Chapter 5 Nutritional Assesment and Malnutrition.pptx

Chapter 5 Nutritional Assesment and Malnutrition.pptx

1. Dr Ready Mulugeta NUTRITIONAL ASSESMENT AND PROTEIN ENERGY MALNUTRITION

2. LEARNING OBJECTIVES By the end of this lecture the reader should be able to: To know the different methods for assessing the nutritional status To understand the basic anthropometric techniques, applications, & reference standards Etiology of PEM Pathophysiology of PEM Clinical feature of PEM Managements of PEM

3. HUMAN NUTRITION Nutrients are substances that are crucial for human life, growth & well-being. Macronutrients (carbohydrates, lipids, proteins & water) are needed for energy and cell multiplication & repair. Micronutrients are trace elements & vitamins, which are essential for metabolic processes.

4. HUMAN NUTRITION/2 Obesity & under-nutrition are the 2 ends of the spectrum of malnutrition. A healthy diet provides a balanced nutrients that satisfy the metabolic needs of the body without excess or shortage. Dietary requirements of children vary according to age, sex & development.

5. Assessing the nutritional status of an individual generally is referred to as nutritional assessment it includes: the evaluation of normal growth and health, evaluation for nutritional risk factors contributing to diseases, and the early detection and treatment of nutritional deficiencies and excesses

6. Assessment of Nutritional status “Nutritional Status expresses the degree to which physiologic needs for nutrients are met ” The purpose of nutritional assessment is to : Identify individuals or population groups at risk of becoming malnourished Identify individuals or population groups who are malnourished To develop health care programs that meet the community needs which are defined by the assessment To measure the effectiveness of the nutritional programs & intervention once initiated

7. Cont … Methods: Direct deal with the individual and measure objective criteria. it includes: ABCD Clinical assesment Anthropometric assesment Dietary evaluation methods Laboratory, biochemical, radiology Indirect use community health indices that reflects nutritional influences Health statistics Ecological variables

8. Nutritional Status “Nutritional Status expresses the degree to which physiologic needs for nutrients are met” Optimal NS = Balance between intake and requirement Malnutrition state caused by nutritional deficiency Reversible by providing appropriate nutrition support Deficiency vs Overload (can be combination of both) “whole person” focus, not just disease or condition focus.

9. Nutritional Risk Critically unwell patients may be well nourished but high nutritional risk Illness, injury, infection Metabolic derangements May have significant affect on nutritional status May lead to malnutrition Cannot be corrected by nutrition support alone Patients at high nutritional risk will require early nutritional intervention and close monitoring

10. Nutrition Screening Tools Requirements(it has to be) quick and simple to administer sensitive enough to identify individuals at risk appropriate for client group being screened capable of being used by non-dietitians reproducible when used by different observers able to guide non dietetic staff into taking appropriate action for findings recorded

11. Nutritional Assessment Tools No single / standard way of assessing nutritional status Various validated assessment tools developed some disease specific some age specific

12. Clinical Assessment Useful in severe forms of malnutrition Based on thorough physical examination for features of PEM & vitamin deficiencies. Focuses on skin, eye, hair, mouth & bones. Detection of relevant signs helps in establishing the nutritional diagnosis

13. Clinical signs of nutritional deficiency HAIR and mouth Protein, zinc, biotin deficiency Spare & thin Protein deficiency Easy to pull out Vit C & Vit A deficiency Corkscrew Coiled hair Riboflavin, niacin, folic acid, B12 , pr. Glossitis Vit . C,A, K, folic acid & niacin Bleeding & spongy gums B 2,6,& niacin Angular stomatitis, cheilosis & fissured tongue Vit.A,B12, B-complex, folic acid & niacin leukoplakia Vit B12,6,c, niacin ,folic acid & iron Sore mouth & tongue

14. Clinical signs of nutritional deficiency EYES Vitamin A deficiency Night blindness, exophthalmia Vit B2 & vit A deficiencies Photophobia-blurring, conjunctival inflammation NAILS Iron deficiency Spooning Protein deficiency Transverse lines Thyroid gland Enlarged ( goitor ) Iodine deficiency

