Update on Severe Acute

Malnutrition

D R . B I N I YA M N I G U S S I E
 Outlines

Introduction
Etiology
Assessment of Undernutrition
Pathophysiology
Clinical Manifestations
Management of complication of SAM
Therapeutic Feeding
Discharge Criteria & Outcome
Malnutrition refers to all deviations from
adequate nutrition and can exist in two
forms: over nutrition and undernutrition
of Macronutrients and/ or Micronutrients.
Macronutrients provide the energy required
for growth and replacement of cells, which
are required in large amounts and include
protein, carbohydrate and fat.
Micronutrients are nutrients which are
required in much smaller amounts and
ensure the healthy functioning of organs
and body processes
According to Ethiopian demographic and
health survey ( EDHS) report of 2016 for
under five children: The percentage of
children who are
Stunted - 38%
Severely stunted -18%
Wasted -9%
Underweight -24%
Severely underweight- 7%
There are two types of SAM:
-Non-edematous SAM(marasmus)
-Edematous SAM(kwashiorkor)
Non-edematous SAM was believed to result
primarily from inadequate energy intake or
inadequate intakes of both energy and protein,
whereas edematous SAM was believed to result
primarily from inadequate protein intake.
Protein-energy malnutrition is currently
avoided, as it oversimplifies the complex
multideficiency etiology!
 Micronutrient deficiencies:

A. Type I nutrients are those required for

adequate functioning of the body, such as
iron, Vitamin A, iodine, etc.
B. Type II nutrients are the growth nutrients
required to build new tissue e.g. nitrogen,
essential amino-acids, potassium,
magnesium, Sulphur, phosphorus, zinc,
sodium, etc.
 Causes of Malnutrition

 Immediate: are causes which act on individuals

-Inadequate food intake
-Disease

 Underlying causes: they influence households and communities.

-House hold food insecurity,
-Social and cultural
-Environmental

 Basic causes: they influence communities and societies

-Formal & informal infrastructure,
-Education,
-Country’s political and economical status
Primary malnutrition- resulted from
inadequate food intake

Secondary malnutrition -resulted from

increased nutrient needs, decreased nutrient
absorption, and/or increased nutrient losses
Infants prematurely weaned from breast
milk, exposed to diluted and dirty formula
=>repeated GI infection=>develop
marasmus before age 1yr

Children with prolonged breast feeding,

starchy gruel, family diet & devoid of proteins
=> acute infections => edema (kwashiorkor)
more frequently after age 18months.
10 Things Everyone Should Know about
Child Nutrition in Ethiopia
10
1 Today, more than 2 out of every 5 children in Ethiopia are stunted.
2 As many as 81% of all cases of child undernutrition and its related
pathologies go untreated.
3 44% of the health costs associated with undernutrition occur before
the child turns 1 year-old.
4 28% of all child mortality in Ethiopia is associated with
undernutrition.
5 16% of all repetitions in primary school are associated with stunting
6 Stunted children achieve 1.1 years less in school education.
7 Child mortality associated with undernutrition has reduced Ethiopia’s
workforce by 8%
8 67% of the adult population in Ethiopia suffered from stunting as
children.
9 The annual costs associated with child undernutrition are estimated
at 55.5 billion Ethiopian birr (ETB), which is equivalent to 16.5% of
GDP.
10 Eliminating stunting in Ethiopia is a necessary step for growth and
transformation.

 Ethiopia COHA summary report, June 2016.

