Severe Acute Malnutrition presentation: 2013 WHO IMCI recommendations.

1. SEVERE ACUTE MALNUTRITION
PRESENTED BY: MORACHA KEVIN
(MOI UNIVERSITY-KENYA)
MODERATED BY: DR. MARETE
(CONSULTANT PEDIATRICIAN)

2. INTRODUCTION
• Presence of bilateral edema or severe wasting
(weight for height/length <-3SD) or MUAC
<115mm.
• Both Kwashiorkor and Marasmus are managed
similarly.
• Children who are <-3SD weight for age may be
stunted but not severely wasted. They don’t
require hosp adm unless with serious illness.

3. Formerly PEM:
• WHO: "the cellular imbalance between supply
of nutrients and energy and the body's
demand for them to ensure growth,
maintenance, and specific functions."

4. • Forms: Kwashiorkor, marasmus, marasmic
kwashiorkor, underweight.
• Marasmus involves inadequate intake of
protein and calories, whereas a child with
kwashiorkor has fair-to-normal calorie intake
with inadequate protein intake.

5. EPIDEMIOLOGY
• Worldwide, SAM is among leading causes of
death among children <5Yrs
• More common in the developing states
• Malnutrition causes abt 5.6 to 10 million
deaths/yr, with sever malnutrition
contributing to abt 1.5 million of these deaths
( Heinkens et al. 2008)

7. Cont..
• Prevalence of SAM in developing counties is
40% while in developing countries is 2- 10%
• Factors found to predispose in high income
countries : chronic diseases and congenital
disorders
• In developing countries: Socioeconomic status
– EA journal Vol 81 No. 8 Aug 2004

8. Kenya’s Epidemiology
• 2009, MoH : National figure for acute
malnutrition of under 5’s is approx. 6%
• Variations exist in diff parts of the country:
arid and semi arid areas- 15-20%

9. • It has been noticed that most of the malnourished
children in Kenyan hospitals have hx of:
– poverty
– single mothers,
– single parents,
– displacement by clashes,
– birth out of wedlock,
– mother and child staying separate from father due to
working conditions,
– and sharing of income with extended families
• (EA journal Vol 81 No. 8 Aug 2004)

10. Study at MTRH on risk factors for PEM June
2001 to June 2002 by Prof. Ayaya, Prof. Esamai et al
concluded that poverty, social conditions
under which the child was living, sex of the
child and incomplete immunizations were risk
factors for the severe protein energy
malnutrition.

11. ETIOLOGY
• Primary - when the otherwise healthy
individual's needs for protein, energy, or both
are not met by an adequate diet. (most
common cause worldwide)
• Secondary - result of disease states that may
lead to sub-optimal intake, inadequate
nutrient absorption or use, and/or increased
requirements because of nutrient losses or
increased energy expenditure.

12. PRECIPITATING FACTORS
 Lack of food (famine, poverty)
 Inadequate breast feeding
 Wrong concepts about nutrition
 Diarrhoea & malabsorption
 Infections (worms, measles, T.B)

13. WHO classification
Acute malnutrition
(severity)
MUAC (cm) WHZ
None >13.5 >-1
At risk 12.5 to 13.4 -2 to -1
Moderate 11.5 to 12.4 -3 to -2
Severe
<11.5 <-3
Kwashiorkor

14. • Former classifications include: Welcome
classification, Gomez and Seo anne and
Lathams.

15. Wellcome working party.
NB: If WT >80% with oedema– Kwashiorkor. Parameter: weight for
age + oedema
Weight Oedema
Underweight 80% - 60% -
Kwashiorkor 80% - 60% +
Marasmus <60% -
Marasmus-
Kwashiorkor.
<60% +

16. SAM Pathogenesis- Theories
1. Dietetic Hypothesis (classical)
– Kwashiorkor : Predominantly protein deficiency
– Marasmus : Energy deficiency