15. Clinical Assessment ADVANTAGES Fast & Easy to perform Inexpensive Non-invasive LIMITATIONS Did not detect early cases Trained staff needed

16. ANTHROPOMETRY Objective with high specificity & sensitivity Measuring Ht , Wt , MAC, HC, skin fold thickness, waist & hip ratio & BMI It is an essential component of clinical examination of infants and children Reading are numerical & gradable on standard growth charts Non-expensive & need minimal training

17. ANTHROPOMETRY/2 ADVANTAGES Objective Readings are numerical & gradable on standard growth charts Readings are reproducible. Non-expensive & need minimal training LIMITATIONS Inter-observers’ errors in measurement Limited nutritional diagnosis Problems with reference standards Arbitrary statistical cut-off levels for abnormality

18. CLASSIFICATION DEFINITION GRADING CRITERIA Gomez Weight below % median WFA Mild (grade 1) 75%-90% WFA Moderate (grade 2) 60%-74% WFA Severe (grade 3) <60% WFA Waterlow z scores (SD) below median WFH Mild 80%-90% WFH Moderate 70%-80% WFH Severe <70% WFH WHO (wasting) z scores (SD) below median WFH Moderate −3 ≤ z score <−2 Severe z score <−3 WHO (stunting) z scores (SD) below median HFA Moderate −3 ≤ z score <−2 Severe z score <−3 Kanawati MUAC divided by occipitofrontal head circumference Mild <0.31 Moderate <0.28 Severe <0.25 Cole z scores of BMI for age Grade 1 z score <−1 Grade 2 z score <−2 Grade 3 z score <−3 Definition of malnutrition

19. LAB ASSESSMENT Biochemical Serum proteins, creatinine/ hydroxyproline Hematological CBC, iron, vitamin levels Microbiology Parasites/infection The laboratory evaluation of the child with or at risk for malnutrition is directed by the history and physical examination

20. Objective measures No single test is diagnostic Consider “normal / recommended range” for various and combination of conditions, eg. age, gender, physiological state, disease type and stage Consider clinical significance of test result Test result may reflect immediate intake (eg glucose) or long term status (HbA1c)

21. Identify nutritional deficiencies before clinical findings are evident ( eg , iron deficiency) Confirm the presence of nutrient deficiencies that commonly are associated with specific disease entities Monitor recovery from malnutrition that occurs as a complication of illness

22. Other factors to Consider… Other factors can mask/influence test results eg. Acute phase response due to stress / injury ( reduced albumin) GI bleed (higher urea) blood transfusion (higher serum K and Hb) Surgery (lower Hb and albumin)

23. Acute Phase Response Inflammatory processes (shock, trauma, sepsis) liver protein synthesis shifts from visceral proteins, e.g. albumin and prealbumin to acute phase proteins Visceral proteins may reflect ‘nutritional risk’ not nutritional status

24. Nutritional Indicators Ideal indicator or marker is sensitive and specific to nutritional intake Commonly Used “Nutritional Indicators” Albumin Pre-albumin Transferrin Retinol-binding protein

25. Albumin Synthesised in the liver May be useful indicator of nutritional status in “healthy” person. Not a good indicator of protein status during critical illness (due to acute phase response) Long half life (14-20 days) and large body pool  slow to respond to improvements in clinical status

26. Factors Affecting Serum Albumin Levels Increased in: Dehydration, blood transfusions, exogenous albumin Decreased in: Overhydration , hepatic failure, inflammation, infection, metabolic stress, post-op, bed rest, pregnancy, nephrotic syndrome.

27. Pre-albumin Also known as Transthyretin, thyroxine binding protein. Synthesised in the liver Relatively short half life (2 days) Negative acute phase reactant -  with inflammatory response May be useful in healthy population

28. Transferrin and RBP Transferrin Half life 8-10 days Poor correlation with nutrition status Involved with iron transport, influenced by iron status Retinol Binding Protein (RBP) Half life 12 hours Affected by renal function, Vitamin A and Zn status Unreliable measure of nutritional status

29. B iochemistry & other Blood Tests, cont’d (See also disease/condition specific lectures) Interference – drugs, sampling Nutrient-nutrient interactions, drug-nutrient interactions Be aware of hydration status Must interpret lab results with other nutritional parameters

30. Advantages of Biochemical Method It is useful in detecting early changes in body metabolism & nutrition before the appearance of overt clinical signs. It is precise, accurate and reproducible. Useful to validate data obtained from dietary methods e.g. comparing salt intake with 24-hour urinary excretion.

