Management of Severe Acute Malnutrition.pptx

Severe acute malnutrition is a standard term referred to a condition where a child has severe wasting and/or bilateral pedal edema.

The health, social and economic burden of this condition cannot be overemphasised. It is needful and timely yet again to reiterate and summarily but comprehensively outline the management of this condition. Thus, this presentation is a comprehensive summary of the management of severe acute malnutrition as outlined in standard paediatric textbooks.
A detailed explanation should however be sourced from standard texts and updated journals.

This presentation is cannot be cited or referenced in publications, presentations nor public fora.

The presenters:
Dr Efosa Emmanuel Aimien is a Paediatric Resident on outside posting at the National Hospital Abuja. He had his medical training at the prestigious College of Health Sciences, Ahmadu Bello Univeristy, Zaria. Nigeria.
Dr Zarah Fatima Abdu is a Paediatric Senior Resident at the Department of Paediatrics, National Hospital Abuja. Her vastness and clinical acumen in child health especially malnutrition is without question.

We hope this presentation contributes to the ease of gaining medical knowledge especially in Paediatrics.

Thank you.

1. Department Of Paediatrics, National Hospital Abuja. Nigeria. MANAGEMENT OF SEVERE ACUTE MALNUTRITION BY DR EFOSA AIMIEN & DR ZARAH ABDU

2. OUTLINE Introduction Definition Epidemiology Etiology Classification Pathophysiology Clinical Manifestations Medical Complications Management Prevention Conclusion References

3. INTRODUCTION Malnutrition refers to a group of pathological entities resulting from an imbalance between the supply and intake of essential nutrients and the body’s requirement for these nutrients. Severe acute malnutrition (SAM) is predominantly seen in under 5 year old children (commonly 6 – 18 months). SAM is responsible for 45% of death among children under 5 years (WHO 2015). Management according to the WHO guidelines in a hospital setting reduces mortality by 55%.

4. DEFINITION Severe acute malnutrition can be defined as:- Severe wasting, i.e extreme thinness. - Weight for Length (Height) <-3 z score of the WHO child growth standards. - Mid-upper arm circumference(MUAC) <115mm in children aged 6- 59 months. And/or presence of bilateral pedal edema.

5. DEFINITION Other terms include:- Marasmus - severe wasting. Kwashiorkor - characterized by edema. Marasmic-Kwashiorkor - severe wasting and edema.

6. EPIDEMIOLOGY According to WHO 2018 data , 52 million children < 5yrs wasted, nearly 20 million children globally are severely malnourished and out of these, about 1 million die yearly. Most of these children are in the Sub-Saharan Africa and south Asia. In Nigeria, nearly 6 million under-five year old children in the Northwest and Northeast are expected to suffer from acute malnutrition - IPC snapshot assessment May 2022 - April 2023.

7. EPIDEMIOLOGY Nigeria has the second highest burden of stunted children in the world. About 2 million children suffer from SAM and only 2 in every 10 children get to receiv e hospital treatment - UNICEF. In National Hospital Abuja, a total of 13 cases of SAM were admitted between October 2022 and September 2023. The male to female ratio was 1.3:1. Four of these patients died from complications and five were discharged to the follow up clinic.

8. ETIOLOGY There are three level of causality: Immediate cause (individual level) Inadequate dietary intake. Disease/poor health status - infectious diseases such as diarrheal disease, measles, helminthiasis, TB, HIV/AIDs, malabsorption, congenital anomalies, malignancies. Child neglect.

9. ETIOLOGY Underlying cause ( Household/Family level ) Poverty - Food insecurity, Maternal - Teenage/single mother, poor nutritional status during pregnancy, maternal smoking/drug use during pregnancy, ignorance, lack of knowledge on feeding, hygiene, and weaning practices. Large family size. High birth order. Poor health seeking behavior.

10. ETIOLOGY Basic/Remote cause ( Community/Society level ) Lack of political will. Natural disasters - Drought, flood. Man-made disasters - Wars. Economic instability - currently fuel subsidy removal, hike in prices of food. Inadequate health care services. Poor environmental hygiene.

