Recognizing and

Treating Malnutrition
in Children

REHEMA MARANDO MD,MMED

(PEDIATRICIAN)
Outline

 Background
 Definitions and Diagnosis
 Causes of malnutrition
 Reductive adaptation
 Refeeding syndrome
 WHO’s 10 Steps
 Complications and Challenges
 Summary
Background
 Malnutrition contributes to ~6 million deaths
annually to children < 5
 Over a third of child deaths are due to maternal and
child undernutrition
 80% of the world’s undernourished live in just 20
countries – Tanzania is ONE of them!
 Demographic and Health Survey data 2005,
Tanzania
 40,000 severely malnourished children
 450,000 moderately wasted children
 2.4 million chronically malnourished children
Diagnosing Severe
Malnutrition
Definitions
 The World Health Organization (WHO)
defines malnutrition as
 “the cellular imbalance between the
supply of nutrients and energy, and the
body’s demand for them to ensure
growth, maintenance and specific
functions’’
Classification of malnutrition

 Severe acute malnutrition is defined as:

 -Severe wasting (weight for height/length <70% or <-3SD or
MUAC <11.5 cm) and/or
 - Oedema of both feet

 Moderate acute malnutrition is defined as:

 - Moderate wasting (weight for height/length 70-79% or -3SD and
<-2SD or MUAC ≥11.5 and < 12.5cm) with no oedema
 
 
 Acute Malnutrition is classified into severe acute malnutrition
(SAM) and moderate acute malnutrition (MAM) according to the
degree of wasting and the presence or absence of oedema.
 Currently used Anthropometric
Measurements are:
 
 Weight for Length or Height (Wt/Lt or Ht) = Wasting
 Length or Height for Age (Lt or Ht/Age) = Stunting
 Mid-Upper Arm Circumference for Age (MUAC/Age) = Wasting

 
 The Interpretation:
 Weight for Length or Height; If it is:
 Between Median and Minus one standard deviation: Median and –1SD: Normal
 Between Minus one standard deviation and minus two standard deviation: -
 1SD and -2SD; Mild Wasting (Mild Malnutrition)
 Between Minus two standard deviation and minus three standard deviation
 -2SD and -3SD: Moderate Wasting (Moderate Malnutrition).
 Below Minus three standard deviation:
<-3SD: Severe Wasting (Severe Malnutrition).
 

 
Conceptual framework for
causes of malnutrition
 Causes of malnutrition including severe malnutrition
are diverse and interrelated. The causes can be
explained in three levels; Immediate, Underlying
and Basic. Immediate caused by inadequate
dietary intake and diseases, Underlying caused by
insufficient household food security, Inadequate
child and maternal care, insufficient health services
and unhealthy environment; Basic causes include
fundamental issues surrounding policy, political will
and the institutional framework and structures
governing access to and distribution of resources for
human development.
 Physiological changes that occur in severe
malnutrition

Reductive Adaptation
 When a child’s intake is insufficient, fat stores are mobilised to
provide energy. Later protein is mobilised from muscle, skin and
the gut. Physiological and metabolic changes also take place to
conserve energy. These changes take place in an orderly
progression called reductive adaptation. Energy is conserved
mainly by:
 Reducing physical activity and growth
 Reducing basal metabolism by:
 - Slowing protein turnover
 - Reducing the functional reserve of organs
 - Slowing the sodium and potassium pumps in cell
membranes and reducing their number
 Reducing inflammatory and immune responses
 Malnourished children are not usually brought to hospital because
of their malnutrition. They usually come because they have
diarrhoea, or pneumonia.
Consequences (1)
T The liver is less able to make glucose, increasing the risk of hypoglycaemia and
hypothermia. The liver is also less able to excrete excess dietary protein and toxins. These
changes have implications for feeding. First, long gaps without food must be avoided. This
needs processing children quickly in the outpatient queue, giving frequent feeds day and
night, and using a nasogastric tube if reluctant to eat. Second, a ready source of glucose is
needed. Third we must limit the amount of protein to avoid stressing the liver.