 Assessment of Undernutrition

 WHO (wasting) weight-for-height

-<−2 to >−3 SD=Moderate
-<−3 =Severe

 WHO (stunting) height-for-age

- <−2 to >−3 SD=Moderate
-<−3 = Severe

 WHO (wasting)(for age group6-59 mo)MUAC

-115-125mm -Moderate
-<115 mm -Severe
 Pathophysiology

The physiology of severely malnourished children

is highly atypical due to reductive adaptation,
which is known as reduced body homeostasis to
minimize energy expenditure and allow survival.
Even though the definition and identification of
the severely malnourished is by anthropometric
measurements, there is not a perfect correlation
between anthropometric and metabolic
malnutrition.
It is mainly metabolic malnutrition that causes
death.
Often, the only sign of severe metabolic
malnutrition is a reduction in appetite.
 Pathophysiology in kwashiokor
13

 Excess carbohydrate, with low protein intake in

malnourished child reverses the adaptive
responses
 Mobilization of body protein stores
 Reduced muscle protein break down
 Decreased albumin synthesis
 Fatty liver- raised lipogenesis and low apolipoprotein

 Aflatoxin poisoning;
 diarrhea,

 impaired renal function

 decreased Na+ K+ ATPase activity

 Metabolic changes

 Energy mobilization:
Decreased energy expenditure compensate for the
insufficient intake initially,
Later on; body fat mobilization, decrease in adiposity
and muscle protein catabolism occurs.

 Protein metabolism
Preservation body protein and the essential protein-
dependent functions, in long term causing breakdown
of muscle protein
In kwashiokor, early loss of visceral protein
 Endocrine changes

 The decreased food intake tends to reduce insulin

secretion

 The low plasma amino acid levels, stimulate the secretion

of human growth hormone, thereby favoring amino acid
recycling;

 Low food intake and acute illnesses stimulate

epinephrine release and corticosteroid secretion,

 Triiodothyronine and thyroxine levels are reduced from

decrease in iodine uptake; decreasing thermogenesis and
oxygen consumption, leading to energy conservation.
 Hematology and Oxygen Transport

 The reduction in hemoglobin concentration and red

cell mass, following
-Reduction in lean body mass and lower physical
activity
-Decrease in dietary amino acids
-Concomitant dietary deficiency

 Due to reductive adaptation, a severely

malnourished child makes less hemoglobin than
usual. Iron that is not used for making hemoglobin is
put into storage. Thus, there is “extra” iron stored in
the body, even though the child may appear anemic.
Hence, providing iron early in treatment does not
cure anemia, rather it fatally harms children.
 Cardiovascular and Renal Functions

Cardiac output, heart rate, and blood pressure are

all decreased
In severe PEM, there is peripheral circulatory failure

Hemodynamic compensation is primarily through

tachycardia, rather than from increased stroke
volume.

Reduction of renal plasma flow and GFR from

decreased cardiac output,
Water clearance and the ability to concentrate and
urine remain unimpaired
 Water and Electrolytes

Total body intracellular water is decreased owing to

the loss in lean body mass
Decreased Total body potassium due to reduction in
muscle proteins and loss of intracellular potassium.
Impaired Na-K ATPase results in
-Decreased potassium
-Increased intracellular sodium.

Intracellular overhydration may occur.

These partly explain increased fatigability and
reduced strength of skeletal muscle
 Gastrointestinal Functions

 Impaired intestinal absorption of lipids, glucose

and disaccharides
 Decrease in gastric, pancreatic, and bile production
 Villi atrophy
 Functional impairment from protein deficit
 Repeated infections

 Increased incidence of diarrhea due to;

 Decreased absorptive function
 Irregular intestinal motility
 Gastrointestinal bacterial overgrowth
 Super- and co-infections
 Nervous System and Cognitive Functions

 Severe malnutrition at an early age causes decreased

brain growth,
nerve myelination,
neurotransmitter production, and velocity of nervous
conduction.
impairs cognitive function and IQ deficits

 Severity, timing, and duration of nutritional

deprivation, the quality of rehabilitation, emotional,
and psychosocial support, influence outcome of
neurobehavioral development and cognitive functions.
 Immune System

 Marked defect in function and development of T lymphocytes

and the complement system

 Depletion of lymphocytes from the thymus, spleen and

lymphnodes.

 Defects in opsonic and complement functional activities.