17. 2. Adaptation Hypothesis (Gopalan’s )
– Marasmus : Extreme case of adaptation
– Kwashiorkor : A stage of adaptation failure
• Continued prolongation of stress
• Sudden precipitation or aggravation by a
fulminant infection like measles, whooping cough,
diarrhoea or pneumonia

18. 3. Free Radical Hypothesis (Golden’s)
• Kwashiorkor from over production of free radicals
and breakdown of protective mechanisms. Low serum
iron causes increased production of free O2 radicals
These oxides (free O2 radicals) are normally buffered by
protein and mopped up by anti-oxidants such as
• Vitamins A,C,E
• Glutathione:-Defc causes toxic accum of free O2
radicals
• Zinc.
• Selenium

19. 4. Jelliffe’s Hypothesis
• A mixture of interactions and sequelae of dietary
imbalances, infections and infestations, emotional
trauma and toxins
5. Aflatoxin Hypothesis
• Contamination of food.
• In kwash, free O2 radicals potentially toxic to cell
membrane are produced during infections or as a
result of ingesting aflatoxin from aspergillus
flavus fungi growing in moist grains and ground
nuts.

20. 6.Role of hormones
Kwashiorkor – Low plasma cortisol – Muscle
protein NOT mobilized –Low plasma A.A –
stimulate the pituitary to secrete high GH – G.H
is lypolytic causing high plasma free fatty acid –
low synthesis of lipoproteins – Fat accumulates
in the liver – impaired hepatic fat metabolism-
Fatty liver.

21. Marasmus
• High plasma cortisol in marasmus > kwash
• Raised cortisol levels leads to breakdown of muscle protein
and the amino acids released are diverted to the liver for the
synthesis of plasma protein.
• The plasma concentration of β-Lipoproteins is well maintained
facilitating mobilization of triglycerides from the liver .The
metabolic integrity of the liver remains unimpaired in
marasmus.

22. 7.ROLE OF INFECTION
• Kwash is often preceded by an episode of infection with
diarrhoea and respiratory infection being the most common
precipitating factors.
• Others –measles, chicken pox, HIV, Whooping cough, TB,
Malaria et.
• Why does infection affect nutritional status?
– Poor appetite
– Dietary restriction –misconception of low feeds during diarrhoea.
– Malabsorption of nutrients
– Frank protein-losing enteropathy e.g. in measles, HIV.

23. 8. Serum iron status
• Low serum iron increases free oxygen radicals
in circulation
• Proteins , vit A,C, and E, Zn, Se, and
glutathione help mop up free radicals. These
are reduced in Kwash. Thus free radical excess

24. PATHOPHYSIOLOGY of SYMPTOMS
OEDEMA
Cause:
• Protein-deficient, hypoalbuminaemia, reduced plasma oncotic
pressure, shift to interstitium
• Free radical damage of cell membrane, Na+/K+ ATPase malfxtn-leaks
• Hypovolemia reduced GFR, activation of RAAS, Na+ and water
retention.
• Incr levels of leukotrienes cause uncontrolled vasodilation-hypovolemia-
low BP-decr peritubular hydrostatic pressure – incr
tubular reabsorption of salt and water.

25. PATHOPHYSIOLOGY Cont’d
WASTING
• Calorie def – fats and tissue proteins mobilized
to supply energy for metabolic processes.
• Recurrent infections coupled with
hypoglycemia cause acute stress response-cortisol
released- wasting
• Effects of associated infections e.g. HIV
wasting syndrome

26. PATHOPHYSIOLOGY- Cont’d
HAIR CHANGES
• Keratin synthesis impaired coz of cysteine and
methionine def , thus brittle hair easily pulled off
/breaks
• Pigment melanin formed from tyrosine deficiency in
kwash. Hair changes colour to reddish or grey.
• Periods of good nutrition alternating with poor
nutrition- flag sign.
• Dullness and lack of lustre due to weathering of the hair
cuticle.
• Bleaching effects of H202

27. PATHOPHYSIOLOGY- Cont’d
SKIN CHANGES
•Ulcerations and flaky paint rash due to Zn
def.
•Atrophy of sweat and sebaceous glands
leads to excessive dryness of the skin.
•Hyperpigmentation, erythema, duskiness
of exposed areas – niacin def
•Cracking and fissuring of hyper pigmented
•Generalized hypopigmentation due to
stretching of the skin by the edema.