Consequences (2)
The heart is smaller and weaker and has a reduced output. Any excess fluid in the circulation
stresses the heart and can lead to death from heart failure. This means that fluid intake
must be carefully controlled initially. Also feeds, and rehydration fluid, must be low in
sodium.

The kidneys are less able to excrete excess fluid and sodium. So excess fluid (from feeds or
rehydration fluid) can quickly build up in the circulation.

The gut produces less acid and smaller amounts of enzymes and Villi become flattened.
Motility is reduced and bacteria may colonise the stomach and small bowel, damaging the
mucosa and de-conjugating bile acids. So, initially, feeds must be small to avoid exceeding
the gut’s functional capacity, and the composition of feeds must also be considered.
  
 Consequences (3)
 During reductive adaptation, sodium goes into cells due to fewer
and slower pumps, leading to excess body sodium. Potassium
leaks out of cells and is lost in urine, contributing to electrolyte
imbalance, anorexia, fluid retention and heart failure. So we need
to restrict sodium, and provide potassium. We must also provide
Magnesium to help the potassium get into cells.

 Consequences (4)
 Reduction in muscle mass is accompanied by loss of
intracellular nutrients (of K, Mg, Zn and Cu) and smaller reserves
of muscle glycogen.

 Red cell mass is also reduced, liberating iron. Conversion of

ferrous (harmful ‘free’ iron) to ferritin needs glucose and amino
acids, and there may not be enough available to put all the iron
into safe storage. Free iron promotes the growth of pathogens
and the production of free radicals which damage cell
membranes. So during initial feeding, we need to withhold iron,
and provide vitamins and minerals to help mop up free radicals.
  
  Children with protein-energy malnutrition (PEM) also may
have deficiencies of the fat-soluble vitamins: A, D, E, and k

 Vitamin A — Vitamin A deficiency is common in resource-

limited countries . It is associated with a group of ocular
signs known as xerophthalmia.
 The earliest symptom is night blindness, which is followed
by xerosis (dryness) of the conjunctiva and cornea , and
development of Bitot's spots (triangular areas of abnormal
squamous cell proliferation and keratinization of the
conjunctiva) (p].
 Progression of disease includes keratomalacia (softening),
ulceration, perforation and scarring of the cornea; prolapse
of the lens; and blindness. Other features of vitamin A
deficiency include follicular hyperkeratosis, pruritus, growth
retardation, and increased susceptibility to infection .
Randomized trials have shown that routine vitamin A
supplementation to children in endemic areas is associated
with a reduction in diarrhea-related and possibly in all-
cause mortality.
 Vitamin D — Deficiency of vitamin D, typically caused by dietary
deficiency and inadequate exposure to sunlight, is associated
with hypocalcemia, hypophosphatemia, and rickets in children
and osteomalacia in adults Defective bone growth is caused by
a failure of mineralization of uncalcified osteoid and cartilage
resulting in a wide irregular zone of poorly supported tissue and
numerous characteristic skeletal abnormalities including:

 ●Craniotabes, caused by thinning of the outer table of the skull

 ●Enlargement and delayed closure of the anterior fontanelle
 ●Frontal bossing of the skull
 ●Delayed eruption of the teeth and tooth enamel defects
 ●Beading of the ribs (rachitic rosary)
 ●Scoliosis
 ●Exaggerated lordosis
 ●Bowlegs in older infants
 ●Greenstick fractures in the long bones
 Radiographic changes include widening, concave cupping, and
frayed poorly demarcated ends of long bones with metaphyseal
flaring.
 Vitamin E — Tocopherol deficiency can be
associated with a progressive sensory and
motor neuropathy, ataxia, retinal
degeneration, and a hemolytic anemia.
 Vitamin K — Deficiency of vitamin K results
in a bleeding diathesis. Bleeding may be
seen in the skin, the gastrointestinal tract,
genitourinary tract, gingiva, lungs, joints, or
the central nervous system.
 WATER SOLUBLE VITAMIN DEFICIENCIES 