- Phagocytosis
- Chemotaxis predisposition to G-ve bacterial
sepsis
- Intracellular killing

 The B-lymphocyte and immunoglobulin function are relatively

normal,
 22
 Increased free radical
 Increased production with sepsis, toxins, iron stores
 Diminished removal from low antioxidant and enzymes
 Leads to edema, fatty liver, skin lesion

 Infection
 Shift of production to acute phase reactant
 Increased protein catabolism and loss
 Consumption of aminoacid for energy production
 Formation of free radical

o Renal blood flow/GFR, hypokalemia, increased ferritin are

postulated to further retain water and sodium
 Clinical Manifestation

Marasmus
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
Apathetic and anxious
Monkey’s or old person’s face
 Kwashiokor

Anorexia is almost universal.

Bilateral pitting edema, or anasarca
Rounded prominence of the cheeks ("moon-
face")
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
 Investigations

Hct and Hgb

WBC count and differential
RBS
Urinalysis and urine culture
Chest X-ray
Blood culture
Total serum protein
Ratio of non essential to essential a.a-
Reduced urinary creatinine clearance
 Management Of SAM

Principles of Treatment
Treatment of Medical Complications

Routine Medicines and Antibiotics

Therapeutic Feeding

Monitoring (Surveillance)
 Appetite test

An appetite test is done for children aged 6 to

59 months who have no medical
complications
30
Criteria for inpatient (6month-5yrs)
31
Criteria for inpatient (5-18yrs)
32
Ten essential steps of Rx(SAM)
34
 Medical Complications of SAM

• Poor appetite
• Intractable Vomiting
• Convulsion
• Lethargy, not alert
• Unconsciousness
• Hypoglycemia
• High fever (Axillary Temperature ≥38.50.C)
• Hypothermia
• Dehydration
• Lower respiratory tract infection (e.g. Pneumonia)
• Severe anemia
• Persistent diarrhea
• Eye sign of vitamin A deficiency
• Severe Skin lesions (e.g. severe dermatosis)
 Treatment Of Complication

Hypoglycemia
Important cause of death in 1st 2days
At risk because of alteration in glucose
metabolism
Signs –low body temperature, lethargy, eye
lid retraction, twitching or convulsion
RBS<54 mg/dl
 37

If conscious: If unconscious:

1. 10% glucose (50 mL), or 1. Immediately give sterile

a feed or 1 teaspoon 10% glucose (5 mL/kg) by
sugar under the tongue- IV
whichever is quickest 2. Feed every 2 hr for at
2. Feed every 2 hr for at least first day. Initially
least the first day. Initially give 1/4 of feed every 30
give 1/4 of feed every 30 min. Use nasogastric (NG)
min tube if unable to drink
3. Keep warm 3. Keep warm.
4. Start broad-spectrum 4. Start broad-spectrum
antibiotics antibiotics
 Hypothermia

Body temperature <35.5 degree,

axillary or 35 degree rectal
Due to impaired thermoregulatory
mechanism, reduced fuel
substrate or severe infection
Use kangaroo technique, put a hat
and the room should be kept warm
(b/n 28 -32 degree)
The child should always sleep with
the mother.
 Dehydration

History of vomiting or diarrhea.

Useful signs –thirst, dry tongue and mouth, low
urinary output, weak and rapid pulse, low blood
pressure, cool and moist extremities, and declining
state of consciousness
Unreliable signs – sunken eyeball, decreased skin
turgor, irritability and apathy
Rehydration should be preferably orally or through
NG tube
Solution should contain less Na and more K – ORS
( not ideal) Resomal (best)
Indication for iv fluid – shock and coma
 40
Hx of vomiting or diarrhea, Recent weight loss, tachypnea, tachycardia

Yes

Resomal 5ml/kg Q30’ for 2hrs then 5-10ml/kg/hr for 10hrs

Unconscious, weak pulse, delayed capillary refill Mana

ge as
shock

No
No dehydration
Replace loss with Resomal
 Shock
41
Tachycardia,
Tachypnea, Cold
extremities,
SHOCK
Delayed c-refill, No
UOP !
15ml/kg/hr
RL-5%dexrose
1/2NS-
5%dextrose