28. PATHOPHYSIOLOGY- Cont’d
HEPATOMEGALY/ FATTY LIVER
– Free radicals damage mitochondrial enzymes in the liver
causing reduced synthesis of proteins.
– Beta LP def – accumulation of TG in the liver – fatty liver –
Hepatomegally.
POT BELLY
– Hypotonic muscles of abdominal wall resulting in muscle
wasting.
– Overgrowth of bacteria in the gut due to reduced immunity-
– Paralytic ileus due to hypokalemia
– Hepatomegally coz of fatty liver

29. PATHOPHYSIOLOGY- Cont’d
DIARRHOEA
• Caused by recurrent infxns due to reduced
immunity- low sIgA and reduced secretion of
acid in stomach.
• Malabsorption – deficiency of pancreatic
enzymes resulting from pancreatic
atrophy/protein deficiency.
• Villous atrophy- reduced absorptive surface

30. PATHOPHYSIOLOGY- Cont’d
Recurrent infections
• Atrophy of thymo-lymphatic glands cause
depletion of T lymphocytes and depressed CMI
thus infxns like Herpes, candidiasis common.
• Reduced phagocytic and bactericidal activity of
leucocytes- NADPH oxidase and lysozyme def
• C3,C5, and factor b levels reduced – opsonization
and phagocytosis reduced.
• Immune response reduced due to inability to
synthesis IL-1,IL-6.TNF alpha due to lack of supply
of essential AA.

31. PATHOPHYSIOLOGY- Cont’d
The “Vicious Cycle”of Undernutrition & Infection
Disease:
. incidence
.severity
.duration
Appetite loss
Nutrient loss
Malabsorption
Altered metabolism
Inadequate dietary intake
Weight loss
Growth faltering
Lowered immunity
Mucosal damage
Figure 2. The Synergistic cycle of infection and malnutrition

32. PATHOPHYSIOLOGY- Cont’d
ANAEMIA
• Due to dietary deficiency of iron and folate
• Parasitic infxtns e.g. hookworm.
• Malabsorption due to recurrent diarrhea.
• Reduced protein intake and synthesis.
APATHY
• Hypokalemia- muscle weakness and easy fatigability of muscles-child
lacks in energy
• Lack of stimulation and deprivation causes reduced growth of
brain and nerve thus mental slowing.
• Reduced BMR
• Apathy also attributed to Zinc deficiency.

33. PATHOPHYSIOLOGY- Cont’d
ELECTROLYTE/ MINERAL DEFICIENCIES –
Magnesium
• Good evidence that magnesium deficiency is common in
severe malnutrition
• Consequences:
– Muscular twitching
– Arrhythmias
– Convulsions
– Predisposes to K+ deficiency

34. PATHOPHYSIOLOGY- Cont’d
sodium
– Plasma sodium can be low and on occasions is
extremely low in children with marasmic
kwashiorkor.
• However total body sodium is often increased
• So large amounts of additional sodium (fluids and
feeds) are poorly tolerated.

35. PATHOPHYSIOLOGY- Cont’d
Micronutrients / Trace Elements
• Zinc
• Copper
• Selenium
Consequences of Zinc deficiency
• Reduced appetite
• Reduced immunity
• Reduced gastrointestinal function
– longer period of diarrhoea
• Reduced ability to gain weight
even when there is adequate
feeding
Consequences of Copper and
Selenium deficiency
• Copper is required for adequate
tissue growth and repair,
anaemia and poor bone growth
may particularly be associated
with inadequate copper (there
is very little in milk).
• Selenium deficiency may be
associated with reduced cardiac
muscle function.