 Deficiencies of water-soluble vitamins are seen with

protein-energy malnutrition (PEM) in resource-limited
countries but are less common than are deficiencies of fat-
soluble vitamins

 Folate — Folate deficiency is characterized by

hypersegmentation of neutrophils, megaloblastosis and
anemia. Folate deficiency can cause growth faltering, even
in the absence of anemia. Low serum folate levels are also
found in children with zinc and vitamin B12 deficiencies.
Medications such as phenobarbital increase the need for
folate .

 The World Health Organization (WHO) recommends

empiric treatment of all severely malnourished children with
folate . It is also important to provide adequate amounts of
zinc at the same time, as part of overall nutritional
rehabilitation, because folic acid treatment can inhibit zinc
absorption.
 Niacin — Niacin (vitamin B3) deficiency results in pellagra
with dermatitis, diarrhea, dementia, and weakness.
 ●The dermatitis is localized to sun-exposed areas of the
body. The skin is dry, cracked, hyperkeratotic, and
hyperpigmented.
 ●Watery diarrhea, as well as colitis, may be pronounced.
Vomiting also may occur.
 ●Neurologic findings include peripheral neuropathy,
irritability, headache, insomnia, loss of memory, emotional
instability, toxic psychosis associated with delirium and
catatonia, seizures, and coma.
 ●Oral manifestations include cheilosis, angular fissures,
atrophy of the tongue, hypertrophy of the fungiform
papillae, and painful inflammation of the mouth, which may
lead to refusal of food.
 Pyeridoxin — Pyridoxine (vitamin B6) deficiency manifests
as nonspecific stomatitis, glossitis , cheilosis, irritability,
confusion, weight loss, and depression. Peripheral
neuropathy occurs in adolescents, whereas younger
children develop encephalopathy with seizures
 Thiamine — Thiamine (vitamin B1) deficiency is
classically associated with beriberi, characterized by
high output cardiomyopathy and polyneuritis.
Infantile beriberi occurs in infants between one and
four months of age who have protein-energy
malnutrition, are receiving unsupplemented
hyperalimentation fluid or boiled milk, or are
breastfed by mothers who are deficient in thiamine .
Infants with beriberi have a characteristic
hoarseness or aphonic cry caused by laryngeal
paralysis.

 Riboflavin — Riboflavin (vitamin B2) deficiency is

characterized classically by angular stomatitis,
glossitis (magenta tongue) , seborrheic dermatitis
around the nose and scrotum, and vascularization of
the cornea .
 Pyridoxine — Pyridoxine (vitamin B6) deficiency
manifests as nonspecific stomatitis, glossitis , cheilosis,
irritability, confusion, weight loss, and depression.
Peripheral neuropathy occurs in adolescents, whereas
younger children develop encephalopathy with seizures.

 Vitamin B12 — Vitamin B12 deficiency is uncommon in

children but can occur in exclusively breastfed infants of
mothers eating a strict vegetarian (vegan) diet, or with
vitamin B12 malabsorption due to gastric bypass, short
bowel syndrome, or pernicious anemia . In under-
nourished children, subclinical vitamin B12 deficiency
contributes to poor linear growth and weight gain . Overt
deficiency may cause megaloblastic anemia , atrophic
glossitis , neuropathy, and demyelination of the central
nervous system. Infants may present with nonspecific
symptoms, including weakness, failure to thrive, tremors,
and irritability . If untreated, irreversible cognitive deficits
may occur
Weight-for-
Height
Reference
Table

© 2007 Baylor College of Medicine

 Wasting vs Stunting

Wasting Stunting
 Decreased weight  Weight and height
relative to height decreased
 Almost always from  Weight-for-height normal
acute nutritional
deficiency resulting in
 Can result from any chronic
loss of subcutaneous disease
fat  Do not require hospital
 Severely wasted admission unless they have
children frequently another serious illness
require hospital
admission
Marasmus
(‘Wasting Malnutrition’)