Repeat, if improvement
Transfuse:
continue with Resomal. whole blood
If not…assume SEPTC Antibiotics
SHOCK
Close monitor
If there are no signs of improvement assume
septic shock and:
1. Give maintenance fluid IV (4 mL/kg/hr) while
waiting for blood
2. Order 10 mL/kg fresh whole blood and
transfuse slowly over 3 hr. If signs of heart
failure, give 5-7 mL/kg packed cells rather than
whole blood.
3. Give furosemide 1 mg/kg IV at the start of
the transfusion
 Signs of Overhydration

Stop ReSoMal if any of the following signs appear:

• Increased respiratory rate by five breaths and
pulse rate by 25 beats per minute (Both must
increase to be considered a problem.)
• Jugular veins engorged. (Pulse wave can be seen
in the neck.)
• Sudden increase in liver size and tenderness
• Increasing oedema (e.g., puffy eyelids).
• Increasing weight with clinical deterioration
• Bilateral chest crepitation
 Severe Anemia
44

If very severe anemia Hgb <4 g/dl; or

Hemoglobin 4-6 g/dl with respiratory distress
or HF:

 Give whole blood 10 ml/kg slowly over 3 hr. If signs of

heart failure, give 5-7 mL/kg packed cells rather than
whole blood
 Hold transfusion after 48hrs of admission till 2weeks
 Fe treatment in phase II.
 Heart failure
45
 Usually starts after management of SAM- IV
infusion/ORS/high Na diet, blood or plasma
transfusion,

 Respiratory Distress with weight gain

 Tachypnea, grunting, crepitation's, prominent
superficial & neck veins and gallop, plus enlarged
tender liver

 Stop all oral or IV intakes/fluid for 24-48 hours

until managed
 Furosemide 1mg/kg single dose
 Digoxin 5microgram/kg single dose
 If there is severe anemia, treat the HF first
46
 Infections

Clinical manifestations may be mild

Classical signs (fever, tachycardia and
leukocytosis) may be absent
Major complications lead to a loss of appetite
Assume that children with severe malnutrition
have a bacterial infection
Gram positive and gram negative
Safer to treat all with broad spectrum antibiotics
Po route is preferred unless the patient is in septic
shock (a fast and weak pulse, cold extremities, low
BP and disturbed consciousness)
Management of abdominal distension
with absent bowel sounds, gastric
dilatation and intestinal splash.
-Give IV second line antibiotics
-Consider adding third line antibiotics like
ceftriaxone
-Stop all other drugs that may be causing
toxicity (such as metronidazole)
-Give a single IM injection of magnesium
sulphate (2 ml of 50 per cent solution).
-Insert an NG-tube and aspirate the contents of
the stomach, then “irrigate” the stomach and
check for the absorptive capacity of the
stomach using 10 per cent sugar water.
-Monitor for 6 hours and If there is intestinal
improvement then start to give small amounts
of F75 by NG tube.
Management of corneal clouding and ulceration

Give Vitamin A and Atropine 1% for corneal

ulceration.
 If the child has corneal clouding and
ulceration, give Vitamin A immediately.
All severely malnourished children with eye
signs need Vitamin A on Day 1,
Routine Medicines
Antibiotics
52
 Vitamin A
53
A high dose of vitamin A on admission is
given if the therapeutic foods that are not
fortified
Otherwise, enough supplemental amount
of Vit. A is found in F75/F100.
Do not give vitamin A for children
except those:
 with eye signs of vitamin A deficiency or
 recent measles
 Given at day 1,2,15
 Therapeutic Feeding
54

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
 Child is very weak

 Use NGT only in Phase I and for max 3 days, try oral
feeding at every feeding
 •F75(130ml = 100kcal)

Phase I
•“starter” formula
•for 2-7days until the child is stabilized
•Return of appetite, edema reduced, clinically well, no NGT or IV line

55

Transition phase
•F100(100ml=100kcal)
•Expected weight gain 6g/kg/day.
•A good appetite, taking at least 90% of the RUTF/F100, edema<+,

Phase II
•F100
•no major medical complication
•Expected weight more than 8 g/kg/day.
56
 Failure To Respond
59

Failure to respond can be

 primary failure- during the first phase

 Secondary failure- regress after having progressed

satisfactorily to Phase 2 with a good appetite and
deteriorates afterwards or on initial response as an
out-patients
Criteria for Failure
60
Monitoring Of SAM Patients
 Discharge /Transfer
62 Criteria

If admission was with anthropometric

measurement, indication of nutritional recovery
 Wt-for-height/length is ≥–2 Z-score and no edema for at
least 2 weeks, OR
 MUAC is ≥125 mm and no edema for at least 2weeks.