31. Limitations of Biochemical Method Time consuming Expensive They cannot be applied on large scale Needs trained personnel & facilities

32. DIETARY ASSESSMENT Includes: 24 hours dietary recall Food frequency questionnaire Dietary history since early life Food dairy technique Observed food consumption

33. 24 Hours Dietary Recall A trained interviewer asks the subject to recall all food & drink taken in the previous 24 hours. It is quick, easy, & depends on short-term memory, but may not be truly representative of the person’s usual intake

34. Food Frequency Questionnaire In this method the subject is given a list of around 100 food items to indicate his or her intake (frequency & quantity) perday , per week & per month . inexpensive, more representative & easy to use.

35. Food Frequency Questionnaire/2 Limitations: long Questionnaire Errors with estimating serving size. Needs updating with new commercial food products to keep pace with changing dietary habits.

36. DIETARY HISTORY It is an accurate method for assessing the nutritional status. The information should be collected by a trained interviewer. Details about usual intake, types, amount, frequency & timing needs to be obtained. Cross-checking to verify data is important.

37. FOOD DAIRY Food intake (types & amounts) should be recorded by the subject at the time of consumption. The length of the collection period range between 1-7 days. Reliable but difficult to maintain.

38. Observed Food Consumption The most unused method in clinical practice, but it is recommended for research purposes. The meal eaten by the individual is weighed and contents are exactly calculated. The method is characterized by having a high degree of accuracy but expensive & needs time & efforts.

39. Protein is 0.9 gm /100ml Is lower than in other animal Higher animal protein overload immature neonate with nitrogen waste It is whey protein which is easily digestible than casein of cows milk contain alpha lactoalbumin and cow milk contain beta lactaglobulin which can infant become intolerant Vitamin and minerals All are adequate except vitamin D IRON AND ZINC are low but high bioavailability and absorption

40. Protein Energy Malnutrition 45 Introduction PEM results when the body’s need for protein, energy or both cannot be satisfied by diet Dietary energy & protein deficiencies usually occur together, but one may predominate Kwashiorkor Marasmus Marasmic kwashiorkor – chronic energy deficiency & chronic or acute protein deficit

41. ETIOLOGY: 46 Primary Results from inadequate food intake Secondary Results from other diseases that lead to: Low food ingestion Inadequate nutrient absorption or utilization Increased nutritional requirements &/or Increased nutrient losses

42. Etiology 47 Is multi-factorial 1. Social & economic factors Poverty Migrations – rural to urban Ignorance – by itself or associated with poverty Lack of awareness Suboptimal breast feeding practice Social problems Food taboos Child abuse, abandonment

43. Etiology 48 2 . Biological factors Maternal malnutrition Infectious diseases  negative protein & energy balance Poor food preparation 3. Environmental factors Overcrowding &/or unsanitary living  frequent infections Agricultural patterns Drought, floods, & war Forced migrations

44. AGE OF THE HOST 50 More common among infants & young children Nutritional requirement Dependent When living under unhygienic conditions  d/t disease Older children usually have milder PEM Natural selection of the more fit Pregnant & lactating women – high requirement, but Consequences usually affect the fetus, newborn & infants Adolescents, adult men, non lactating – lowest prevalence

45. Pathophysiology & Adaptive Responses 51 PEM develops gradually in weeks or months allowing metabolic & behavioral adjustments that result in:- Decreased nutrient demands Nutritional equilibrium compatible with a lower level of cellular nutrient availability

46. Pathophysio … 52 Patients whose PEM develops slowly, as in marasmus , are better adapted & maintain a less fragile metabolic equilibrium than patients with acute PEM, as in kwashiorkor of rapid onset