 Generally wasted
 Thin arms
 Thin face; “old man”
 Ribs visible
 Sunken eyes
 Lack of skin turgor
Marasmus
(‘Wasting Malnutrition’)

Not only seen in the very

young
HIV serology should be
done if status unknown
Kwashiorkor
(‘Edematous Malnutrition’)

 Must have bilateral,

(usually) pitting edema
 Commonly associated
features:
 Apathetic/miserable
 Enlarged liver
 Dermatosis
 Mucous membrane
changes/angular chelitis
 Hair changes:
 Thin/sparse
 Discoloured; fragile
Kwashiorkor
Kwashiorkor
 Classification of Edema

 Kwash edema starts at

feet and spreads up:
 1+ feet only
 2+ feet & shins
 3+ whole body, including
face
  firm pressure, 5 seconds
Maggie’s Wt/Ht is <60%
Diagnosis?

 CHECK CHART for

wt/ht!
 Make sure she has no
edema – she may be
Marasmic-Kwash rather
than just Marasmus
Severely Malnourished
Children Need Different Care
 WHY?
 Loss of muscle and a damaged liver  high risk for
hypoglycemia
 Loss of body fat  increased risk for hypothermia
 Gut and liver cannot cope with normal meals
 The heart EASILY goes into failure if too much fluid is
given
 Loss of fat and muscle make it difficult to diagnose
dehydration
 Weakened immune system  infections may easily be
missed
Severely Malnourished
Children Need Different Care
 This Means That Severely Malnourished
Children Must Be:
 Fed differently
 Rehydrated differently
 Treated with antibiotics even if no clinical signs of
infection
 Given special nutrients to correct imbalances
 Given special care (not kept waiting for
admission, kept warm, etc.)
WHO’S 10 Steps: Management
of Severe Acute Malnutrition
1. Prevent/treat hypoglycemia
2. Prevent/treat hypothermia
3. Prevent/treat dehydration
4. Correct electrolyte imbalances
5. Treat/prevent infections
6. Correct micronutrient deficiencies
7. Start cautious feeding
8. Give catch-up diet
9. Sensory stimulation
10. Discharge and follow-up
Step 1: Prevent/Treat
Hypoglycemia
 Diagnosis:
 RBG < 3 mmol
 Hypothermia (<35.5 C)
 Drowsiness; change in level of consciousness
 Treatment:
 If conscious: 50 ml 10% glucose soln or formula
 If unconscious or convulsing: IV 10% glucose
solution, 5 ml/kg body weight
 If IV access cannot be established quickly, give 50 ml
of 10% glucose solution by nasogastric tube
Step 1: Prevent/Treat
Hypoglycemia
 Prevention:
 Feed starter formula (F75) immediately
 Feed every 3 hours day and night (every 2 hours
if the child is very ill)
 Keep the child warm to preserve glucose
 Start antibiotics immediately
Step 2: Prevent/Treat
Hypothermia
 Diagnosis:
 Axillary temperature < 35 C
 Rectal temperature < 35.5 C
 Prevention and Treatment:
 Feed immediately (rehydrate first if necessary)
 Dress in warm clothes, cover the head, wrap in
blanket; or skin to skin contact with caregiver
 Monitor temperature every 2 hours until rewarmed
(36.5 C)
Step 3: Prevent/Treat
Dehydration
Diagnosis Is a Challenge…
Signs in Dehydration Signs in Severe
 Skin pinch slow Malnutrition
 Eyes sunken  Skin pinch slow
 Dry mouth  Eyes sunken
 More thirsty than  Dry mouth
usual
Step 3: Prevent/Treat
Dehydration
Treatment:

Do not use IV fluids for

rehydration – except in
cases of shock!