11. CLASSIFICATION Modified Wellcome classification Gomez classification WHO classification Waterlow classification Others: Jellife’s, Bengoa’s, Udani’s, and Composite classification scheme(Mclaren and Read).

12. Modified Wellcome Classification % Body weight Without edema With edema Nutritional Status >120% - - Obese 80 -120% + - Normal 80 -120% - + Overweight kwashiorkor 60 -80% + - Underweight 60 -80% - + Underweight kwashiorkor <60% + - Marasmus <60% - + Marasmic-kwashiokor

13. Gomez Classification % Weight for age Nutritional Status >90 Normal 75 - <90 1st Degree Malnutrition 60 - <75 2nd Degree Malnutrition <60 3rd Degree Malnutrition

14. WHO Classification Indicators Mild Moderate Severe Weight for Height(Length) <-1 to >-2 z score < -2 to >-3 z score < - 3 z score Height for age <-1 to >-2 z score < -2 to >-3 z score < - 3 z score Bilateral edema No No Yes MUAC - >115 - < 125mm < 115mm

15. Waterlow Classification Indicators Mild Moderate Severe Weight for Height(Length) 80 - 89% 70 - 79% < 70% Height for age 90 - 95% 85 - 90% <85%

16. PATHOPHYSIOLOGY THEORIES OF MALNUTRITION Dysadaptation theory ( Gopalan , 1968). Aflatoxin hypothesis ( Hendrickse , 1982). Free radical theory (Golden and Ramdath , 1987). Hypoalbuminemia ( Coulthard , 1980’s).

17. DYSADAPTATION THEORY OF GOPALAN It postulates that a child with better adaptation to low calories and proteins(marasmus). would preserve the structural and functional integrity of the liver at the expense of less important organs i.e skin and muscles. Effective catabolism and near normal anabolism in marasmus and failure of the latter in kwashiorkor.

18. AFLATOXIN HYPOTHESIS In kwashiorkor, there is either a greater exposure to aflatoxins or impaired transport and excretion of aflatoxins. A resultant hepatotoxicity occurs leading to the formation of unstable epoxides of AFB1, thereby initiating biologic and metabolic derangements.

19. FREE RADICAL THEORY It states that the free radicals produced due to various infection and toxins, cause some hepatic damage resulting in fatty liver. There is absence of the protective pathways(Vitamin A and E deficiency) involved in free radical scavenging. These lead to iron catalyses chain reaction with inadequate repair of leaky membranes, edema, skin and hair changes.

20. HYPOALBUMINEMIA There is a link between severe acute malnutrition and low plasma oncotic pressure due to extreme hypoalbuminemia.

21. PATHOLOGIC AND METABOLIC CHANGES Reductive adaptation. Fat stores are mobilized to provide energy and subsequently from the muscles, skin, and gastrointestinal tract. Energy is conserved by reducing physical activity and growth, reduce basal metabolism, and functional reserves of organs, and reducing inflammatory and immune responses.

22. PATHOLOGIC AND METABOLIC CHANGES These leads to important consequences:- Liver - Becomes fatty and it makes glucose less readily available. It also produces less transport proteins such as albumin and transferrin. Pancreas - Impaired exocrine and endocrine function. GIT - Less gastric acid is produced, atrophy of the intestinal mucosa leading to flattening of the villous processes with accompanied disaccharidase deficiency, and reduced motility. Digestion and absorption is impaired.

23. PATHOLOGIC AND METABOLIC CHANGES Heart :- Cardiac muscle wasting leading to decreased cardiac output. Kidneys :- Decreased ability to excrete excess fluid and sodium, and fluid easily accumulates in the circulation increasing the risk of fluid overload. CNS :- Apathy and irritability. Basal metabolism :- The basal metabolic rate is reduced due to impairment of the oxidative phosphorylation and energy producing mechanism in the muscle, hence hypothermia ensues.