47. Pathophysiology & … 53 1. ENERGY MOBILIZATION & EXPENDITURE in energy intake  in energy expenditure, Metabolism of body fat  wt loss Lean body mass diminishes due to muscle protein catabolism with increased efflux of amino acids Muscular wasting

48. Pathophysiology & … 54 Blood glucose concentration remains normal, at the expense of Gluconeogenic amino acids, & Glycerol from fats, and it falls in severe PEM or when complicated by serious infections or fasting

49. Pathophysiology & … 55 2. PROTEIN BREAKDOWN & SYNTHESIS The poor availability of dietary proteins  Reduces protein synthesis Loss of body protein, primarily from skeletal muscle Adaptations lead to the Sparing of essential body proteins & Preserve essential protein dependent functions until the nonessential tissue proteins are depleted

50. Pathophysiology & … 56 The above mentioned changes result in:- Decrease in total nitrogen or amino acid turnover Decrease in amino acid catabolism Adaptive Increase to 90-95% in the proportion that is recycled for synthesis Reduces urea synthesis & urinary nitrogen excretion Increase in half life of several proteins - albumin

51. Pathophysiology & … 57 BUT when protein depletion becomes too severe:- The adaptive mechanisms fail, The concentration of serum proteins, & especially albumin, decreases Reduction in oncotic pressure & Out flow of water into the exravascular space Contributing to the development of edema in kwashiorkor

52. … & ADAPTIVE RESPONSES 58 3. Endocrine changes Contribute to the maintenance of energy homesotasis through Increased glycolysis & lipolysis Increased amino acid mobilization Preservation of visceral proteins – via breakdown of muscle proteins Decreased storage of glycogen, fats, & proteins Decreased energy metabolism

53. Pathophysiology &… 59 …Endocrine changes Circulating levels of hormones Vs altered cellular responses to hormonal stimulation a . low food intake  reduces plasma glucose & free amino acids  Reduce insulin secretion & Increase glucagon & epinephrine release

54. … & Adaptive responses 60 b . The low amino acid levels, seen in kwashiorkor Stimulate secretion of human GH & Reduce somatomedins / insulin like GFs/ activity Further increase in GH levels due to absence of feed back inhibition The increase in GH & Epi influence the reduction of urea synthesis, favoring amino acid recycling

55. … & Adaptive responses 61 C . The stress induced by PEM also stimulate epinephrine & corticosteroid secretion The increase in plasma concentration of GH, Epi , & corticosteroids  lipolysis  increase in plasma free fatty acid level  increased resistance to peripheral action of insulin

56. … & Adaptive responses 62 d . A decrease in the activity of 5’-monodeiodonase reduces the production of triiodothyronine & increase in the inactive reverse T3 Thyroxine levels are also reduced possibly by a decrease in iodine uptake by the thyroid The reduction in active thyroid hormones decreases thermogenesis & oxygen consumption , leading to energy conservation

57. …. & Adaptive responses 63 4. Hematology Reduction in hgb & RBC mass related to lower tissue oxygen needs Reduced amino acids  reduced hematopoietic activity sparing amino acids for synthesis of more necessary proteins

58. …. & Adaptive responses 64 But, When tissue synthesis, lean body mass, & physical activity begin improving with treatment  rise in oxygen demand  accelerated hematopoiesis If iron, folic acid, & vit . B 12 are not available in sufficient amount, functional anemia with tissue hypoxia will develop

59. …. & Adaptive responses 65 5. Cardiovascular & renal function Reduction in cardiac output, heart rate & BP Central circulation takes precedence over peripheral circulation Altered CV reflexes  postural hypotension, & reduced venous return Renal plasma flow, and glomerular filtration rate may be reduced , But Water clearance & ability to concentrate & acidify urine appear unimpaired

60. …. & Adaptive responses 66 6. Elecrtolytes Reduction in Na excretion/ acid excretion total body K + due to reduction in muscle proteins & loss of intracellular potassium Low insulin action & intracellular energy substrates  reduced ATP & phosphocreatine  altered Na + & K + exchange  K + loss & increased IC Na + & thus water  intracellular over hydration, although total body water is decreased