Problems with Standard ORS:

High in sodium
Low in Potassium
Severely malnourished children are salt-sensitive and
potassium-deficient
Step 3: Prevent/Treat
Dehydration
 Rehydrate orally or by NGT with ReSoMal
 (Rehydration Solution for Malnutrition)

 Recipe for ReSoMal

Ingredient Amount
Water 2 litres
WHO-ORS One 1-L packet
Sucrose 50 g
Electrolyte/Mineral Solution* 40 ml
*If no EMS, use 45 ml of KCl solution instead
Step 3: Prevent/Treat
Dehydration
ReSoMal ORS
 37.5 mmol Na  75 mmol Na

 40 mmol K  20 mmol K

 3 mmol Mg  0 mmol Mg

 35 g sugar  20 g sugar

(Per litre) (Per litre)

Step 3: Prevent/Treat
Dehydration
 Treat: 5 ml/kg ReSoMal every 30 minutes x 2
hours (orally or NGT)
 Then 5-10 ml/kg/hour for the next 4-10 hours
 Monitor closely for signs of overhydration
(which may cause heart failure)
 Increase in respiratory rate by > 5/minute AND/OR
 Increase in pulse rate by > 15/minute 
STOP ReSoMal immediately and
reassess after one hour
 Prevent: 50-100 ml ReSoMal after each loose
motion
Step 4: Correct Electrolyte
Imbalances
 Severely malnourished children have excess
body sodium and deficiencies of potassium
and magnesium
 Give:
In
 Extra Potassium: 3-4 mmol/kg/day standard
 Extra Magnesium: 0.4-0.6 mmol/kg/day F-75,
F-100
 When rehydrating, give low sodium fluid
(ReSoMal)
 Prepare food without salt
Step 5: Treat/Prevent
Infections
 Signs of infection often masked
 Broad-spectrum antibiotics are given
routinely on admission

If the child appears severely ill, has or not has

complications give:
 Ampicillin and Gentamycin
Step 6: Correct Micronutrient
Deficiencies
 All severely malnourished children have
vitamin and mineral deficiencies
 Vitamin A on days 1&2
 Multivitamin supplement
 Folic acid
 Zinc
 Copper (if available)
 Iron (NOT given initially but typically after child is
completely stable and/or nearing discharge)
Vitamin A Deficiency
Bitot’s spot on the conjunctiva Keratomalacia
Step 7: Start Cautious Feeding
 The severely malnourished child has:
 Fragile physiological state
 Reduced homeostatic capacity
 Feeding in the stabilization phase are:
 Small and frequent (3 hourly)
 Low osmolarity and low lactose
 130 ml/kg/day (100 ml/kg/day if severe edema)
 Provide 100 kcal/kg/day and 1-1.5 g protein/kg/day
 Starter formula: F75 = 75 kcal/100 ml and 0.9 g protein/100 ml
 No weight gain expected
 Weight loss expected if kwashiorkor
Step 8: Give Catch-Up Diet
 Once child is clinically stable, finishing
feeds/has appetite, and edema mostly gone
 F-100: 100 kcal/100 ml; 2.9 g protein/100 ml
 Replace F-100 for F-75: same amount for at
least 48 hours
 Then gradually increase F-100 by ~10
ml/feed until some remains uneaten
 Usually occurs at 200 ml/kg/day
 Target weight gain is at least 10 g/kg/day
Monitor respirations and pulse
If RR 5 breaths/min and pulse 25
beats/min for 2 successive 4-hourly
readings, reduce feeding volume

‘‘REFEEDING SYNDROME’’

4-hourly 16 mL/kg/feed x 24h, then

19 mL/kg/feed x 24h, then
22 mL/kg/feed x 48h, then
Increase each feed by 10mL as
above
Refeeding syndrome
  The refeeding syndrome is defined as the clinical complications that
occur as a result of fluid and electrolyte shifts during nutritional
rehabilitation of malnourished patients .

