Showing posts with label children. Show all posts
Showing posts with label children. Show all posts

Protein energy malnutrition in children

March 2013
Home > Nutritional deficiency diseases > Protein energy malnutrition in children
What is protein energy malnutrition?
Also known as protein-calorie malnutrition, this type of malnutrition results from the acute insufficiency of both dietary energy and proteins.
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Considering the time and origin its cause can be primarily due to lack of amino acids and energy nutrients in the diet or secondarily due to debilitating health conditions. In children losing up to 10% of body weight is considered as mild, whereas losing 10-20% is moderate and above 20% is severe malnutrition.

Causes of protein energy malnutrition in children

The primary malnutrition develops in children when their intake of proteins and energy sources is grossly insufficient to support their metabolic needs. This type of malnutrition is seen mostly in developing countries and also in regions ravaged by wars, famines and natural calamities.

The secondary type of malnutrition in children is prevalent even in developed countries. It is usually concurrent with major health problems like AIDS, chronic diarrhea, cancer, chronic kidney failure, chronic obstructive pulmonary disease (COPD), liver cirrhosis, Crohn disease and ulcerative colitis. In these debilitating illnesses, the body's ability to digest, absorb or use the nutrients is impaired. Severe malnutrition may occur in persons on long-term hemodialysis and in those affected by acute illness, severe burns, trauma, or sepsis.

When malnutrition syndrome reaches an advanced disease stage, depending upon the type of deficiency, it is variously named as Kwashiorkor or marasmus.

Kwashiorkor

Kwashiorkor
1.protein-energy malnutrition
Kwashiorkor affected child
This is an advanced disease stage of malnutrition wherein there is acute protein deficiency. Symptoms of kwashiorkor include, protruding belly, liver enlargement and ascites, edema, dry and peeling skin, changes in skin pigment, loss of muscle mass, diarrhea, anemia, change in hair color and texture, apathy, irritability, dermatitis and severe infections. Delay in treatment can lead to permanent mental and physical disability, coma, shock and death. This condition is seen in children feeding on highly amino acid deficit diet after stoppage of breast feeding.

Marasmus

Unlike kwashiorkor, in marasmus there is severe protein and also calorie/energy deficiency. There is no edema. Marasmus is characterized by wasted muscles and tissues. Marasmus may appear in children who have very little to eat after stoppage of breast feeding. The symptoms include profound weakness, emaciation, baggy, wrinkled skin, lack of energy, extremely thin arms and legs, weakened immune system, low body temperature and mental and behavioral retardation.
marasmus
2.protein-energy malnutrition
marasmus affected child
In children with marasmus if severe infections and complications occur, edema may be caused and the malnutrition syndrome is now termed as marasmic kwashiorkor.

Like children, elderly people are also dependent on others for getting the right type of nutrition and in addition their digestive and absorptive capacities are reduced. Like children, they are also at the high risk of developing the secondary malnutrition.

Diagnosis

Malnutrition can be recognized by correlating the symptoms with the visual observation and physical examination of body fat, eating habits, appetite, weight loss, edema and muscle strength. The history of general illnesses, diarrhea and gastrointestinal ailments can give an idea on the patients nutritional status. Blood and urine analysis will further help in the diagnosis.

Treatment

Immediate step in the treatment of malnutrition is correcting fluid and electrolyte imbalances. Antibiotics are given for treating infections. Gradually essential nutrients are replenished, first the carbohydrates and then the amino acids and micronutrients. Physiotherapy is given to make the patient gain the muscle strength. Once the affected children are free from complications energy dense dietary formulas are used to restore normal weight for the height. If the treatment is delayed, protein energy malnutrition can leave lasting effects on physical and mental health of children and they may not reach their full growth potential.
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Related topics:
Carbohydrate Deficiency Diseases.
Protein deficiency diseases.
Protein-energy malnutrition (PEM).
Vitamin deficiency diseases.
Fat deficiency diseases.
Mineral deficiency diseases.
Image 1 source: http://phil.cdc.gov/
Content Providers: CDC/ Dr. Lyle Conrad
License: Public domain
Image 2 source: http://phil.cdc.gov/
Content Providers: CDC/ Don Eddins
License: Public domain