61. …. & Adaptive responses 67 7. Immune system Depletion of T-lymphocytes from thymus, spleen, & LNs Reduction in production & function of complements Impaired phagocytosis , chemotaxis , & intracellular killing despite normal number of phagocytes B-cells and immunoglobulins are relatively normal but there may be defect in antibody production

62. …. & Adaptive responses 68 8. Gastrointestinal function Decreased gastric, pancreatic, & bile production  Impaired absorption Structural alteration of intestinal epithelial cells, atrophy of villi Altered / irregular GI motility & bacterial overgrowth  prone to diarrhea Fatty liver  hepatomegally

63. …. & Adaptive responses 69 9. CNS & PNS Decreased brain growth Decreased neurotransmitter production Decreased myelination Decreased velocity of nervous conduction Long term effects – not clearly understood and Can not be correlated with later behavior & level of intelligence

64. Pathogenesis of edema in severe PEM 70 1. Hypoalbuminemia through a reduction in colloid osmotic pressure of the plasma Outflow of fluid from the capillaries into interstitial space.

65. Pathogenesis of edema in severe PEM 71 2. Reduced renal blood flow & GFR  sodium retention & production of renin & aldosterone  edema due to increased tubular reabsorption of Na + & H 2 O 3. Increase in ferritin  stimulate production of ADH 4. Energy deficiency for the function of Na + pump & restoration of IC potassium

66. Pathogenesis of edema in severe PEM 72 5. Free Radical Theory Increased production of free radicals due to infections, toxins, trauma, catalysts /e.g. iron/, or sunlight, and Decreased scavenger /antioxidant/ mechanisms that remove free radicals ( vit . A, C, E, zinc, selenium & glutathione) Accumulation of free radicals Damage of cell membranes Alterations seen kwashiorkor: fatty liver, edema, skin changes…

67. 73 Infections in undernourished children also can precipitate the onset of kwashiorkor - mechanisms may be: Infections may divert the meager amino acid pool to the production of globulins and acute-phase reactant proteins, instead of albumin and transport proteins The increase of acute-phase reactant proteins that are proteinase inhibitors, such as alpha 1 -antitrypsin and alpha 1 -antichymotrypsin, may impair muscle protein breakdown

68. 74 Impaired production and utilization of ketone bodies for energy during infections  the use of more amino acids for gluconeogenesis Protein catabolism and nitrogen losses are enhanced by many viral and febrile infections, probably through increased epinephrine and cortisol actions.

69. 75 Regardless of the mechanisms involved, protein losses during severe infections can amount to as much as 2% of muscle protein per day Leukocytes stimulated by infectious organisms produce large quantities of superoxide and hydrogen peroxide. These are released into the surrounding medium and contribute to the production of kwashiorkor, according to the free-radical theory.

70. DISRUPTION OF ADAPTATION 76 When the supply for tissue & cell energy can no longer be maintained, a serious decompensation occurs causing:- Hypoglycemia Hypothermia Impaired circulatory & renal functions Acidosis Coma, & Death All These can occur within a few hours

71. DISRUPTION OF ADAPTATION 77 Metabolic decompensations due to severe protein deficiency Hemorrhagic diathesis & jaundice due to liver failure Renal failure with acidosis Water & sodium retention Decreased cardiac work Pulmonary congestion Susceptibility to infections Coma & death

72. Classification of PEM 78 Welcome classification Wt for Age No edema With edema 60 – 80% Under weight Kwashiorkor <60% Marasmus Marasmic kwashiorkor

73. Classification… 79 Water-low classification Grade of malnutrition Wt for ht /wasting/ Ht for age /stunting/ Normal >90% >95% Mild/ grade I/ 81 – 90% 90 – 95% Moderate/ grade II/ 70 – 80% 85 – 89% Severe /grade III/ <70% <85%

74. Clinical manifestations 80 Marasmus Wasting & loss of subcutaneous fat – wizened old man appearance “skin & bone” appearance Hair is sparse, thin, dry and easily pulled out Skin is dry, thin with little elasticity & wrinkles easily Watery diarrhea – common Heart rate, BP, & body temperature may be low Abdominal distension Anorexia - seldom