 PATHOGENESIS AND CLINICAL FEATURES — In significantly

malnourished patients, the initial stage of oral, enteral, or parenteral
nutritional replenishment causes electrolyte and fluid shifts that may
precipitate disabling or fatal medical complications .
 The refeeding syndrome is marked by:
 ●Hypophosphatemia
 ●Hypokalemia
 ●Vitamin (eg, thiamine) deficiencies
 ●Congestive heart failure
 ●Peripheral edema
 Hypophosphatemia
 Is the hallmark of the syndrome and predominant cause of the
refeeding syndrome. The risk of hypophosphatemia during refeeding
appears to be greater in patients who are more severely malnourished .
 The pathogenesis of hypophosphatemia begins when stores of
phosphate are depleted during episodes of starvation. When nutritional
replenishment begins and patients are fed carbohydrates, glucose
causes release of insulin, which triggers cellular uptake of phosphate
(and potassium and magnesium).
 Insulin also causes cells to produce a variety of depleted molecules
that require phosphate (eg, adenosine triphosphate (ATP) and 2,3-
diphosphoglycerate), which further depletes the body’s stores of
phosphate . The lack of phosphorylated intermediates causes tissue
hypoxia and resultant myocardial dysfunction and respiratory failure
due to an inability of the diaphragm to contract.
 Vitamin and trace mineral deficiencies are due to starvation . These
deficiencies are exacerbated by the onset of anabolic processes that
accompany refeeding the patient.  
 Volume overload begins with an increase in insulin secretion during the
early stage of refeeding the patient . This eventually increases renal
sodium reabsorption and retention, and then fluid retention.
 Pulmonary — Impaired diaphragmatic
contractility due to overall weakness or to
hypophosphatemia may occur, leading to
dyspnea and impaired respiratory function.
Respiratory failure and the need for mechanical
ventilation are rare . Heart failure may
secondarily lead to respiratory symptoms and
failure.

 Muscular — Impaired contractility, weakness,

myalgia, and tetany may occur .
Hypophosphatemia may also cause
rhabdomyolysis, which is suggested by an
abnormally high creatine kinase (CK) .
  Gastrointestinal -Liver function tests may be elevated,
and several gastrointestinal symptoms may develop.
Liver function tests, including aspartate aminotransferase
(AST) and alanine aminotransferase (ALT), are often mildly
elevated during the first few weeks of refeeding the patient
due to excessive calories and fat deposition or due to cell
death-apoptosis from malnutrition . These elevations are
usually not clinically significant and resolve by reducing the
rate of nutritional replenishment or by continuing nutritional
rehabilitation. However, malnutrition and hepatic apoptosis
can also elevate liver enzymes, which normalize with
nutritional replenishment.
Diarrhea may occur, due to atrophy of the intestinal
mucosa and pancreatic impairment . Nausea and vomiting
may also arise . These symptoms may require decreasing
the rate of refeeding or temporarily terminating the process.
 Neurologic-Patients may develop tremors,
paresthesias, delirium, and seizures as a result
of electrolyte abnormalities during the early
stages of refeeding.

The malnourished patient may be thiamine

deficient at baseline. With refeeding, intracellular
uptake of electrolytes leads to increased
utilization of thiamine, and Wernicke’s
encephalopathy may occur, with signs that
include encephalopathy, oculomotor
dysfunction, and gait ataxia . Thiamine at a dose
of 100 mg should be given at least 30 minutes
before starting nutritional replenishment .
 PREVENTION AND MANAGEMENT — The refeeding
syndrome can be avoided by restoring weight with an amount
of calories that is close to and above the resting energy
expenditure, avoiding rapid increases in the daily caloric
intake, and monitoring the patient clinically and biochemically
during the refeeding process. Complications of the syndrome
may be reduced by slowing the rate of nutritional support;
proactively correcting electrolyte abnormalities, especially
phosphorous levels; and monitoring for and treating
cardiovascular and pulmonary complications.

