this is sever acute malnutrition ppt

1. SEVERE ACUTE
MALNUTRITION
Nigus Chanie,MD(pediatrician)

2. Terms/Acronyms
 F75 -Therapeutic milk used only in Phase 1 of treatment for SAM
 F100 -Therapeutic milk used in Transition Phase and Phase 2 of
treatment of SAM (for inpatients only)
 IU -International Units
 MUAC- Mid Upper Arm Circumference
 OTP -Out-patient Therapeutic Programme (treatment of SAM at
home)
 ReSoMal -Oral REhydration SOlution for severely MALnourished
patients
 RUTF- Ready-to-Use Therapeutic Food
 SAM -Severe Acute Malnutrition (wasting and/or nutritional oedema)
 SFP- Supplementary Feeding Programme
 TFU- Therapeutic Feeding Unit (in hospital, health centre or other
facility)
 TFP- Therapeutic Feeding Programme

3. Introduction
• Food insecurity indicates inadequate access
to food for whatever reason.
• Hunger is the immediate physiologic
manifestation of inadequate food intake.
• Undernutrition describes the biochemical
and/or physical consequences of long-term
inadequate intake.
• Food insecurity, hunger, and undernutrition
are viewed as a continuum, with food
insecurity resulting in hunger, and ultimately,
if sufficiently severe and/or of sufficient
duration, in undernutrition.

4. • Approximately 18% of all individuals in
developing countries are undernourished.
In Ethiopia
 Stunting: National=47%
 wasting : National=10.5%
 Severe wasting: National=2.2%
 Underweight: National=38.4%
 More than 50% under five deaths have underlying malnutrition
 Most health facilities currently have over 20% mortality due to
SAM

5. Causes
 Immediate: Inadequate food intake & Disease
 Underlying causes: House Hold food insecurity,
Care & social env’t(drought,war) , poor access
to health & the health env't.
 Basic causes: Formal & Informal
Infrastructure,education, Political Ideology &
Resources.

6. Problems and causes of under
nutrition
 low birth weight
 maternal under nutrition
 deficiencies of specific nutrients (iodine, vitamin A,
iron, zinc)
 diarrhea
 HIV infection and other infectious diseases
 chronic illness
 inadequate infant and child feeding practices
 time constraints
 limited household income
 limited agricultural production
 food insecurity, environmental degradation
 urbanization

7. Prevention
 food insecurity and undernutrition arise
from a variety of social, economic, and
ecologic situations that vary from time to
time and from place to place.

8. SEVERE CHILDHOOD
UNDERNUTRITION
• Deficiency of a single nutrient is an example of
undernutrition or malnutrition, but deficiency of a
single nutrient usually is accompanied by a
deficiency of several other nutrients.
• Protein-energy malnutrition (PEM) is manifested
primarily by inadequate dietary intakes of protein
and energy, either because the dietary intakes of
these 2 nutrients are less than required for normal
growth or because the needs for growth are
greater than can be supplied by what otherwise
would be adequate intakes. However, PEM is
almost always accompanied by deficiencies of
other nutrients. For this reason, the term severe
childhood undernutrition, which more accurately
describes the condition, is preferred.

9.  primary malnutrition resulted from
inadequate food intake.
 secondary malnutrition resulted from
increased nutrient needs, decreased
nutrient absorption, and/or increased
nutrient losses.
 malnourished children often present with
gastroenteritis or pneumonia.

10.  Marasmus (Non-edematous SCU) believed
to result primarily from inadequate energy
intake or inadequate intakes of both energy
and protein, whereas kwashiorkor
(edematous SCU )was believed to result
primarily from inadequate protein intake.
 marasmic kwashiorkor, has features of
both disorders (wasting and edema).

11. underlying causes
• social and economic factors such as
– poverty and ignorance,
– social factors such as food taboos,
• biologic factors maternal
malnutritionLBW(prematurity)
• inadequate intakes of breast milk and other
foods
• environmental factors such as
overcrowded and unsanitary living
conditions.