24. PATHOLOGIC AND METABOLIC CHANGES Endocrine glands :- Increased cortisol and growth hormone, and decreased insulin, triiodothyronine, and IGF-1. Body fluids and electrolyte :- There is increased extracellular water while serum potassium and sodium are low. However, the total body sodium content is high. Micronutrients :- Reduced calcium, phosphate, magnesium, zinc, copper, iron, manganese. Skin and endothelial lining :- Loss of the integrity leads to translocation of infective organism to the blood.

25. PATHOLOGIC AND METABOLIC CHANGES Immune system :- There is extensive atrophy of the lymphoreticular tissues which compromises both hum o ral and cell immunity, lymphokine production, and the number of circulating lymphocytes. The monocyte chemotaxis and intracellular killing capabilities are depressed. Complement levels are decreased, particularly C3.

26. Pathologic and metabolic changes Caption

27. CLINICAL MANIFESTATIONS This depends on the severity or degree of under nutrition, aetiology and inter-current illness The child may have presented to the clinic for other complaints and discovered to be malnourished on physical examination

28. KWASHIOKOR CONSTANT FEATURES Edema Mental changes Growth retardation Wasting USUALLY PRESENT SIGNS Moon face Hair changes Skin changes Anemia OCCASIONALLY PRESENT Flaky paint dermatosis Hepatomegaly Signs of vitamin deficiencies Signs of in fection 29

29. MARASMUS Poor growth Muscle wasting-prominent ribs and bony points, multiple skin folds around the buttocks (baggy pant sign), thighs and upper arms Mental alertness-they are mentally alert and less miserable, wizened facial expression Appetite- intact and often voracious Diarrhea Skin and hair changes Anaemia Vitamin deficiency

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32. COMPLICATIONS Dehydration Shock Hypoglycemia Hypothermia Infection Electrolyte imbalance Severe anemia Micronutrient deficiencies Dermatoses Helminthiasis Persistent diarrhea and dysentery Re-feeding syndrome

33. CHECKLIST OF POINTS FOR TAKING THE CHILD’S MEDICAL HISTORY Usual diet before current episode of illness (24 hours diet recall and also FADUS) AFASS (in the setting of breast milk substitute) Breastfeeding history Food and fluid taken in past few days Recent sinking of eyes Duration and frequency of vomiting or diarrhea, appearance of vomit or diarrheal stools Time when urine was last passed Contact with people with measles or tuberculosis

34. CHECKLIST OF POINTS FOR TAKING THE CHILD’S MEDICAL HISTORY Any death of siblings Birth weight Milestones reached (sitting up, standing, etc ) Immunizations Level of education of the parents especially mother Occupation of parents Communal food taboos / superstitions Any communal unrest e.g. from terrorism

35. PHYSICAL EXAMINATION

36. INVESTIGATIONS Full blood count with peripheral blood film - Anemia, leukopenia/leukocytosis. Blood glucose - hypoglycemia( < 3mmol/L or < 54mg/dL). Serum electrolytes, urea, creatinine - dyselectrolytemia. Serum total protein and albumin - hypoproteinemia/hypoalbuminemia. Urinalysis.

37. INVESTIGATIONS Blood smear for malaria. Screening for HIV. Cultures- urine, stool, blood, and swab specimens from skin ulcers. Stool microscopy for ova, cyst , parasite; stool for occult blood and reducing substances. Tuberculin skin test. Chest x-ray.

38. TREATMENT This is multidisciplinary : paediatricians , dieticians, social welfare, etc Those without complications can have outpatient care: Oedema is +/++ MUAC >115mm Good appetite ( indicates less metabolic disturbaces ), clinically well and alert Those with complications can have inpatient care: Severe oedema +++ MUAC <115mm Those with anorexia , clinically unwell and not alert

39. TREATMENT The mainstay of treatment is dietary therapy requiring the provision of appropriate amounts of protein, energy, and micronutrients. The treatment plan can be divided into 3 main phases:- Stabilization phase (1 - 7 days). Rehabilitation phase (2 - 6 weeks). Follow-up ( 6 - 26 weeks).