Reference: Alderman H, Shekar M. Nutrition, food security, and health.In: Kliegman RM,Behrman RE, Jenson HB, Stanton BF, eds.Nelson Textbook of Pediatrics.19th ed. Philadelphia, Pa: Saunders Elsevier; 2011:chap 43.
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Rachitis disease in children

› › Rachitis disease in children

Rachitis is the disorder of the bones in children leading to their weakening and softening due to deficiency of vitamin D and then calcium.

Rickets is believed to be the distortion of the word 'wrickken'(meaning 'twist') used in the old English dialect. The scientific name 'rachitis' is derived from Greek meaning 'inflammation of the spine'.
It is caused primarily due to deficiency of vitamin D (Cholecalciferol) and also calcium and phosphate.
Although the deficiency of vitamin D may occur in adults it is called osteomalacia. Mostly, the incidence of this disease is found in malnourished children with deficiency in sun exposure.
Calcium is an essential mineral for the formation of bones and its absorption in intestine is dependent upon the availability of vitamin D in the system.
With sufficient sun exposure all the required vitamin D can be synthesized by the skin.
In youngsters with poor exposure to sunlight, the synthesis of this nutrient is affected causing rachitis.
This in turn affects the absorption of calcium in the intestines and rachitis disease is caused.
Moreover Cholecalciferol controls the levels of like and phosphorus in the blood.
Deformities in the skeleton like pigeon chest, bowed legs and spinal and pelvic deformities are some of the signs of rachitis.
Breast-fed infants who are not exposed to sufficient sun light may develop the condition.
Infants of mothers who are not exposed to sunlight can also develop the disease.
Children who are lactose intolerant and are with darker skin are also predisposed to develop rachitis.
rachitis disease rickets children
Children are affected by rachitis (enlarge)(courtesy: Dr. Tom and Rosie Thacher)

Children in the age group of six months to two years are among the high risk groups for this disease as their bone growth is at a faster rate.
Vitamin D supplements are advised for breastfed infants above 2 months.
Any deficiency at this age and negligence can cause bowed legs and bent backs leading to permanent disability and affliction of rachitis.
Some of the symptoms are pain and tenderness in the bones, muscular pains and predisposition for bone fractures; dental deformities like delay in the formation of teeth and defects in their structure is also seen in rachitis affected.
Distorted skull formation and retarded growth are the other effects of the disease.
Blood tests of the affected children show low levels of serum calcium and serum phosphorus rachitis affected.
This deficiency of vitamin D caused rachitis can be corrected completely, if diagnosed early and treated.
Exposure to sun light, intake of food rich in all essential nutrients and minerals and intake of supplements when required can cure rachitis.
Sufficient intake of milk, milk products, vegetables, fish,egg and fish liver oils in addition to sunlight can prevent the disease in children.
Renal disorders and hereditary factors can also become the causative factors of rachitis disease in children.

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Vitamin D deficiency causes rickets in children

Home > Vitamin D deficiency causes rickets

Deficiency of vitamin D or/and calcium and phosphorus are the causes of the nutritional disorders and rickets disease in children.

A number of factors including lack of sunlight exposure and nutritional vitamin D deficiency cause rickets. Certain metabolic disorders, digestive disorders and genetic factors can also lead to rickets.

Lack of sufficient exposure to sunlight (ultraviolet B light) causes rickets

Most of the vertebrate animals including man produce vitamin D in their skin photochemically, with the exception of cats, dogs and a few other animals.
The ultraviolet B light (UVB) from the sun reacts with 7-dehydrocholesterol in the stratum basale and stratum spinosum of the epidermis layer (upper layer of skin) and by a chemical process cholecalciferol is synthesized.
The melanin pigment deposits in the skin function as UVB filter and the dark-skinned people have to be exposed to, more sunlight than the light colored people to produce the same quantity of cholecalciferol.
Children and people who always live and work indoors and are rarely exposed to sunlight are high risk group for developing deficiency of vitamin D.
The intensity of sunlight decreases with higher latitudes and in children living there deficiency of cholecalciferol arises in winter especially if they are dark skinned.