36. INITIAL ASSESSMENT
HISTORY
• Assess for danger signs or emergency signs and
take history concerning:
– Recent intake of food
– Usual diet before current illness: quantity, quality,
frequency
– Breastfeeding Hx
– Duration and frequency of diarrhea & vomiting
– Type of diarrhea(watery/bloody)
– Loss of appetite

37. – Family circumstances: Socioeconomic status i.e.
Income, Housing, food &Water supply, Sanitation
– Cough>2wks
– Contact with TB
– Recent contact with measles
– Known or suspected HIV infn or exposure

38. Further History
1. Birth history: birth weight
2. Immunization history
3. Milestones: achieved/delayed
4. Past medical hx: Resp. infxns, TB, measles,
HIV
5. Family history: Parents, Siblings, health
status, family occupation, education

39. PHYSICAL EXAM
• Shock: lethargic or unconscious; with cold peripheries,
slow cap refill(>3sc), or weak rapid pulse or low BP
• Signs of deH20
• Severe pallor
• Bilateral pitting edema
• Eye signs of vitamin A def
– Dry conjuctival or cornea, Bitot spots
– Corneal ulceration
– keratomalacia

40. • Vitamin A def: likely to be photophobic – keep
eyes closed. Examine eyes gently to avoid
corneal rupture.
• Localizing signs of infxn: ear discharge, throat
infxns, skin infxns or pneumonia
• Signs of HIV infxn
• Fever : >37.5 c or Hypothermia (rectal: <35.5c)
• Mouth ulcers

41. • Skin changes
– Hypo/hyperpigmentation
– Desquamation
– Ulceration
– Exudative lesions
• Conduct appetite test: ready to use
therapeutic food

42. Features of Kwashiorkor
1.Always present
• Generalized edema, Pitting edema over the lower limbs
• Growth failure: wasting (may be masked by edema).
• Psychomotor changes: apathy, irritability
2.Usually present
• Hair changes: fine but coarse in chronic d’se, easy
pluckability, discoloured, light-colored hair streaky
red/gray, sparseness (areas of alopecia),Alternate areas
of hypo and normal pigmentation-flag sign
• Anemia
• Loose stools

43. 3.Occasionaly present
• Hepatomegaly
• Signs of vitamin deficiencies
• Skin changes
A. Diffuse/patchy areas of hypo/hyperpigmentn
B. Thin, shiny, taut skin over edematous areas
C. Moist ulcerations over flexural/pressure points
D. Super infectns e.g.. scabies
Classical lesions
– Flaky paint dermatosis: hyper pigmented, desqumation
area(flake) over raw skin.
– Crazy pavement dermatosis: dry, hyperkeratotic ,fissured
skin with alternate areas of hyper/hypo pigmentation
– Mosaic dermatosis: mixed lesions in mosaic form

44. Features of Marasmus
1.Always present
• Extreme growth failure,<60% WA
• Marked muscle wasting, loss of subcut fat
• Alert, with good appetite
• Face is shriveled like ‘little old man, monkey like- Relatively larger
head, wrinkled skin, loose skin folds over buttocks, thighs, axilla
2.Occasionaly present
• Anemia
• Diarrhea with signs of dehydration
• Vit deficiencies: cheilosis,dermatosis,rickets
• Infxns: resp,TB,measles

45. • Mosaic
dermatosis ↓

46. Flaky paint dermatosis

47. • Flag sign

48. Organization of care
• Those who pass appetite test: Rx as O/Ps for
uncomplicated SAM
• Those with Edema +++, lack of appetite, one
or more danger signs or with medical
conditions requiring admission- Rx as I/Ps
• Separate I/Ps from infectious children and
keep them warm (25-30⁰c). Special nutrition
unit if available

49. Out patients
• Respond rapidly to therapy unless have other infections.
• Mainstay is enough fresh affordable balanced food.
• Milk alone is adequate for an infant 4-6mths
• Nutritional education to the caretaker.
• Weight monitoring as a follow-up measure.
• Their daily requirements:
– Calories 120cal/kg/day
– Protein 2-3g/kg/day
– Vit. A 1500 I.U/day.