 Percentage weight gain/target weight should not be used

as a discharge criterion.
 Infant under six month
63

Severe acute malnutrition <6month is defined as:

 Visible severe wasting
 WFL <-3Z
 Bilateral edema

 Admission if there is:

 Any medical complication
 recent weight loss or failure to gain weight;
 Ineffective feeding
 Any pitting edema;
 Infants who have poor weight gain
 Any medical or social issue (e.g. regarding caregiver, or other
social issues)
 Principles of Treatment

Treatment should always be in in-patient unit

Objective is to return to full exclusive breast
feeding.
Treatment of complications
Feeding
Diluted F 100 130ml/kg/day in 8 feeds/day
No separate phases of feeding
F75, if child is edematous
Supplemental Suckling
 Breast milk output is stimulated by the (SS) technique; it is important to
put the child to the breast as often as
65possible.
 66

P T P
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Discharge criteria
67

Infants < 6 months on Breastfeeding

 Infant gaining weight on breast milk alone

 No medical complication
 Have a weight-for-length ≥–2 Z-score.
 OTP Management
68

Candidates:
 Children 6 to 59 months who have:
 MUAC<11.5cm,
 Weight for height z-score <-3 or
 Edema +/++ AND:
1. who pass the appetite test,
2. without medical complications

 Should be without +++ edema or marasmic

Kwashiorkor!
Components
Feeding 69
 RUTF, per kilogram
Antibiotics:
 AMOXYCILLIN 50-100mg/Kg/day in two doses for 7
days
Folic acid-
 if clinical signs of anemia

Vitamin A-
 if overt deficiency or measles
Deworming-
 Albendazole, at second visit
Measles
Iron- not recommended
 Discharge Outcomes

1. Successful outcome: 70
Cured (Recovered): child that has reached the
discharge criteria for in-patient care
Transfer Out to OTP: Child that is transferred from
inpatient care to OTP.
2. Adverse outcomes:
Defaulter: Child that is absent for 2 consecutive days
in in-patient care
Death: Patient that has died while s/he was in the
inpatient care.

3. Non-responder: Patient that has not reached

the discharge criteria after 40 days in the inpatient
care
 71

 Retrospective descriptive study was conducted in

children between 6 months and 5 years of age with
SAM admitted to Yekatit 12 hospital from a period of
September 2012- September2013.
 A total of 193 patients with severe acute malnutrition

were admitted over one year period of study.

 Management outcome of severe acute

malnutrition from 6 months to 5 years of
age children admitted to Yekatit 12 hospital-
August 2014
The outcome of these children was 74.4% had
improved, 12.4% dead and 72 the same 12.4%
withdraw the treatment.
 There is no significant association between type of
malnutrition, age of the child, serum albumin level
and presence of complications with treatment.
 Mean age of hospital stay was around 16 days (15 days
for those dead Vs 16 for those improved).
 The risk of death in the first one week is high.

The study showed increased rate of death in

patients with:
 Seropositivity for HIV infection
 Early age of admission
 References
73

 Modern nutrition, in health and disease- 10th

edition
 Nelson textbook of pediatrics- 20h edition
 Guidelines for the Management of Acute
Malnutrition- April,2016
 WHO guideline- Updates on the management of
SAM, in infants and children- 2013
 Literature reviews
 Management outcome of severe acute

malnutrition from 6 months to 5 years of age

children admitted to yekatit 12 hospital- August
2014
 Thank
You!!!