75. C/m… 81 Marasmus Common complications are Acute gastroenteritis, Dehydration Hypoglycemia Hypothermia Respiratory infections Eye lesions due to hypovitaminosis A Systemic infections  s eptic shock or IV clotting

76. Kwashiorkor 82 Edema Soft, painless, pitting /feet, & legs Severe – perineum, upper extremity, & face Skin lesions: usually present Pigmentation, desquamation, ulceration – flaky paint dermatitis, +/- erythematous , (peeling of epidermis  infection) Affected sites: legs, buttocks, & perineum Severe cases – seem burn

77. Kwash …. 83 Subcutaneous fat is prserved & Limited muscle wasting Mucous membrane Angular stomatitis , cheilosis , & smooth tongue Hair Fine, straight, sparse, without its normal sheen & pulled out easily Color changes usually to brown/ red/ gray/ yellowish white Flag sign – alternating bands of depigmentation & normal hair

78. Kwashiorkor…. 84 Pallor, & cold and cyanotic extrimities Mental changes Irritable, cry easily Expression of misery & sadness GI system anorexia, post prandial vomiting & diarrhea Fatty infiltration of liver – hepatomegally with soft rounded edge

79. C/m… 85 Kwash … Protruding abdomen due to distended stomach & intestinal loops slow & irregular peristalsis Reduced muscle tone & strength Tachycardia Hypoglycemia, & hypothermia

80. Complications in kwash … 86 Similar with marasmus , but Diarrhea and infections /respiratory & skin/ are more frequent & serious Severe, fatal infections could occur frequently with out Fever, tachycardia, respiratory distress, or Appropriate leukocytosis

81. Complications in kwashiorkor 87 Most common causes of death are pulmonary edema with Bronchopneumonia Septicemia Gastroenteritis, and Water & electrolyte disturbance

82. Lab studies 88 Tests that might be helpful Blood glucose – normal or low Hgb , or Hct Urine microscopy & culture S/E CxR Skin test for tuberculosis Blood film Serum electrolyte Serum protein / albumin

83. Mgt of severe acute malnutrition 89 Admission Inpatient mgt Phase 1 (acute phase) Transition phase Phase 2 (recovery phase ) Discharge Follow up

84. Mgt of SAM 90 Criteria for diagnosis weight-for-height/length <–3 Z-score MUAC < 115 m m for a child with length >65cm or age > 6month Bilateral pitting edema of nutritional origin

85. Indication for inpatient treatment Children who have medical complications, severe oedema (+++), or poor appetite (fail the appetite test), or Present with one or more Integrated Management of Childhood Illness (IMCI) danger signs

86. Phase - I 92 1. Nutritional Rx - Feed the patient F75 2. Give routine medications 3. Monitor the patient 4. Prevent, diagnose, and treat complications:- Hypoglycemia** Hypothermia** Dehydration**

87. Phase 1 93 … complications Infection** Heart failure Severe Anemia Septic shock Electrolyte disturbance

88. Phase 1 94 1. Nutritional Rx – F75 F75 = 75kcal/100ml Has less Na, protein, fat, lower osmolality & renal solute load than F100 Is Less energy dense Quantities = 100kcal/130ml/kg/day Feed by cup or NG tube

89. F 75 :- 95 Use NG tube when:- The child is taking less than 75% of prescribed diet Pneumonia with fast breathing Painful lesions of the mouth Cleft palate or other physical deformity Impaired consciousness

90. Phase 1 96 2 . Routine medications Vitamin A On day 1 & at admission when there is: Wasting with out edema Vitamin A not given in the last 6 months For every patient on the day of discharge Dosage: 6 to 12 months = 100,000 IU > 12 month = 200,000 IU

91. Phase 1 97 … Routine medications Folic acid - 5mg po single dose Antibiotics During phase I + 4 days 1 st line – amoxicillin 2 nd line – chloramphenicol or gentamycin Measles vaccine if not vaccinated and >6 to 9 months