50. INVESTIGATIONS
a)For general screening and monitoring
Hematological
FHG, PBF, Blood glucose profile, LFT:albumin
Septic screening
BS for MPS, Blood culture, Stool MCS,CXR
Mantoux test, PITC, Urine: urinalysis, M/C/S
Biochemical
Electrolytes: rarely helpful, may lead to inappropriate therapy,
LFTs
Iron tests: serum Fe, TIBC, ferritin
Vitamins and minerals:B12,folate,D,K,calcium,magnesium

51. DIFFERENTIALS
KWASHIORKOR
• Nephrotic syndrome
• Liver disease
• Protein losing enteropathy
• Angio-neurotic edema
• CCF
MARASMUS
• Malignancies
• HIV wasting syndrome
• TB, Other chronic illnesses
KWASH DERMATITIS
• Acrodermatitis Enteropathica -zinc deficiency.
• Scurvy
• Pellagra

52. 10 step mgt of malnutrition
1. Hypoglycemia
2. Hypothermia
3. Dehydration
4. Electrolyte imbalance
5. Infections
6. Micronutrient def.s
7. Initial feeding
8. Catch up growth
9. Sensory stimulation
10. Follow up

53. STABILIZATION REHABILITATION
DAY 1-2 DAY 3-7 WEEKS 2-6
Hypoglycemia -------------
Hypothermia -------------
Dehydration 10 step approach
-------------
Electrolyte imbalance ---------------------------------------------------------------------
Infections ----------------------------------
Micronutrient ------NO IRON-----------------------WITH IRON------------
Initiate feeding -----------------------------------
Catch up growth ---------------------------
Sensory stimulation --------------------------------------------------------------------
Prepare for follow-up ---------------------------

54. Hypoglycemia
Dx: blood glucose < 3mmol/l
• Rx:
– 50mls of 10% glucose or sucrose sol (1 rounded
teaspoon of sugar in 3 tablespoons of water) orally or
by NGT, followed by 1st feed ASAP
– Give 1st feed of F75 therapeutic milk if available and
then CT with feeds 2hrly for 24hrs; then CT feeds 2 or
3hrly day and night
– If unconscious: Rx with IV 10% glucose at 5mls/kg or if
no IV access then 10% glucose by NGT
– Start on appropriate IV or IM Abx

55. • Monitoring: after 30 mins. If BG still
<3mmol/L-repeat
• Check for abd distension.
• If Deh2o rehydrate 1st

56. Hypothermia
• Often indicates coexisting hypoglycemia or
serious infxn
• Dx: Axillary temp <35oc rectal <35.5oc
• Rx:
– Feed immediately and then 2hrly unless with abd
distension
– Dress warmly-cover with a warmed blanket
– Keep dry, away from draught
– Heaters or lamp
– Put child on mothers bare chest or abdomen
– Avoid exposure to cold during procedures, bathing

57. • Monitoring:
– Monitor temp 2hrly- rectal till rises to 36.5oc,half
hourly if heater is being used.
– Ensure child is covered at all times
– Check for hypoglycemia
• Prevention
– Feed 2-3hrly
– Kangaroo technique
– Avoid child exposure to cold
– Don’t use hot water bottle of fluorescent lamp
– Change wet nappies

58. Dehydration
• Dx: assume that all children with watery
diarrhea or reduced urine output have some
dehydration
• Rx:
– No IV route unless in shock
– Resomal 5ml/kg oral every 30 mins for first 2
hours. Then 5 – 10 mls/kg each for the next 4-10
hrs on alternate hrs, with F75 formula. (the exact
amt depends on how much the child wants, vol of
stool loss and whether the child is vomiting.)