40. THE WHO 10 STEPS Caption

41. TREATMENT STABILIZATION PHASE: The aim is to repair cellular function, correct fluid and electrolyte imbalance, restore homeostasis, and prevent death. It involves 24 - 48 hours intensive care to treat/prevent life threatening complications. Hypogycemia, hypothermia, and dehydration should be treated within the 1st 48hrs

42. TREATMENT - HYPOGLYCEMIA Defined as RBG < 3mmol/L (< 54mg/dL). If Conscious and able to drink: Give 50mls of 10% glucose or sucrose solution(1 teaspoon of sugar in 3½ tablespoons of water orally or through nasogastric tube or 1 t ea sp oonful sugar under tongue, whichever is quickest ). Feed 2hly for at least the first day. Keep warm and commence broad spectrum antibiotics

43. TREATMENT - HYPOGLYCEMIA If unconscious: Give 5ml/kg of sterile 10% glucose solution intravenously. Feed via NGT every 2 hr for at least the 1st day. Initially ¼ of initial feed every 30minutes until the blood glucose stabilizes. Other care similar to the p re vious.

44. TREATMENT - HYPOTHERMIA Defined as axillary temperature < 35 ℃ (< 95 F) or rectal temperature < 35.5 ℃ (< 95.9 F). Actively rewarm by: Kangaroo technique or dress in warmed clothings , wrap in warmed blankets or provide heat using radiant warmer for infants. Keep room warm (25 ℃ – 30 ℃ )

45. TREATMENT - HYPOTHERMIA Feed child immediately if not contraindicated. Monitor temperature hourly( every 30mins if using heater) Stop rewarming when rectal temperature is 36.5 C(97.7F)

46. TREATMENT - DEHYDRATION Give ReSoMal orally or via NGT at 5 mL/kg every 30mins for 1st 2 hours. Then give 5 - 10 mL/kg in alternate hours for up to 10 hr. Feed with same volume in the other alternate hour. Give 5-10 mL /Kg of ReSoMal for each lo ss Do not interrupt breastfeeding.

47. TREATMENT - DEHYDRATION Monitor hourly and stop if signs of overload develop (PR increases by 25bpm, RR increases by 5 breaths/min; increasing edema; engorged jugular veins). Stop when rehydrated ( > 3 signs of hydration: less thirsty, passing urine, moist mouth, tears, less lethargic, improved pulse and respiratory rate). NOTE:- DO NOT GIVE IV FLUIDS UNLESS CHILD IS IN SHOCK.

48. TREATMENT - SHOCK PARAMETERS: Lethargic or unconscious, cold hands plus either slow capillary refill(>3 sec) or weak fast pulse. Commence on Oxygen Give sterile 10% glucose( 5mL/kg) rapidly by IV route Give IV fluid at 15 mL/kg over 1 hour, using: Ringer’s lactate with 5% dextrose or Half-strength Darrow solution with 5% dextrose or Half- normal saline with 5% dextrose or

49. TREATMENT - SHOCK If all the above not available, use Ringer’s lactate Repeat IV fluid at 15 mL/kg for 1 more hour if there are signs of improvement. Then switch to oral or NGT rehydration with ReSoMal, 5 - 10mL/kg in alternate hour. If no signs of improvement, assume septic shock and : Give maintenance IV fluid at 4mL/kg/hr(while awaiting blood). Order for fresh whole blood at 10mL/kg over 3 hours( if in heat failure, give 5 - 7mL/kg packed cells). IV frusemide 1mL/kg at start of transfusion.

50. TREATMENT - SEVERE ANAEMIA Blood transfusion should be given when the child presents with : Hb < 4g/dL(PCV <12%). Hb 4 - 6g/dL( PCV 12 - 18%) and has respiratory distress. Transfuse with whole blood at 10mL/kg over 3 hours. If in heat failure, give 5 - 7mL/kg packed cells. IV frusemide 1mL/kg at start of transfusion.