92. Monitoring 98 Weight - each day Degree of edema – each day Body temperature – twice per day Stool, vomiting, dehydration, cough, respiratory rate, liver size & tenderness – each day MUAC – each week Height – after 21 days

93. Diagnosis & Mgt of Complications: 99 1. Dehydration:- Malnourished children are sensitive to excess Na + intake All signs of dehydration in a normal child occur in a severely malnourished child who is not dehydrated Thus only a history of recent fluid loss & very recent change in appearance can be used Misdiagnosis of dehydration & giving inappropriate treatment is the commonest cause of death in severe malnutrition

94. Rx of dehydration... 100 Give 50 -100ml/kg of ReSomal over 12 hours 5ml/kg/30min. ReSoMal for 2hours, then 5-10ml/kg/hour Stop rehydartion as soon as target weight is reached Monitor every hour:- The weight, RR, & PR The liver edge, marked before any rehydration Rx The heart sound

95. Rx of dehydration… 101 Make a major reassessment after two hours, and 1. If there is continued weight loss Increase rate of ReSoMal administration by 10ml/kg/hr & Reassess in one hour 2. If there is no weight gain Increase rate of ReSoMal by 5ml/kg/hr & Reassess every hour

96. Rx of dehydration… 102 3. If there is weight gain with:- a. Deterioration of child’s condition, diagnosis of DHN was definitely wrong Stop ReSoMal and go for F75 treatment b. No clinical improvement Diagnosis of DHN was probably wrong Either change to F75 or alternate F75 & Resomal c. Clinical improvement but still signs of DHN Continue until weight gain is achieved d. Resolution of clinical signs – stop rehydration & start F75

97. Indications for IV rehydration 104 Defined signs of dehydrations, & Patient has all of the following:- Semiconscious / unconscious Rapid weak pulse Cold hands & feet Give 15ml/kg/hour darrow’s solution i.e. Ringer lactate with 5% DW, OR Half strength saline with 5% DW, AND

98. Iv rehydration… 105 Then reassess the child after an hour & decide If improving / weight loss continue for one more hour - 15ml/kg If became conscious- oral/ NG tube – Resomal 10ml/kg/hr If not improving & wt gain – consider septic shock & stop fluid intake

99. Dehydration Rx 106 All rehydration /oral or IV/ therapies should be stopped immediately if Target weight is achieved Visible veins become full Development of edema - overhydration Development of Prominent neck veins Increase in liver size by >1cm & development of tenderness Increase in RR by 5 or more per minute Development grunting Development of crepitations in the lungs Development of S 3 gallop

100. 107 Fast weak pulse, cold peripheries, pallor, drowsiness No history of recent fluid loss No history of recent change in appearance Eye lid drooping / normal, OR Closed when asleep/unconscious Eye lid retracted or slightly open When asleep / unconscious 2. Signs of septic shock & Rx Septic shock with hypoglycemia Septic shock

101. Rx of septic shock 108 Give darrow’s solution 15ml/kg/hr Reassess every 10min. Give second & first line antibiotics together – IV Keep warm to prevent or treat hypothermia Give sugar water to prevent hypoglycemia – orally /NG tube If possible blood transfusion 10ml/kg in 03 hours If improved  F75

102. Dehydration in kwashakor If wt loss is > 2 % Watery diarrhea Treatment-30 ml of ReSoMaL per each diarrhea

103. 3. Dx & Rx of Heart Failure 110 Signs include- Deterioration with weight gain Increase in heart rate, RR Grunting Distended neck veins Increase in liver size / tender S3 gallop A fall in Hgb level is usually a sign of fluid overload

104. … Rx of CHF 111 Stop all intake of fluids or feeds /oral or IV/ No fluid or feed should be given until stabilization ( 24 -48 hrs) Small amount of sugar water can be given orally Give furosemide 1 mg/kg/dose – usually not very effective Single dose digoxin can be given (5mcg/kg) Even if anemic don’t transfuse – heart failure treatment takes precedence

105. 4. Anemia 112 Hgb < 4mg/dl or Hct <12% during the first 48 hours after admission Give 10ml/kg whole blood over 3-4 hours All children should be fasted for 3 hours after transfusion

106. 4. Hypoglycemia 113 Best prevented by regular feeding Often there are no clinical signs at all Mgt:- If conscious give 50ml of 5gm sugar water or F75 by mouth If loosing consciousness 50 ml of 5gm sugar or Dextrose 10% via NG tube If unconscious:- sugar via NG tube or glucose as single IV injection (5ml/kg Dextrose 10%) Start 1 st & 2 nd line antibiotics together Reassess after 15min.