 Electrolyte deficiencies that are present in patients with

malnutrition should be corrected prior to initiating the
refeeding process. Although one clinical guideline states that
clinicians may correct electrolyte imbalances during the
feeding process rather than beforehand , we suggest that
nutritional replenishment not commence until electrolyte
levels are normal, based upon multiple reviews. Treating
electrolyte abnormalities usually requires no more than 12 to
24 hours .
 Treatment — If the refeeding syndrome
occurs, clinicians should reduce nutritional
support and correct hypophosphatemia,
hypokalemia, and hypomagnesemia .
Moderately to severely ill patients with
marked edema or a serum phosphorous < 2
mg/dL should be hospitalized to
intravenously correct electrolyte deficiencies
and for close monitoring. Continuous
telemetry may be needed to monitor
cardiopulmonary physiology.
Step 8: Give Catch-Up Diet
 How do you know when the child is ready to
move from F-75 (stablilization phase) to F-
100 (transition phase)?
 Finishing all 3-hourly feeds; does not need NGT
 Has appetite; crying for more
 Clinically improving
 More alert, active; diarrhea improving, no sepsis etc.
 Loss of most of edema, if kwashiorkor
 Does not have to be completely resolved, but should be
significantly improved
Step 8: Give Catch-Up Diet
 Plumpy Nut can also be introduced once the
child is in the rehabilitation phase
 Can be given along with F-100
 Is nutritionally equivalent to F-100
 Ideally, plumpy nut should gradually replace
F-100 milk
 Should always be introduced and “tested” on
child before discharge, as this is what the
child will be going home on!
 F75 and F100 recipes