51. TREATMENT - MICRONUTRIENT DEFICIENCIES

52. TREATMENT - INFECTIONS Give broad-spectrum antibiotics. For children attending OTP: Oral Amoxicillin 15mg/kg/dose b.d x 5/7 For Severely ill, necessitating inpatient care: First line - IV Amoxycillin 50mg/kg/dose 12 hourly x 3/7, then PO at 50mg/kg/dose 12 hourly to complete 1/52 OR IV Cefotaxime 50mg/kg 12hourly x 5/7. Add IV/IM Gentamycin 3 - 5mg/kg/day daily x 1/52.

53. TREATMENT - INFECTIONS +/- IV Metronidazole 7.5 - 10mg/kg/day 12 hourly x 3/7, then PO at 10mg/kg/day 12 hourly to complete 1/52. Second line - If child fails to improve clinically within 48hrs or deteriorates after 24hrs change to: IV Ciprofloxacin 10mg/kg/dose 12 hourly for 1/52 OR IV Ceftriaxone 50 - 100mg/kg/day in 2 d.d.

54. TREATMENT - INFECTIONS Deworm drugs should be given at OTP but if the child must remain in IPF, then during the rehabilitation phase they should receive a single dose of any of the following: Albendazole ( 12 -23mo 200mg ; >24mo 400mg) stat OR Mebendazole 100mg PO, twice daily for 3 days for children > 6mo ( not recommended below 6 months). Antimalarials for patient with RDT positive Give measles vaccine if child > 6months and not immunized.

55. TREATMENT - CAUTIOUS FEEDING The milk based diet used in this phase(stabilization) is F-75. Give frequent oral small feeds every 3 hr( 2hr for the ill child) for the 1 - 2 days, then 5 - 6 feed per day The feed should provide 130ml/kg/day, 100kcal/day, and 1 - 1.5g protein/kg/day.( volume to be reduced to 100ml/kg/day if grossly edematous ). Children < 23 months and still breastfeeding should still continue. Keep a 24hr intake chart and measure feeds carefully including left overs.

56. TREATMENT - CAUTIOUS FEEDING Use NG tube for feeding if Child takes <80% of the amount offered. Unconscious or has a n orofacial deformity. Painful mouth lesions. Severely ill. Weigh daily

57. TREATMENT REHABILITATION PHASE(2 -6weeks): The aim is to restore wasted tissues The signals for entry to this phase are reduced or minimal edema and return of appetite. A controlled transition over 2-3 days is recommended to prevent re-feeding syndrome. Iron is added at 3mg/kg/day. Continued emotional stimulation and sensorial development.

58. TREATMENT - CATCH-UP GROWTH FEEDING The milk based diet used in this phase(rehabilitation) after transition is RUTF(preferably) or F-100. Give 5 - 6 feed per day. The feed should provide 200ml/kg/day, 150-220kcal/kg/day and 4-6g protein/kg/day. Continue breast feeding 30mins before each scheduled feed time. Monitor and record weight and keep 24hr feeding chart.

59. REFEEDING SYNDROME A potentially fatal physiologic response to increase in energy from any source(parenteral or enteral) either given too soon or too vigorously. Onset is usually 24 - 48hours after start of high energy feeding. Characterized by hypokalemia, hypophosphatemia, hypomagnesemia, sodium retention, hyperglycemia, and thiamine deficiency which can lead to cardiac and respiratory failure, neurologic, and hematologic abnormalities.

60. REFEEDING SYNDROME Diagnostic criteria - Reduction in serum levels in one or any of the electrolytes by: 10 - 20% - Mild re-feeding syndrome 20 -30% - Moderate re-feeding syndrome >30% - Severe re-feeding syndrome

61. REFEEDING SYNDROME Prevention is key. Principles of management include: Correct biochemical abnormalities and fluid imbalances. Cautious re-introduction of feeds( use 50% of goal). Micronutrient supplementation( Thiamine, Zinc, Multivitamins). IV Frusemide and digoxin

62. SAM in children < 6 months Return and/or encourage full exclusive breast feeding. Supplemental suckling technique using supplemental suckling milk -F-75, infant formula, or F-100 dilu te . . Treat infections and other complications. Care for the mothers.