107. Complications…. 114 Hypothermia:- Axillary temperature < 35 c, rectal <35.5 c Nearly all hypothermia is due to low room T , lack of cover, or washing Check that the child sleeps with his/her mother - KMC Thermoneutrate temp. range is 28 c – 32 c Do not wash severely sick child

108. Hypothermia… 115 Put a hat on the head and wrap the child with the mother Give hot drinks to the mother  warm skin Treat for hypoglycemia and Start IV antibiotics: 1 st & 2 nd line

109. Fever in SAM 116 Check if the child is on routine antibiotics Most cases are due to high environmental temp Treat with sponging with room temperature Give extra water to drink Do not give antipyretics – aspirin or paracetamol These does not work in SAM & liver function is impaired - poisoning

110. Transition phase 117 Criteria to progress from phase I to transition phase Beginning of loss of edema Return of good appetite No NG tube, IV line, and No Severe medical complications

111. Transition phase 118 Feed the patient in exactly the same way as in phase 1 except that F100 (100kcal/100ml) is given instead of F75 The same volume is given so that energy intake is increased by 30% & the child starts to gain tissue Expected weight gain is 6gm/kg/day

112. Transition phase 119 Criteria to move back to phase 1 from transition phase Rate of wt gain >10gm/kg/day Increasing edema or development of refeeding edema Increase in liver size & tenderness Signs of fluid overload, CHF, or respiratory distress Development of tense abdominal distension If there is sufficient diarrhea to give weight loss If complication develops that require IV infusion of drugs

113. Phase II 120 Criteria to progress from transition phase to phase II Good appetite At least two days for wasted patients Complete loss of edema No medical complications/ problems

114. Phase II 121 Medical part of treatment is now complete The patients takes large amount of their diet & gain weight rapidly Pt can be undertaken in a nutrition unit /TFC, or take home therapy Give F100 5 times/day & plus porridge Ready to use therapeutic food – plumpy nut

115. Phase 2 122 Give routine medicines Iron sulfate is added to the diet /200mg in 2 liters of F100/ De-worming:- Mebendazole 100mg po BID for 03 days Vitamin A Measles vaccine – on discharge If signs of morbidity – return the patient to phase 1

116. Criteria for discharge 123 Wt for ht > 85%//-2 Z score MUAC > 125 mm No edema for 10 days Education has been complete Immunization is up to date Adequate arrangement have been made for follow up

117. Out patient Mgt 124 Pts with good appetite & no complications are directly admitted to phase 2 as out patient RUTF – ready to use therapeutic food is used for nutritional treatment Need longer time to recover than inpatient Mgt

118. Treatment failure 125 Primary failure to respond Criteria Time after admission Failure to gain appetite Day 4 Failure to loose edema Day 4 Edema still present Day 10 Failure to enter phase 2 & gain >5gm/kg/day Day 10 Secondary failure to respond Failure to gain weight >5gm/kg/day for 03 successive days During phase 2

119. 126

120. Cause of failure to respond 127 Problems in treatment facility Poor environment Insufficient or poorly trained staff Food prepared or given incorrectly Problems of individual children - Underlying disease such as:- Malabsorption Regurgitation Diarrhea Infections…

121. Poor prognostic factors 128 Age <6mo Deficit wt/ht >30% or wt/age >40% Altered mental status Infections Bleeding tendencies Heart failure Low serum protein (<3gm/dl) Severe anemia Extensive exudative or exfoliative cutaneous lesions Hypoglycemia or hypothermia Jaundice on admission

122. THE END