Marasmus kwashiorkor

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Marasmus kwashiorkor

  1. 1. MALNUTRITION (PEM) Marasmus/ Kwashiorkor Najah Kh. Qasem Qassim University1
  2. 2. OBJECTIVES Define the definition of malnutrition,kwashiorkor, and marasmus. Discuss pathphysiology of Kwashiorkor. List etiology factors for kwashiorkor, and marasmus. Explain assessment findings, laboratory findings in kwashiorkor, and marasmus. Identify the complications of PEM. Identify treatment steps for PEM. Formulate nursing care plan for malnourished infants.2
  3. 3. OVERVIEW OF PEM The term protein - energy malnutrition has been adopted by WHO in 1976. WHO defines malnutrition as "the cellular imbalance between the supply of nutrients and energy and the bodys demand for them to ensure growth, maintenance, and specific functions.3
  4. 4. OVERVIEW OF PEM " The term protein-energy malnutrition (PEM) applies to a group of related disorders. that include marasmus, kwashiorkor, and intermediate states of marasmus- kwashiorkor. • occurring most frequently in infants and young children and commonly4 associated with infection
  5. 5. OVERVIEW OF PEM  Although several factors may contribute to the production of PEM, the basic problem is usually a lack of food intake. Sometimes, there may be poor absorption of one or more of food components. Other time, the cause is lack of parental education regarding infants and childrens nutrition5
  6. 6. Mortality / Morbidity  In 2000 WHO estimated that 32% of <5 years old children in developing countries are underweight (182 million).  Around 150 million children younger than 5 years are malnourished when measured in terms of weight for age.  The reciprocal interaction between PEM & infection is the major cause of death & morbidity in young children.6
  7. 7. Cont..  In south central Asia and eastern Africa, about half the children have growth retardation due to protein-energy malnutrition. This figure is 5 times the prevalence in the western world.  Approximately 50% of the 10 million deaths each year in developing countries occur because of malnutrition in children < than 5 years.7
  8. 8. 8
  9. 9. Kwashiorkor - Definition It is an acute form of childhood protein-energy malnutrition characterized by inadequate protein intake with reasonable caloric (energy) intake; it tends to occur after weaning, when children change from breast milk to a diet consisting mainly of carbohydrates. Studies suggest that kwashiorkor represents a maladaptive response to starvation9
  10. 10. Cont..  characterized by edema, irritability, anorexia, ulcerating dermatoses, and an enlarged liver with fatty infiltrates.  The presence of edema caused by poor nutrition defines kwashiorkor  The term Kwashiorkor is taken from the Ga language of Ghana & means “the sickness of the weaning” .10
  11. 11. Pathophysiology_ Kwashiorkor.  Decreased protein intake decreased synthesis of visceral proteins.  Decreased visceral protein hypo- albuminemia contributes to extravascular fluid accumulation.  Impaired synthesis of B-lipoprotein produced a fatty liver.11
  12. 12. Etiology:  Dietary Inadequacy: occurs when there is a rapid period of transition from the balanced diet supplied by the breast milk to an unbalanced inadequate diet, which is very low in protein, and consists mainly of carbohydrates due to socio - economic status such as:12
  13. 13. Cont..  Poverty  Ignorance  Inadequate weaning practice  Lack of basic health education and nutritional knowledge.  Child abuse13
  14. 14. Precipitating Factor: i) Acute infections like acute infantile diarrhea and measles due to:  Catabolic effect of the infections.  Anorexia, which usually accompanies infections.  The bad habit of withholding food during measles and diarrhea up to the degree of starvation. ii) Malaria and severe parasitic infestations may play a role in the development of kwashiorkor in some region of the world.14
  15. 15. Cont.. iii) Studies suggest that aflatoxin poisoning is an important factor in the development of kwashiorkor.  Aflatoxins are produced by molds and ingested with moldy foods.  Aflatoxins damage liver DNA.15
  16. 16. Assessment (signs & symptoms) The clinical assessment of kwashiorkor is divided into 3 groups:  Constant manifestation.  Usual manifestations.  Occasional manifestations16
  17. 17. Clinical Manifistation  Clinical manifistation is affected by: • The degree of deficiency • The duration of deficiency • The speed of onset • The age at onset • Presence of conditioning factors • Genetic factors17
  18. 18. Constant Manifestations 1. Growth retardation: this is reflected by:  Weight is markedly diminished.  Retarded linear growth (length).  Head circumference may also be affected.  Bone age may be retarded.18
  19. 19. Constant Manifestations 2. Edema:  The main factor is hypoproteinemia. It starts in the feet and lower parts of the legs then becomes-generalized. It is usually soft and pitting, affecting more the dependent parts (back and dorsum of hands and feet). The cheeks become bulky, pale and waxy in appearance (doll-like cheecks). Ascites is unusual.19