12. Victims of SAM
 chronically ill patients in neonatal or
pediatric intensive care units
 patients with burns, HIV, cystic fibrosis,
failure to thrive, chronic diarrhea
syndromes, malignancies, bone marrow
transplantation, and inborn errors of
metabolism

13. PATHOPHYSIOLOGY OF SCU
• Many of the manifestations of SCU
represent adaptive responses to
inadequate energy and/or protein intakes.
In the face of inadequate intakes, activity
and energy expenditure decrease.
However, despite this adaptive response,
fat stores are mobilized to meet the
ongoing, albeit lower, energy requirement.
Once these stores are depleted, protein
catabolism must provide the ongoing
substrates for maintaining basal
metabolism.

14. • Why edematous SCU develops in some children
and non-edematous SCU develops in others is
unknown.
• Possible explanations:
1) the variability among infants in nutrient
requirements and in body composition at the time
the dietary deficit is incurred.
2) giving excess carbohydrate to a child with non-
edematous SCU reverses the adaptive responses
to low protein intake, resulting in mobilization of
body protein stores. Eventually, albumin synthesis
decreases, resulting in hypoalbuminemia with
edema. Fatty liver also develops secondary,
perhaps, to lipogenesis from the excess
carbohydrate intake and reduced apolipoprotein
synthesis.

15. 3). Aflatoxin poisoning as well as diarrhea,
impaired renal function and decreased Na+
K+ ATPase activity.
4). Free radical damage has been proposed as
an important factor in the development of
edematous SCU. This proposal is supported
by low plasma concentrations of
methionine, a dietary precursor of cysteine,
which is needed for synthesis of the major
antioxidant factor, glutathione. This
possibility also is supported by lower rates
of glutathione synthesis in children with
edematous compared with non-edematous

16. End organ effects of
malnutrition
 Body composition
 Total body water increases(ECF)
 Increased Na+
 Decreased K+ and Mg++
 Muscle and fat loss
 GIT
 Villus atrophy
 Reduced enzymes
 Bacterial over growth

17. End organ effects of
malnutrition
 Liver
 Reduced synthesis of protein
 Impaired gluconeogenesis
 Decreased metabolism of toxins and substances
 Cardiac
 Myocardial atrophy, reduced cardiac out put ,
decreased BP
 Hematology :anemia
 Metabolic
 Hypoglycemia
 Reduced metabolic rate

18. End organ effects of
malnutrition
 Immunity
 Impaired especially the Cell mediated
 Reduced IgA
 Reduced phagocytosis
 Inflammatory response
 Impaired acute phase response
 Reduced chemotaxis of WBC to site of infection/
inflammation
 Prone to infectious agents/subtle signs

19. Marasmus
• characterized by the wasting of muscle mass and the
depletion of body fat stores.
• It is the most common form of PEM and is caused by
inadequate intake of all nutrients, but especially
dietary energy sources (total calories
• Physical examination findings include:
• Diminished weight and height for age
• Emaciated and weak appearance
• Bradycardia, hypotension, and hypothermia
• Thin, dry skin
• Redundant skin folds caused by loss of subcutaneous fat
• Thin, sparse hair that is easily plucked

20. Kwashiorkor
• characterized by marked muscle atrophy with normal or
increased body fat
• caused by inadequate protein intake in the presence of
fair to good energy intake.
• Anorexia is almost universal.
• Physical examination findings include:
• Normal or nearly normal weight and height for age
• Anasarca
• Pitting edema in the lower extremities and periorbitally
• Rounded prominence of the cheeks ("moon-face")
• Pursed appearance of the mouth
•

21. Kwashiorkor
 Dry, atrophic, peeling skin with confluent areas
of hyperkeratosis and hyperpigmentation
• Dry, dull, hypopigmented hair that falls out or is
easily plucked
• Hepatomegaly (from fatty liver infiltrates)
• Distended abdomen with dilated intestinal loops.
• Adequate protein intake restores hair color,
resulting in alternating loss of hair color
interspersed between bands of normal
pigmentation (flag sign)

24. Marasmus -kwashiorkor
• occur in a child who has inadequate dietary
intake of all nutrients and subsequently
develops a common infectious illness of
childhood.
• the undernourished child develops
hypoalbuminemia and edema because the
acute loss of nutrients associated with an
inflammatory response is superimposed on the
chronic wasting of body fat and muscle
nutrient stores.

