea from excess calories is rare in adults and should be considered only when other causes have been excluded.
DCP can affect heart and kidney functions, so overhydration can cause intravascular volume overload. The treatment lowers extracellular potassium and magnesium levels. The depletion of potassium or magnesium can cause arrhythmias. The carbohydrate metabolism that occurs during treatment stimulates the release of insulin, which carries the phosphate into the cells. Hypophosphatemia can cause muscle weakness, paresthesias, seizures, coma, and arrhythmias. Phosphate levels can change rapidly during enteral feeding, so they must be determined regularly.
During treatment, endogenous insulin can become ineffective, and this leads to hyperglycemia. There may be dehydration and hyperosmolarity. Fatal ventricular arrhythmias can develop, possibly caused by a prolonged QT interval.