Nutritional deficiency of calcium and phosphorus causes rickets

Calcium and phosphorus are very important for the formation and growth of bone tissue and bones. Any insufficiency of these minerals lead to bone deformities and rickets disease.

Maternal deficiency of cholecalciferol, calcium and phosphorus causes rickets in the newborns

The deficiency in pregnant women reduces the availability of these to the fetus.
Bone formation in the fetus may be affected and the density of the bones is reduced and results low birth weight.
Further if the shortfall is not cured by supplements, birth deformities occur in the newborn children.
Nursing mother's nutritional deficiency causes rickets disease in the infant.
The human milk has just sufficient quantities of cholecalciferol in a healthy woman.
If the lactating mother is not having sufficient reserves of it and is poorly nourished having little exposure to sunlight, the milk becomes poor in this nutrient.

Lactose intolerance and food habits causes rickets disease

Milk and milk products which are rich in calcium are not tolerated by some people and they have problem digesting them.
Unless they eat other sources of calcium they develop vitamin D deficiency.
Vegans who do not include milk and milk products are among the high risk groups to get vitamin D deficiency.

Malabsorption of fats from intestine causes rickets disease

Vitamin D is fat-soluble and requires dietary fat in the intestine for absorption.
In various conditions and ailments like Crohn's disease, cystic fibrosis and in certain liver disorders fat and vitamin D absorption from the intestine is affected and results in its deficiency.

Certain medication causes rickets disease

Phenobarbital and phenytoin are used for preventing and controlling epileptic seizures.
These drugs convert vitamin D into inactive compounds by increasing the hepatic metabolism. This leads to reduction in calcium absorption. Orlistat (weight-loss drug) and cholestyramine (cholesterol-lowering drug) reduces absorption of fat soluble vitamin D.
Corticosteroids like prednisone can affect cholecalciferol metabolism and decrease calcium absorption and result in rickets.

Hereditary predisposition for rickets disease

Vitamin D resistant rickets is hereditary. Here the rickets disease is inherited as a sex-linked genetic disorder. In this condition kidney is impaired from retaining phosphate.
Excessive use of sunscreen and spending more time in-doors causes this ailment.
Understanding the causes and proper preventive measures and treatment can resolve rickets disease.

Related topics:
Rickets disease overview
Symptoms
Diagnosis
Treatment
Prevention
Osteomalacia (in adults)
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Rickets signs and symptoms in children

Home > Rickets - Symptoms - Signs
The most important rickets symptoms and signs are bone deformity and pain in the bone
A number of skeletal, muscular and dental symptoms are observed in children in this disease.

Early rickets symptoms and signs

The initial symptoms are poor sleep, restlessness, profuse sweating in the head even in winter.
Then digestive disorders like unnaturally high appetite, stomach upsets, diarrhea and bloated abdomen can be seen as further rickets signs.
The patient's feeling of weakness, dullness, loss of weight, getting easily tired, and complains of pain in the bones, joints and muscles are tell-tale rickets symptoms.