63. SENSORY STIMULATION & EMOTIONAL SUPPORT Emotional and physical stimulation through play program can substantially reduced the risk of permanent mental and emotional damage. Provide cheerful stimulating environment. Structured play therapy( 15 - 30mins/day). Physical activity as soon as child is well enough.

64. WHO CRITERIA FOR DISCHARGE Criteria for transferring children from inpatient facility to outpatient therapeutic program(or outpatient clinic): Appetite has returned( pass the appetite test). Bilateral edema is consistently resolving or resolved. Medical complications have resolved. Mental status has improved. Parents/caregiver have received appropriate health education and training on how to prevent recurrence as well has have resources to feed child.

65. WHO CRITERIA FOR DISCHARGE Criteria for discharging children from treatment: Children with SAM should only be discharged from treatment when their:- Weight for length/height is ≧ -2 Z score and have had no edema for at least 2 weeks OR Mid-upper arm circumference is ≧125mm and have had no edema for at least 2 weeks. The anthropometric indicator used to confirm SAM should also be used to assess whether a child has reached nutritional recovery. Children admitted with only bilateral pitting edema should be discharged when it has resolved and based on whichever anthropometric indicator is routinely used.

66. FOLLOW-UP Discharged children with SAM should be periodically monitored to avoid a recurrence. Enroll patient in nutritional support clinic for 4-6months. Every 2 weekly for the first 2 months, then monthly as progress is satisfactory. Ensuring immunization schedules are up to date. Continuous health education and training for parents/caregivers.

67. PREVENTION GENERAL HEALTH PROMOTION Education and counseling of mothers and care givers on how to adequately feed their children through balance diet Provide free micronutrient supplements to children Strengthening policies as done by UNICEF, government systems and accountability to ensure adequate finance for nutrition Support humanitarian assistance Exclusive breastfeeding for 6months and cont breastfeeding for 2years

68. PREVENTION SPECIFIC PREVENTION Focus antenatal care Preventing anemia Prevent LBW babies through improved calories malaria prophylaxis/folic acid supplementation Encourage family planning Prevention and control of pneumonia and diarrhea, immunization, deworming, oral rehydration therapy, distribution of insecticides treated mosquito net, and adolescent and maternal nutrition

69. PREVENTION EARLY DIAGNOSIS AND TREATMENT Early identification through growth monitoring via charts Treatment of infections/dehydration/hypoglycemia Correction of nutritional deficiency LIMITATION OF DISABILITY Through SAM treatment programmes . REHABILITATION Join rehabilitation groups. Clinic follow ups.

70. CONCLUSION SAM remains a major contributor to childhood morbidity and mortality accounting for about 45% of under-5 mortalities. Adequate nutrition is the cornerstone to mitigating against these potentially fatal problem. Management of SAM according to the WHO guideline reduces mortality by 55% thus informing the need to adequately equip the medical personnel on the knowledge of the management of SAM

71. REFERENCE WHO. Guideline: Updates on the management of severe acute malnutrition in infants and children . Geneva: World Health Organization; 2013. UNICEF/WHO/World Bank Group - Joint Child Malnutrition Estimates 2017 edition. WHO, WFP. UNSCN, UNICEF. Community-based management of severe acute malnutrition. A joint statement by the WHO, World Food Programme , United Nations Standing Committee on Nutrition, United Ntions Children’s Fund. Geneva World Health Organization;2007. WHO, Management of Severe malnutrition: a manual for physicians and other senior health workers. Geneva, WHO:1999. Nelson Essentials of Paediatrics , 20 th Edition. Azubuike, J.C. and Nkanginieme , K.E.O., Eds., Paediatrics and Child Health in a Tropical Region. 3 rd Ed. Educational Printing and Publishing Lagos, pg-701 Morbidity and mortality statistics for the Dept of Paediatrics , National Hospital Abuja (Oct 2022 – Sept 2023)