25. Anthropometric assessment
– During periods of nutritional deprivation, weight
deficits occur initially, followed by length or height
deficits and, finally, by head circumference deficits.
– height-for-age an index of the cumulative effects
of under nutrition during the life of the child.
– weight-for-age reflects the combined effects of
both recent and longer-term levels of nutrition.
– weight-for-height reflects recent nutritional
experiences.
– Values <80–90% of expected are considered
abnormally low.
– Non specific to reflect causes

26. Gomez , welcome, waterlaw
 Gomez : wt for age=wt of subject/wt of normal
child of same ageX100
 Short comings
 Did not differentiate b/n acute vs chronic and
types of malnutrition.
 Age may not be known in developing countries
Wt for age Degree of malnutrition
90-109% normal
75-89% mild
60-74 moderate
<60 severe

27.  Welcome uses the weight for age measured
by Harvard curve. It differentiate b/n the types
of malnutrition but not whether whether acute
or chronic.
Wt for age
Edema 60-80% <60%
absent Under wt Marasmus
present kwashiorkor Marasmic-
kwsahiorkor

28.  Water low is better in understanding the type
of malnutrition and its duration. Wasting
showing acute malnutrition and stunting
showing chronic malnutrition.
Wt for ht % Nutritional
status
Ht for age% Nutritional
status
90-100 normal >95 normal
85-90 Mild wasting 90-95 Mild stunting
75-85 Moderate
wasting
85-90 moderate
<75 Severe wasting <85 Severe stunting

29. Wasting
• The severity of wasting is determined as a percentage
of the expected weight for height for the population.
• The expected weight for height is determined by
plotting the child's height on the 50th percentile line of
the standard growth curve (usually reflecting the size
of a younger child) to determine the child's height age
and then finding the 50th percentile weight for that
age. Severity is assigned as follows :
•Less than 90 percent: First-degree (mild) acute malnutrition
•Less than 80 percent: Second-degree (moderate) acute
malnutrition
•Less than 70 percent: Third-degree (severe) acute
malnutrition.

30. Stunting
• The severity of stunting is determined as a
percentage of the expected height for age . The
measured height is divided by the expected height
for age and multiplied by 100. Severity is assigned
as follows
• Less than 95 percent: First-degree (mild) chronic
malnutrition
• Less than 90 percent: Second-degree (moderate)
chronic malnutrition
• Less than 85 percent: Third-degree (severe) chronic
malnutrition

31. Arm/head circumference
• McLaren described an alternative approach to estimate the
degree of acute malnutrition in children younger than three
years of age and for whom accurate measures of weight or
height cannot be obtained .
• This method uses the mid-upper arm circumference as a
proxy for weight, and head circumference as a proxy for
height. Its accuracy requires that no malformation of the head
(eg, microcephaly or hydrocephalus) is present.
• The degree of acute malnutrition is calculated by dividing the
mid-upper arm circumference by the fronto-occipital (head)
circumference. Severity is assigned according to the ratio as
follows
• Less than 0.31: First-degree (mild) acute malnutrition
• Less than 0.28: Second-degree (moderate) acute malnutrition
• Less than 0.25: Third-degree (severe) acute malnutrition

33. Laboratory Features of Severe
Malnutrition
VARIABLES INFORMATION DERIVED
Hemoglobin, hematocrit, erythrocyte count,
mean corpuscular volume
Degree of dehydration and anemia; type of
anemia (iron/folate and vitamin B12
deficiency, hemolysis, malaria)
Glucose Hypoglycemia
Electrolytes and alkalinity
Sodium Hyponatremia, type of dehydration
Potassium Hypokalemia
Chloride, pH, bicarbonate Metabolic alkalosis or acidosis
Total protein, transferrin,(pre-)albumin Degree of protein deficiency
Creatinine Renal function
C-reactive protein, lymphocyte count,
serology, thick and thin blood films
Presence of bacterial or viral infection or
malaria
Stool examination Presence of parasites

34.  As needed urine, stool, and blood culture cane
be done .
 If there is any clue for pneumonia, tuberculosis
or CXR can be ordered.

35. SAM/SCU
Management

37. Appetite TEST
Why do we do appetite test?
No signs of clinical infection in children with SAM
No perfect correlation between metabolic malnutrition & anthropometric
malnutrition
Metabolic malnutrition is the common cause of death and often its sign is
loss of appetite
Appetite test is the most important criteria to admit SAM either to inpatient
or OTP
Poor appetite means significant infection or metabolic
dysfunctions like liver dysfunction, electrolyte imbalance and
high risk of death.