© 2007 Baylor College of Medicine

Commonly Asked Questions
Regarding Therapeutic Feeds
 Can mothers continue to breastfeed while their
children are being therapeutically fed?
 YES, and they should!
 Can children eat other food while undergoing
inpatient malnutrition therapy?
 NO, they need only the therapeutic milk and/or Plumpy
Nut. Other food can be harmful if given during the
stabilization phase, and may hinder weight gain if given
during the transition/rehabilitation phases.
 What if the child does not like Plumpy Nut?
 Continue to offer it! Most children get used to it and
eventually love it!
Special Feeding Circumstances
 Children with kwashiorkor with severe (3+)
edema:
 Reduce initial F-75 feeds to 100 ml/kg/day (rather
than 130 ml/kg/day)
 Amount can be increased to standard once
edema has reduced
 Children < 6 months:
 Stabilization phase: Breast milk or formula only
(NO F-75)
 Transition/Rehabilitation phase: Dilute F-100
Step 9: Sensory Stimulation
 With severe malnutrition there is delayed
mental and behavioral development
 Provide:
 Tender loving care
 A cheerful, stimulating environment
 Structured play therapy – 15-30 min/day
 Physical activity when child is well enough
 Maternal involvement
Step 10: Discharge/Follow-Up
 A child who is 85% weight/length
 For 2 consecutive days inpatient OR
 For 2 weeks outpatient AND
 Has no edema
 For 10 days (inpatient)
 For 14 days (outpatient)
 Is considered to be recovered
Step 10: Discharge/Follow-Up
 Discharge home on RUTF with follow-up
every 2 weeks until “cure”
 RUTF = Ready to Use Therapeutic Food
Fortified peanut butter,
equivalent to F100
500 kcal/sachet
Low water content
means long shelf life
No refrigeration or
preparation required
Complications and Challenges
 The severely malnourished child with:
 Shock
 Severe Anemia
 Failure to Respond to Therapy
Complications and
Challenges: Shock
 The severely malnourished child in shock:
 Give 15 ml/kg over one hour using one of the
following (in order of preference):
 Ringer’s lactate with 5% dextrose
 Half-normal saline with 5% dextrose
 Half-strength Darrow’s solution with 5% dextrose
 Ringer’s lactate
 Measure pulse and breathing every 10 minutes
 Pulse and respiratory rate will fall with improvement
Complications and
Challenges: Shock
 If improvement:
 Give repeat 15 ml/kg over one hour
 Then switch to oral or NG rehydration with
ReSoMal 10 ml/kg/hour up to 10 hours
 Initiate refeeding with F-75
 If no improvement after first 15 ml/kg,
assume septic shock:
 Give maintenance fluid (4 ml/kg/hour)
 Transfuse whole blood 10 ml/kg slowly
 Initiate refeeding and start antibiotics
Complications and
Challenges: Severe Anemia
 Severe Anemia:
 Hb < 4 g/dl
 Hb > 4 g/dl and signs of heart failure
 Transition must be given slower and of smaller
volume
 Whole blood, 10 ml/kg over 3 hours
 Furosemide, 1 mg/kg IV at start of transfusion
 Monitor pulse and respiratory rate every 15 minutes
during transfusion
 Increase by > 5 breaths/minute or pulse by > 25
beats/minute, transfuse more slowly
Associated conditions (1)
 Vitamin A deficiency
 For any eye signs, give vitamin A days 1, 2, and 14
 >12 months: 200,000 IU
 6-12 months: 100,000 IU
 0-5 months: 50,000 IU
 For corneal clouding or ulceration, give
 Chloramphenicol or tetracycline eye drops 2-3 hourly for 7-10 days
 Atropine eye drops, 1 drop TDS for 3-5 days
 Cover with eye pads soaked in saline solution and bandage
 Dermatosis
 Hypo- or hyperpigmentation, desquamation, ulceration, exudative lesions
 Apply barrier cream to raw areas (zinc and castor oil ointment, petroleum jelly or paraffin
gauze)
 Omit nappies so perineum can dry
 Parasitic worms
 Mebendazole 100mg BD x 3 days
Associated conditions (2)
 Continuing diarrhea
 Very common, usually subsides during the 1st week of treatment
 Loose, poorly formed stools during rehabilitation are not concerning if
weight gain is adequate
 Consider mucosal damage/ giardiasis
 Metronidazole (7.5 mg/kg TDS x 7 days)
 Consider lactose intolerance (rare)
 Substitute milk feeds with yoghurt or lactose-free infant formula
 Reintroduce mild feeds gradually in rehabilitation phase
 Consider osmotic diarrhea
 Use isotonic F75 or low osmolar cereal-based F75
 Introduce F100 gradually
 TB
 Must have high suspicion in malnourished chidren
 Perform Mantoux if possible (false negatives occur frequently) and chest x-
ray if possible
 If strong suspicion or positive test, treat according to national TB guidelines
Complications and Challenges:
Failure to Respond
 High mortality
 Case fatality rates vary widely
 >20% is considered unacceptable
 Goal is < 5%
 Poor weight gain during rehabilitation phase:
 Poor: < 5 g/kg/day
 Moderate: 5-10 g/kg/day
 Good: > 10 g/kg/day
Complications and Challenges:
Failure to Respond
 Possible causes:
 Are night feeds given?
 Is child vomiting? Finishing feeds?
 Are there untreated infections?
 HIV/AIDS?
 Tuberculosis?
 Psychological problems?
A three-edged sword
 Malnutrition and HIV

•HIV infection increases metabolic expenditures and frequently coexists with

malnutrition.
•Globally, 30% of severely malnourished children with complications are HIV+.
•In general, malnutrition should be stabilized before ART is initiated.
•Response to malnutrition treatment may be delayed and more limited in HIV-infected
children.
•ARVS are more effective if nutritional status is also optimized.
•Doses of ARVs must be frequently reviewed in children rapidly gaining weight.
Summary
 Severely malnourished children are at high
risk for hypoglycemia, hypothermia, and
serious bacterial infections
 It is a significant challenge to diagnose
dehydration in the severely malnourished
 They are sodium-overloaded and potassium-
deficient
 They easily go into heart failure from fluid
overload
 They should never get IV fluids unless in
shock
Questions?