59. – If not available: ½ strength standard WHO ORS
with added k+ and glucose.
– If rehydration is still required at 10hrs, give starter
F75 instead of Resomal, at the same times. Use
same vol of F75 as of Resomal
– If in shock or severe deH20 bt cannot be
rehydrated orally or by NGT, give IVF, either RL/ ½
strength darrows with D5W. If neither is available,
0.45%saline with D5W is used

60. • Monitoring: expect RR, PR to fall and urine to be
passed. Return of tears, moist mouth, less sunken
eyes and frontanelle and improved skin tugor
– Monitor every 30 mins for 2hrs then hrly for the next
4-10 hrs
• Prevention:
– CT breastfeeding
– Initiate re-feeding with starter F75
– Give 50-100mls Resomal per loose motion

61. Na+
Mmol/l
K+
Mmol/l
Lactate*
(HCO-)
3
Glucose
Mmol/l
ORS 75 20 10 111
ReSoMal 37.5 40 5 ~ 200
INGREDIENT AMOUNT
Water 2LTRS
WHO-ORS ONE 1LTR PACKET
Sucrose 50g
Electrolyte/mineral soln 40ml

62. Electrolyte imbalance
• All severely malnourished children have
deficiencies in K+ & Mg2+
• May take 2 weeks to correct
• Ideally should receive Mg, Zn, Cu and Se as
part of mineral mix – added to milk feed.
• Rx:
– Extra K+ 3- 4 mmol/kg daily
– Extra Mg2+ 0.4 – 0.6mmol/daily

63. Infection
• Signs like fever may be absent but still infxn
present, assume all malnourished children have
an infection
• Rx:
– Start BS abx, measles vaccine if >6mths unimmunized
or vaccinated before 9mo age, albendazole
– No complications: PO amoxicillin(50mg/kg/d BD) X5
days
– Complications(hypogly,hypotherm,lethargy):Im/iv
xpen (50000IU QID) or ampicillin(50mg/kg BD) X2
days, then oral amoxicillin( 25-40 mg/kg TID) X 5 days
– Plus Genta(7.5mg/kg OD) X7 days.

64. • NB: metronidazole 7.5mg/kg TID X7 days may
be added to the BS Abx but its efficacy has not
been established in clinical trials.
• Rx other infxns as appropriate: meningitis,
pneumonia, dysentery, skin infxns, malaria
and TB)
– Parasitic worms: delay until rehab period. Give
ABZ STAT or MBZ 100mg PO BD X 3/7
– Also do PITC

65. Micronutrients
• Give daily for at least two weeks
• Vitamin A- < 6/12- 50,000 iu, 6/12-1yr-
100,000 iu ,>1 yr- 200,000 iu)on day 1, 2 and
14 – only if child has signs of def eg corneal
ulceration or Hx of measles
• Multivitamins supplement if not on RUTF
– Folic acid- 5 mg on day 1 then 1 mg/day
– Zinc – 2mg/kg/day
– Copper - 0.3 mg/kg/day

66. • NB: Vit A, folic acid , Zn and Cu present in F75,
F100 and RUTF
• Once gaining weight and good appetite,
ferrous sulphate 3mg/kg/day. From the
second week

67. Initial feeding
Essential features
• Frequent small 2-3 hrly feeds of low osmolality ,low
lactose
• Oral/NGT feeds, never parenteral
• 100 kcal/kg/d
• Protein @ 1-1.5g/kg/d
• Liquid @ 130ml/kg/d(100 if with severe edema)
• If child is breastfeeding continue but still give feeds
• Starter F75(75kcal/100ml and 0.9g protein/100ml)
• Monitoring: amt of feed and left over, vomiting ,diarrhea,
daily body wt.

69. Catch up growth
• Signs that a child has reached this phase:
– return of appetite,
– edema gone and
– no episodes of hypoglycemia

70. • Treatment:
– Gradual transition from starter to catch up
– Replace F75 with an equal amnt of
F100(100kcal/100ml and 2.9g protein/100ml) or
RUTF for 2-3 days
– On day 3 increase each successive feed by 10ml till
some remains uneaten at abt 200ml/kg/d
– Aft gradual transition give frequent feeds
unlimited amts, 150-220kcal/kg/d, 4-6g of
protein/d

71. –If on RUTF: start with small but
regular meals and encourage child to
eat often 8 meals/day. If child cannot
take > ½ of RUTF in 12hrs stop and
give F75. reintroduce again in 1-2 days
–Monitor for signs of heart failure due
to fluid overload.
–Assess progress: daily wt gain

72. Sensory stimulation
• Tender, loving care
• Structured play therapy for 15- 30 mins/d
• Physical activity as soon as the child is well
enough.
• A cheerful, stimulating environment.
• Encourage mother’s involvement e.g.
comforting, feeding, bathing, play
• Provide suitable toys for the children.