39. Criteria for OTP(6month-18yrs)
All children with SAM, which means
 weight for height<70%,
 MUAC<11cm
 edema +/++) and:
 Who passed appetite test
 Clinically well
 Alert
 No +++ edema
 Do not have marasmic kwashiorkor

40. Inpatient care(6month-18yrs)
• Bilateral pitting oedema Grade 3 (+++)
• Marasmus-Kwashiorkor (W/H<70% with
oedema or MUAC<11cm with oedema)
• Severe vomiting/ intractable vomiting
• Hypothermia: axillary’s temperature < 35°C or
rectal < 35.5°C
• Fever > 39°C
• respiratory distress

41. Inpatient care(6month-18yrs)
• Extensive skin lesions / infection
• Very weak, lethargic, unconscious
• Fitting/convulsions
• Severe dehydration based on history & clinical
signs
• Any condition that requires an infusion or NG tube
feeding.
• severe anaemia
• Jaundice
• Bleeding tendencies
• Failed appetite test

42. Admission in Adults
 MUAC < 170 mm or
 MUAC < 180 mm with recent weight loss or
underlying chronic illness or
 BMI5 < 16 with or
 Presence of bilateral pitting oedema (unless
there is another clear cut cause)

43. Preparation of F75 and F100
Diets
F75(to prepare 100ml) F100(to prepare 100ml)
Dried skim milk 25 g 80 g
Sugar 70 g 50 g
Cereal flour 35 -
Vegetable oil 27 g 60 g
Mineral mix 20ml 20ml
Vitamin mix 140mg 140mg
Water to make 1000ml 1000ml

45. There are ten essential steps
1.Treat/prevent hypoglycaemia
2.Treat/prevent hypothermia
3.Treat/prevent dehydration
4.Correct electrolyte imbalance
5.Treat/prevent infection
6.Correct micronutrient deficiencies
7.Start cautious feeding
8.Achieve catch-up growth
9.Provide sensory stimulation and emotional support
10. Prepare for follow-up after recovery

46. Ten essential steps of
Rx(SAM)

47. Treatment of complications in SAM
Dehydration
Hypovolemic shock
Septic shock
Absent bowel sounds, gastric dilatation and intestinal
splash with abdominal distension
Heart Failure
Hypothermia
Severe anemia
Hypoglycemia
K.Dermatosis

48. Hypoglycemia
 Blood glucose<3mmol/L(<54mg/dl)
 Important cause of death in 1st 2days
 Hepatic energy production from galactose & fructose is
much slower
 Gluconeogenesis is limited
 Serious infection/not fed in the last 4-6hr, vomited or
too weak to fed or waiting for admission
 S/S include: hypothermia, limpness/drowsiness, lethargy,
loss of conscousness,lid retraction
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49. Treat Hypoglycemia
 50ml 10% glucose/sucrose immediately oral/NGT
 If only 50% glucose: 1 part in 4 part of sterile solution or
boiled water
(5-10ml/kg 10% SW=50ml or F75 or F100 by mouth or NGT)
 Unconscous-5ml/kg 10% glucose solution iv followed by 50ml
10% glucose or sucrose via NGT
 second line antibiotic for all suspected
 Start feeding F75 half an hour after glucose, give 1/4th of the
2hourly dose Q30min in the 1st 2 hrs
 Usually respond rapidly to this treatment, if not suspect other
causes
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50. Marasmus and dehydration
• History is important than the physical findings
• Change in mentation/behavior
• Urine volume decreases if there is dehydration
• Recent change in weight if dehydrated
• Eye ball sunken in both
• Quality of pulse – weak and thready when
dehydrated.
• The oral mucosa is dry if there is dehydration
(may be wet if vomited recently).
• Skin pinch goes slowly in both

51. distinguishing clinical features
b/n dehydration and sepsis
• Hx of diarrhea/vomiting can occur in both
conditions
• Urine amount may be decreased in both
• Hypothermia is common in sepsis than
dehydration
• weak or absent pulses, are likely to occur in
septic shock rather than dehydration (although
cold hands and feet may occur in either
condition)

52. distinguishing clinical features
b/n dehydration and sepsis
• thirst, and sunken eyes and fontanel, which
are characteristic of dehydration and do not
occur in sepsis.
• typical signs of dehydration (eg, lack of
moisture of the mouth and poor skin elasticity)
are not reliable in severely malnourished
children.
• Mental status changes are present in
some/severe dehydration and sepsis.