  20. 20. Constant Manifestations 3. Disturbed muscle/ fat ratio (Muscle wasting) There is a generalized muscle wasting with preservation of some subcutaneous fat. This can be demonstrated clinically by measuring the mid-arm circumference which is diminished in these cases. The children are often weak, hypotonic and unable to stand and walk.20
  21. 21. Constant Manifestations 4. Psychomotor changes: Infants with kwashiorkor have marked apathy; misery and they lack interest in the surrounding. They dont move, look sad and never smile. Their cry is weak.21
  22. 22. Usual Manifestations 1 Hair Changes;  Hair is a spates, especially over the temples and occipital regions.  There is depigmetation of hair. The hair loses its black color and becomes reddish or grayish. Deficiency of pantothenic acid and sulfur containing amino- acids in the hair or a defect in the melanin formation may be responsible for such depigmentation.22
  23. 23. Usual Manifestations  Hair is also atrophic, having lost its curl and tapered nearer to the scalp (like an exclamation mark). 2- Gastro-intestinal Manifestations:  Anorexia sometimes associated with vomiting, especially in severe cases.23
  24. 24. Usual Manifestations  Diarrhea is common and can be due to: - infection with intestinal pathogens or parasites. - Reduction of intestinal and pancreatic enzymes (e.g., amylase, lipase) as a result of protein deficiency. This will lead to inadequate digestion of food and passage of loose stools as a consequence. - Malabsorption of nitrogen, fat, carbohydrates and minerals due to the atrophy of villi.24
  25. 25. Occasional Manifestations 1.Skin Changes: Dermatosis:  The rash appears mainly in areas of increased pigmentation. These pigmented areas subsequently desquamate leaving atrophic, hypopigmented and easily damage skin or even ulcerations.25
  26. 26. Occasional Manifestations 1.Skin Changes:  The characteristic rash is usually seen on the back of thighs and axillae; though other parts of the body may be affected. * Sometimes petechiae may be present, particularly over the abdomen.26
  27. 27. Occasional Manifestations 2. Hepatomegly:  It is caused by fatty infiltration of the liver, which is a constant pathological finding in kwashiorkor that may or may not be accompanied by hepatomegty.27
  28. 28. Occasional Manifestations 3. Anemia: due to:  Deficiency of protein, iron, zinc, copper, folic acid and vitamins A, B, E and or C.  Infections may be responsible by disturbing the iron metabolism. 4. Poor resistance and liability to infections.28
  29. 29. Occasional Manifestations 5. Associated deficiencies of several types of nutrients (Riboflavin, Niacin, Thiamin, Vitamin D and C deficiencies) and minerals as iron, copper, zinc, and magnesium, particularly those involved with anti-oxidant protection (glutathione, albumin, vitamin E, and polyunsaturated fatty acids)29
  30. 30. Laboratory Findings: 1.Reduced total plasma protein (less than 4 gm/dl). 2.Reduced level of serum albumin (less than 2 gm/dl). 3. Urea in blood and urine is markedly reduced because of deficient intake of exogenous protein.30
  31. 31. Laboratory Findings: 4. Total body sodium is higher than normal. Serum sodium may be low due to the excessive amount of water extracellular fluid compartment. 5. Low total body potassium due to potassium losses by diarrhea31
  32. 32. Marasmus - Definition Marasmus is a form of severe PEM occur as result from a negative energy balance that may occur at any age, particularly in early infancy and is characterized by:  Severe wasting (body weight is less than 60% of the expected), the body utilizes all fat stores before using muscles.  Loss of subcutaneous fat.  Gross muscle wasting.  Absence of edema. “marasmus” comes from Greek origin of word “to waste”32
  33. 33. Cont..  Studies suggest that Marasmus represents an adaptive response to starvation  Children adapt to an energy deficiency with: 1- a decrease in physical activity. 2- lethargy. 3- a decrease in basal energy metabolism. 4- slowing of growth. 5- finally, weight loss.33
  34. 34. Etiology: The specific cause may be: 1. Poor feeding habits due to improper training. lack of breast feeding and the use of dilute animal milk. 2. A physical defect e.g. cleft lip or cleft palate or cardiac abnormalities, which prevent the34 infant from taking an adequate diet.
  35. 35. Etiology: 3. Diseases, which interfere with the assimilation of food e.g. cystic fibrosis. 4. Infections, which produce anorexia. 5. Loss of food through vomiting and diarrhea. 6. Emotional problems e.g. disturbed mother- child relationship.35
  36. 36. Assessment (S&S)  Beside the history taking, emphasizing the actual foods taken by the child, the presence of any of the following manifestations should be assessed:36
  37. 37. Assessment (S&S) 1. Growth retardation:  Weight is less than 60% of expected for age and sex.  Length, head, chest, and abdominal circumferences are also affected but to a lesser extent than weight.37
  38. 38. Assessment (S&S) 2. Loss of Subcutaneous Fat from:  The abdominal wall leading to loss of skin elasticity  The limbs (thighs and buttocks): the skin becomes wrinkled and hanging into longitudinal folds.  The buccinators pad of fat is the last to disappear. This leads to hollowing these cheeks, which leads to triangle face and an appearance resembling the38 old man.