Further signs of rickets

The bodies of the affected children become flabby and their muscles becoming flabby and weak. These children have unhealthy skin, sometimes with offensive smell, which can get infected easily causing secondary problems.
The rickets affected may suffer from tetany (uncontrolled muscle spasm) and seizures. Low levels of serum calcium causes tetany.
The ends of the ribs get enlarged and resemble beads (rachitic beads) which are visible and felt at the junction with sternum.
The affected children show symptoms of Harrison grove, a horizontal line seen at the margin of the thorax where the ribs are attached to diaphragm. The pulling of the sternum gives rise to pigeon-chest deformity.
Mild to predominant Scoliosis (curving from side to side) of spine is seen in affected children. The softening of the vertebrae leads to kyphosis (hunchback).
scoliosis
Scoliosis of spine
The weight bearing long bones in the legs get bent and bow-legs or knock-knees occur as signs of the disease in affected children. The bend may cause fracture on one side and this is called greenstick fracture.
In the rickets affected thickening of skull occurs producing frontal bossing and delaying the anterior fontanelle closure giving square forehead look; typical rickets signs.
Radiography shows symptoms like flaring and cupping of the metaphyses of the long bones in the affected children.
These affected persons lose their weight and show increase in vascularity. This hyperemia (increase in blood flow) affects all bones, cartilages, morrow, resulting in irregular and retarded growth of bones and cartilage cell proliferation.
In young affected children the teeth may erupt very late. They may have irregular shape and the enamel may be defective and caries and cavities may occur; another of typical rickets signs.
The rickets affected may show delay in crawling, sitting up and walking. In severe cases there may be respiratory failure in children.
Observing these signs, diagnosis of rickets can be done by visual observations, blood test, urine test and x-ray. If detected early all rickets symptoms can be resolved completely.

Related topics:
Rickets
Causes
Diagnosis
Treatment
Prevention
Osteomalacia (in adults)

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Signs and symptoms of rickets in children
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Rickets diagnosis - vitamin D deficiency - children

Home > Diagnosis of rickets - Vitamin D deficiency in children

Visual observations supported by analytical, radiographic and differential methods confirm the diagnosis of rickets and deficiency of vitamin D in children.
Diagnosis of rickets by visual observations
Sleep pattern of the patient is observed. Affected children sleep poorly and are restless in the night. Their constant movements in the bed, may even cause the hair on their head to wear off. This is a clear sign of vitamin D deficiency and on set of rickets. There is every possibility of wrong interpretation of this sign of rickets as psychosis.
The growth pattern of the children are observed. The growth in the affected is slow and often retarded.
The affected persons will be slow in sitting up, crawling and walking.
The bones of the affected children may bend due to weight of the body and the joints may deform giving deformities like bowed leg and pigeon-breast; a clear diagnosis of vitamin D deficiency.
The muscles of the affected children will be weak and the patients will have pain and distress while moving.
Due to leaching of phosphorus and calcium the bone will be weakened and there can be a history of fractured bones indicating the deficiency of vitamin D.
The broadening and thickening of wrists and ankles is a clear sign of vitamin D deficiency.
The patients show frontal bossing and the forehead becomes prominent and square.
During dental examination, the affected children show delay in emergence of teeth, abnormal tooth structure and cavities.
Diagnosis of rickets by laboratory studies
Serum test and measurements of phosphorus, calcium, parathyroid hormone and alkaline phosphatase are taken for diagnosis of rickets.
In early disease the ionised fraction of calcium will be low, but may be within the reference range.
Serum phosphate will be lower than the reference range.
Parathyroid hormone will show increased values.
Serum calcidiol will show decreased values.
Serum alkaline phosphatase will be more than the reference values.
Levels of serum citrates will be less than 2.5 mg/dl.
Urine calcium will show decrease in levels.
Urine phosphates will show increase in levels.
Diagnosis of rickets by radiography
Radiographic study of long bones, ankles, wrist and knees is made.
In rickets affected children who are able to walk, the defective bone growth give a clear image of bent limbs.
Typical appearance of growth plates with lack of normalcy in mineralisation of the cartilages is seen.
Fraying (irregularity and widening) of the growth plate is seen in radiography.
The metaphysis show concavity (cupping) and the metaphyseal end of bone shows splaying (widening).
Differential diagnosis
Excluding the related signs help. Severe deficiency of calcium and phosphorus can show the symptoms.
Diagnosis to be done to exclude Hypophosphatasia, a rare metabolic bone disease, with confusing symptoms similar to rickets.
A form of short limbed dwarfism, Jansen syndrome may also show metaphyseal chondroplasia.
Hereditary vitamin D -resistant rickets has to be differentiated.

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