53. Diagnose & treat Dehydration
Dehydration Dx and Mgt in Marasmus
Diagnosis
 Difficult, needs definite history of significant fluid
loss/diarrhea AND recent change in child’s appearance-
sunken eyes proven by mother.
 No edema.
 Diagnosis is presumptive not definite.
 Shock with dehydration: weak pulse, cold hands and
feet, if unconscious  severe shock

54. Treatment of dehydration
 Never use the standard protocol for well nourished child & not
ORS but RESOMAL
 Whenever possible hydrate only orally
 IV fluids are dangerous, use only if severe shock with loss of
consciousness from confirmed dehydration
 Re-Hydrate the child until wt deficit is corrected (usually 5%)
 Give a total of 50ml per kg in 12hr
- Start 5ml/kg Q30min for 1st 2hrs then 5-10ml/kg per hour

55. Dehydration Rx …
- Assess wt, liver size, PR, RR, heart sounds Q1hr
- For dehydrated 6-24month child give 30ml Resomal per loss
 If still losing wt=>increase rate of Resomal by 10ml/kg/hr
 If No wt gain=> increase rate by 5ml/kg/hr
 Wt gain and child deteriorates=> stop Resomal & give F75
 Wt gain and no improvement=>change to F75 or alternate
with Resomal
 If improving but still with signs of dhn=> continue until
target wt with Resomal alone or alternate with F75

57. Shock from dehydration
 Definite dehydration+ semi/unconscious, rapid weak
pulse/slow capillary refill & cold feet & hands
 Use IV fluid-R/L with 5%dextrose or half strength
saline with 5%dextrose
 Give 15ml/kg over first hour & reassess, if still wt loss
or stable wt repeat the same until wt gain but if no
improvement assume septic shock and manage
 As soon as child is conscious with good pulse-stop IV,
give oral or by NGT-follow by wt change
 NO IV DRIP NEAR MALNOURISHED CHILD
WHO CAN DRINK OR USE NGT

58. Kwashiorkor and dehydration
 All edematous children have high water and sodium
retention hence over hydrated
 If there is definite watery diarrhea & child clinically
deteriorating-replace with Resomal 30ml per watery
diarrhea
Septic shock
 signs similar with shock of DHN
 Manage the same + antibiotics (1st & 2nd line
antibiotics), treat hypoglycemia, prevent hypothermia

59. Management of heart failure
 HF when?
-usually starts after mgt of SAM-iv infusion/ORS/high Na diet,
blood or plasma transfusion, severe anemia
-deterioration with wt gain
-RD with wt gain -Enlarged tender liver
-Increase in RR-Fast breathing/RD
-grunting, creptations, prominent superficial &
neck veins
-Triple rhythm, increase/appearance of edema
-the 3rd type of shock-Cardiac shock
-Pneumonia is less likely in a child with RD after
wt gain
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61. Treatment of heart failure
 Stop all oral or IV intakes/No fluid or food for 24-48
hours until managed
 Give sugar water to prevent hypoglycemia
 Furosemide 1mg/kg single dose
 Digoxine 5microgram/kg single dose
 If there is also severe anemia, treat the HF first than
the transfusion
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62. Severe anemia
 Hgb<4gm/dl or Hct<12% in first 24 hours after
admission
 Give Packed cell or whole blood 10ml/kg over 3hours
 Keep child NPO during and 3hours after transfusion
 Do not transfuse a child between 48hrs after the start of
F75 and 14days later
 ? Furosemide 1mg/kg iv (WHO)
 No Iron treatment in the first phase
 Exchange transfusion is the best option
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63. Prevent/treat Hypothermia
 Rectal temp <35.5dc or axillary <35dc
 Children should always sleep with their caretakers, dry
well after bath, keep away from open window, cover head
 Keep warm- cover at night kangaroo technique, wrap
with mother, hot drinks to mother, blanket
 Keep room temperature 28-32dc
 Treat hypoglycemia
 Give second line antibiotics/treat infection
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64. Treat Infection/Vit A/FA/Antimalarial
 Start with amoxicillin oral to all cases with SAM
 If complications add Gentamycin / CAF/Augmentin
 Usually add antibiotic if no improvement in 48 hours of
amoxicillin
 Consider 3rd line: Cloxacilline, Ceftriaxone
 Consider antifungal: fluconazole in sepsis
 Treat Oral thrush
 Vit.A (none edema) & FA (for anemic cases)
 Ant malarial(national protocol)
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65. HIV and other condition
• Management of SAM is the same
• Start nutritional treatment at least a week before
ART, anti TB (except miliary TB)
• If a must to start in PI start with reduced dose
• Cotrimoxazole preventive therapy will not replace
amoxil
• Avoid toxic drugs
• Standard doses of drugs for HIV/TB are used in
PII/OTP
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67. Phase 1
• Patients with poor appetite and/or a major
medical complication.
• F75(130ml = 100kcal) promotes recovery of
normal metabolic function and nutrition-
electrolytic balance.
• Breast-fed children should always be offered
breast-milk before the diet and always on
demand.
• Rapid weight gain at this stage is dangerous,
that is why F75 is formulated so that patients
do not gain weight during this stage.