  39. 39. Assessment (S&S) 3. Marked Wasting of Muscles: This together with the loss of subcutaneous fat lead to  Scaphoid abdomen with marked thinning of abdominal wall.  Stick -like appearance of limbs.39
  40. 40. Assessment (S&S) 4. Psychic Changes:  Marasmic infants look anxious, irritable, excessively cry and sleep little. However, they look less miserable than the cases of kwashiorkor.  Marasmic infants are usually hungry and have good appetite. Sometimes, there is anorexia and poor feeding.40
  41. 41. Assessment (S&S) 5. Chronic diarrhea with or without vomiting. 6. Intercurrent infections: Like otitis media, bronchopneumonia, urinary tract infections. 7. Associated deficiencies of iron, vitamin A and D. 8. Hypothermia due to loss of subcutaneous fat.41
  42. 42. Characteristically cases of Marasmus  No edema.  No dermatosis.  No hair changes.  No fatty infiltration of the liver (hepatomegly).42
  43. 43. Laboratory Findings: 1. Plasma protein may be normal or slightly lowered. This is because marasmic infants live on their own muscle protein. 2. Blood urea is low since the protein utilized by the infant is totally endogenous protein. 3. Blood glucose level is low due to deficient glycogen stores in the liver,43
  44. 44. Complications of PEM: 1. Diarrhea, dehydration, electrolyte and acid base disturbances. 2. Infections, such as, bronchopneumonia, T.B, urinary tract infection. 3. Hypoglycemia. 4. Hypothermia. 5. Early prolonged malnutrition may lead to mental retardation.44
  45. 45. The WHO’s Ten Steps to Recovery in Malnourished Children45
  46. 46. Nursing Care Plan: (PEM Infants) 1. Nursing diagnosis:  Altered nutrition: less than body requirements related to knowledge deficit, physical defect, infection, disease interferes with the assimilation of food or emotional problems. Goal:  The patient will gain weight.46
  47. 47. Nursing Care Plan: (PEM Infants) Intervention:  Give high quality protein and adequate carbohydrates in form of milk formula (first skimmed milk then later whole milk). Give the infant breast feeding if still on breast.  Start with liquid food, then semi-solid other chewable food as eggs, beans and meat.47
  48. 48. Nursing Care Plan: (PEM Infants) Intervention:  Feed the infant orally, either by breast, bottle or spoon. If it is impossible feed him through nasogastric tube (gavage feeding).  Give feeding slowly as the child is irritable.  Introduce a positive feeding environment. Avoid interruption of feeding with other activities, such as, laboratory tests or48 radiography.
  49. 49. Nursing Care Plan: (PEM Infants) Intervention:  Weight daily and record to ascertain weight gain. Expected Outcome:  Infant exhibits weight gain appropriate to his age.49
  50. 50. Nursing Care Plan: (PEM Infants) 2. Nursing diagnosis: Body temperature alteration (hypothermia) related to diminished food intake. Goal: The infant will maintain suitable body temperature.50
  51. 51. Nursing Care Plan: (PEM Infants) Intervention:  Place the infant in a warm humidified incubator, radiant warmer or warmly clothed in open crib.  Use hot water bottles.  Dress infant with extra- clothes.  Monitor temperature hourly in unstable infants.51
  52. 52. Nursing Care Plan: (PEM Infants) Intervention:  Avoid situations that might predispose infant to heat loss, such as, exposure to cool drafts, bathing or cold scales.  Check infants temperature in relation of the heating unit.  Observe for signs of collapse (temperature drop, coldness of extremities, slow pulse,52 cyanosis or gray white color of skin.)
  53. 53. Nursing Care Plan: (PEM Infants) Expected Outcome:  Infants axillary temperature remains within normal range (36.5- 37.2°C).53
  54. 54. Nursing Care Plan: (PEM Infants) 3. Nursing diagnosis: Skin integrity impaired related to deficiencies of vitamins intake. Goal: Infant will maintain skin integrity.54
  55. 55. Nursing Care Plan: (PEM Infants) Intervention:  Cleanse skin with clear water and apply oil if needed.  Care of buttocks if infant has diarrhea.  Frequent change of infants position to prevent skin ulcer. Expected Outcome:  Skin remains clean and intact with no55 evidence of irritation or injury.
  56. 56. Nursing Care Plan: (PEM Infants) 4. Nursing diagnosis: High risk for infection related to low body resistance. Goal: Infant will be protected from-infection, Intervention:  Feeding equipments must be sterile to avoid danger of contracting thrush. Infant should56 be kept out of draft.
  57. 57. 57

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