73. Associated conditions
Eye problems
• vitamin A, days 1,2,14
• Signs of corneal clouding/ulceration
– Caf/tetracycline eye drops qid for 7-10 days
– Atropine eyedrops 1 drops tid 3-5 days
– Cover with saline soaked pads
– Bandage eyes

74. Severe Anaemia
• Transfuse: Hb < 4gldl,4-6g/dl in resp distress
• Whole blood – 10 ml/kg slowly for 3hrs +
frusemide 1mg/kg iv at the start of transfusion
• Packed cells – 10 ml/kg if in CCF

75. Dermatitis of kwashiokor
• Due to zinc deficiency – replace.
• Soak/bathe areas in 0.01% potassium
permanganate sol. For 10min/day
• Apply barrier cream zinc and castor oil
ointments, petroleum jelly to raw areas, GV or
nystatin cream toskin sores
• Omit nappies/diapers, perineum can stay dry.

76. Continuing diarrhoea
• Replacement fluids CT
• Stool m/c/s and treat accordingly. giardia;
flagyl 7.5mg/kg TID x 7d
• Osmotic diarrhoea: Diarrhea worsens with
hyperosmolar F75 and ceases when sugar
content and osmolarity are reduced.Rx-lower
osmolar feeds

77. Rehabilitation
• Appetite has returned
• Principles: encourage child to eat as much as
possible, breastfeeding, emotional care,
prepare mum for continued care
• Criteria 4 Discharge : eating well, improved
mental status, normal temp, no
vomiting/diarrhea/edema, gaining weight
>5g/kg/d for 3consecutive days.
• Continue monitoring progress.

78. Discharge and follow-up
Discharge Criteria
• All infections, other conditions have been
treated
• Good appetite and gaining weight (90%
expected WH )
• Lost any oedema
• Appropriate support in the community or
home
• Mother/carer: available, understands child’s
needs, able to supply needs

79. Follow up
• Planned and regular, nutrition clinic
• Risk of relapse greatest aft discharge then
should be seen aft 1wk,2wks,1mth,3mths
• If a problem is identified more frequent visits
• Aft 6mths,do yearly visits till 3yrs of age.

80. PROGNOSIS
• Good if picked early before complications
have set in.
• Long-term effects include
• failure to thrive,
• behavioral and cognitive dysfunction,
• Small stature,
• Obstructed labour,
• Low birth wgt infants

81. PREVENTION
• Appropriate nutrition policies programmes
• Improving food security
• Protection and promotion of good health
• Appropriate care practices for good nutrition
• SUMMARY- GOBIFFF the UNICEF adaptation
– Growth monitoring
– Oral rehydration
– Breast feeding
– Immunization
– Feeds (supplements)
– Female education
– Family spacing

82. REFERENCES
• EA journal Vol. 81 No. 8 Aug 2004
• WHO Guidelines for the management of
common childhood illnesses
• EA medical journal on PEM – Aug 2004

83. ABBREVIATIONS
• WHO: World Health Organization
• I/P: In Patient
• O/P: Out Patient
• GV: Gentian Violet
• AA: Amino Acids
• EA: East Africa
• PEM: Protein Energy Malnutrition
• CT: Continue

84. ABBREVIATIONS
• RUTF: Ready To Use Therapeutic Feeds
• ABZ: Albendazole
• MBZ: Mebendazole
• ORS: Oral Rehydration Solution
• CCF: Congestive Cardiac Failure
• AA: Amino Acids
• TG: Triglycerides
• SAM: Severe Acute Malnutrition
• BS: Broad Spectrum
• Abx: Antibiotics
• LP: Lipoproteins

85. THANK YOU