68. Feeding and NGT use
Indications for NGT use
 Taking <75% of prescribed milk in 24h in phase one
 Pneumonia with rapid RR/Respiratory distress
 Cleft palate or other oral deformities
 Painful mouth lesions
 Unconscious or lethargic child
 Use NGT only in Phase I and for max 3 days, try oral feeding at every
feeding

69. Criteria to move from Phase I to transition phase
or Stabilization Center(SC) /TFU Exit criteria
 Return of appetite
 Edema reduced
 Clinically well
 No NGT or IV line
If there is an OTP these children are transferred to OTP

70. Transition Phase
• Important to avoid electrolyte disequilibrium.
• The diet used is F100(100ml=100kcal)
• Quantity of F100 given is equal to the quantity
of F75 given in Phase 1or an equivalent
amount of RUTF.
• Expected weight gain should be around 6
g/kg/day.

71. Move the child back to Phase 1
 If the patient gains weight more rapidly than
10g/kg/d
 increasing or new onset oedema
 rapid increase in the size of the liver
 significant re-feeding diarrhoea and weight
loss.
 If patient develops medical complication
 If Naso-Gastric Tube is needed
 Patient taking less than 75% of the feeds in
Transition Phase.

72. CRITERIA TO PROGRESS FROM
TRANSITION PHASE TO PHASE 2
 A good appetite, taking at least 90% of the RUTF
or F100 prescribed for Transition Phase.
 Oedematous patients (kwashiorkor) should
remain in Transition Phase until there is a definite
and steady reduction in oedema (now at + level).
 Inpatients should remain in Transition Phase until
they have lost their oedema entirely.
 Out -patients can go when their appetite is good
(taking all the diet in Transition Phase - not just in
the moderate range) and they have reduced their
oedema to ++ or +.

73. Phase 2
• Whenever patients have good appetite and no
major medical complication they enter Phase
2.
• Many patients with a good appetite can be
admitted directly into Phase 2.
• Give RUTF (used in both in-patient and out-
patient settings) or F100 (used in in-patient
settings only) according to look-up tables.
• Expected weight more than 8 g/kg/day.
• Start deworming and iron supplementation

74. MOVE BACK FROM PHASE 2 TO PHASE
1
 Failure of the appetite test
 Increase/development of oedema
 Development of refeeding diarrhoea sufficient to lead
to weight loss.
 Fulfilling any of the criteria of “failure to respond to
treatment”
 Weight loss for 2 consecutive weighing
 Weight loss of more than 5% of body weight at any
visit.
 Static weight for 3 consecutive weighing
 Major illness or death of the main caretaker so that
the substitute caretaker requests inpatient care

75. Surveillance

76. Discharge /transfer criteria
inpatient & outpatient 6mo-18yrs
Option I: WFH >85% if no SFP or >80% where there
is SFP( for 2days in INP and 2 weeks in OTP) and
no edema for 10days in INP or 14days in OTP
Option II: Target weight gain reached and no edema
for 10days in INP or 14days in OTP
All discharges send to Supplementary Feeding Program
(SFP)

77. The Do NOT DOs
1. Do NOT give DIURETICS to treat Edema
2. Do NOT give IRON during the Initial feeding
phase-add iron only after the child has been on
F100 for 2days
3. Do NOT provide high protein formula, over
1.5gm/kg/day in initial phase
4. Do NOT give IV Fluids routinely

78. Infants< 6 months
 ADMISSION CRITERIA
 Infant less than 6 months or less than 3 kg with
no prospect of being breastfed
 W/L (weight-for-length ) < 70% or
 presence of bilateral oedema.

79. PHASE 1 - TRANSITION – PHASE 2
 When there is no prospect of being given
breast milk then severely malnourished, less
than 6 month’ old infants, should be treated
according to the standard protocol with the
following modifications. Phase 1
 Wasted, marasmic infants of less than 6
months can be given F100 diluted in Phase 1.
 Oedematous infants of less than 6 months
should always be given F75 during phase one.

80.  Transition Phase and Phase 2
 During Transition Phase, only F100 diluted should
be used.
 These small infants should not be treated with full
strength F100.
 DISCHARGE CRITERIA
 When they reach 85% weight for length they can
be switched to infant formula.
 All infants less than 6 months old discharged from
therapeutic feeding have to be followed-up
monthly until their reach six months of age.

81. Play, emotional well being,
stimulation
 Emotional and physical stimulation through play
programmes should start during rehabilitation and
continued after discharge can substantially reduce
the risk of permanent mental and emotional
damage.
 understand the emotional needs of malnurished
children and create a friendly supportive
atmosphere.
 the mother should be encouraged to feed, hold,
comfort and play with her child as much as
possible.
 Safe and cheap toys should be available in the

82. FAILURE TO RESPOND
 Problems with the treatment facility
 Problems of individual children

83. Criteria for Failure

84. Problems with the treatment
facility
 In –patients
 Poor environment for malnourished children
 Failure to treat the children in a separate area
 Failure to complete the multichart correctly
 Insufficient staff (particularly at night)
 poorly trained staff
 Inaccurate weighing machines
 Food prepared or given incorrectly

85. Problems with the treatment
facility
 Out – patients
 Inappropriate selection of patients to go directly to
OTP
 Poorly conducted appetite test
 Inadequate instructions given to caretakers
 Wrong amounts of RUTF dispensed to children
 Excessive time between OTP distributions (e.g. two
weekly gives significantly worse results than weekly
visits)

86. Problems of individual
children
In –patients
 Insufficient food given
 Food taken by siblings or caretaker
 Sharing of caretaker’s food
 Vitamin or mineral deficiency
 Malabsorption
 Psychological trauma (particularly in refugee situations
and families living with HIV/AIDS)
 Rumination
 Infection, especially: Diarrhoea, dysentery, pneumonia,
tuberculosis, urinary infection/ Otitis media, malaria,
HIV/AIDS, Schistosomiasis/ Leishmaniasis, Hepatitis/
cirrhosis,
 Other serious underlying disease: congenital abnormalities
(e.g. Down’s syndrome), neurological damage (eg cerebral
palsy), inborn errors of metabolism.

87. Problems of individual
children
Out – patients (In addition to all of the above)
 Sharing within the family
 Sibling rivalry (other children taking the diet)
 All eating from the same plate (the malnourished
child should always have his/her own portion of
food).
 Unwilling caretaker
 Caretaker overwhelmed with other work and
responsibilities

88. Consequences
• acute effects on morbidity and mortality
– severely underweight children (<60% of reference
weight for age) have more than an 8-fold greater
risk of mortality than normally nourished children
– moderately underweight children (60–69% of
reference weight for age) have a 4- to 5-fold
greater risk of death
– mildly underweight children (70–79% of reference
weight for age) have a 2- to 3-fold greater risk.
– >50% of child deaths may be caused directly or
indirectly by undernutrition. Moreover, 83% of
these deaths result from mild to moderate forms
of undernutrition. A major factor is the
potentiation of infectious diseases by
undernutrition.

89. • Survivors of childhood malnutrition have
deficits in cognitive function and school
performance ,work productivity , economic
growth
• Mean deficits in scores on standard tests
of cognition range from 5–15 points.
• severely undernourished children have
greater deficits in cognitive performance
than children with mild or moderate
undernutrition.

90. References
 Nelson text book of pediatrics 18th edition
 Up to date 18.2
 Ethiopian guideline for SAM, March 2007.
 WHO guideline for SAM, 2003
 Pediatrics and child health lecture note for
Health science students, Jimma university,
2006.