This document provides information on protein-energy malnutrition (PEM). It discusses the causes, epidemiology, clinical manifestations, pathophysiology, classification, management, and prognosis of PEM. PEM results from inadequate protein and energy intake and can range from mild growth retardation to more severe forms like marasmus (wasting), kwashiorkor (edema), or a combination of the two. Management involves inpatient or outpatient therapeutic feeding based on severity, with the goal of nutritional rehabilitation. Prognosis is poorer in those with young age, infections, dehydration or other complications.

1. Melese A (MD,GP)

2. PROTEIN-ENERGY MALNUTRITION (PEM)
• PEM results when the body's needs for protein
and energy fuels are not satisfied by the diet.
• It is accompanied by deficiency of several
micronutrients
• Severity ranges from milder forms weight loss or
growth retardation to distinct clinical features
marasmus, kwashiorkor or marasmic
kwashiorkor.

3. Primary PEM- due to inadequate food intake
Secondary PEM- other disease lead to
low food ingestion,
inadequate nutrient absorption or
utilization, increased
nutritional requirements, increased nutrient
losses
causes

4. Epidemiology and etiology
According to the Ethiopian Demographic and
Health Survey (EDHS) preliminary report of 2011
for under five children showed
 The percentage of children who are stunted is 44%; of
which 21% are severely stunted
The percentage of children who are wasted is 10%
And those of underweight is 29%, and 9% of children
are severely underweight

5. Etiology
• Social and Economic Factors
-Poverty
-Ignorance
-Social and cultural problems
• Biological factors
-Maternal malnutrition -
Infection -
Dietary factor bulky foods with low nutritional
value

6. Environmental factors -
Overcrowded and/or unsanitary living
conditions
Agricultural patterns, droughts, floods, wars, and
forced
Age of the host -
more frequent among infants and young
children

7. PATHOPHYSIOLOGY AND ADAPTIVE
RESPONSES
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.

8. Free radical theory
Increased production of free radicals by
infection, toxins, iron, trauma sunlight exposure
and decreased scavenger mechanism that
removes free radicals (vit A, C,E, zinc, selinium)
& glutathione
=>Accumulation of free radicals
=>Damage to cell membrane and vessels
=>Alteration seen in kwashiorkor- fatty liver,
dermatosis,edema

9. Decreased energy intake
↓
Decreased energy expenditure
↓
Fat mobilization and wt loss
↓
Subcutaneous fat markedly reduced and
muscle wasting due to protein catabolism
 Visceral protein in spared in marasmus
longer but early involved in kwashiorkor

10. Endocrine
maintenance of energy homeostasis through
increased glycolysis and lipolysis, increased
amino acid mobilization, preservation of visceral
proteins through increased breakdown of muscle
proteins, decreased storage of glycogen, fats,
and proteins, and decreased energy metabolism

11. Hematology reduction in Hgb
CVS and renal
◦ reduction in CO,HR & BP
◦ reduction in renal blood flow & glomerular filtration rate
Electrolytes
◦ decreased total body potassium and magnesium
◦ increased intracellular sodium
Metabolism hypoglycemia
decreased basal metabolic rate

12. Gastrointestinal
decrease in gastric, pancreatic, and bile production
and decrease in absorption
 villi atrophy , bacterial overgrowth
CNS
severe PEM at an early age may result decreased
brain growth, nerve myelination, neurotransmitter
production, and velocity of nervous conduction

13. Immune system
 reduction of T lymphocytes
 decreased production of complement system
Phagocytosis, chemotaxis, and intracellular killing are
also impaired
B cell and Ig are relatively normal but there may br
defect in antibody production such as secretory
immunoglobulin A

14. Classification of PEM
Welcome system uses weight for age measured
by Harvard curve
Weight for
age
Edema- Edema +
60-80% Underweight Kwashaikor
<60% Marasmic Marasmickwash

15. Water low classification asses severity of
wasting and stunting using the NCHS curve
Grade of
malnutrition
Wt/ht
(Wasting )
Ht /age
(Stunting )
Normal > or=90% > or=95%
Mild 80-89% 90-94%
Moderate 70-79% 85-89%
severe <70% <85%

16. Clinical manifestations
Marasmus = Greek term means to waste
It is an adaptive process
Generalized muscle wasting and absence of
subcutaneous fat “bone and skin appearance” or
old man’s face
Hair sparse, thin, dry & easily pulled out
Skin is dry, thin with little elasticity, and wrinkles
easily


17. Patients are apathetic but usually aware and
have a look of anxiety on their face
Some are anorexic, whereas others are
ravenously hungry
Diarrhea, vomiting, abdominal distension
Heart rate, blood pressure, and body
temperature may be low
Hypoglycemia

18. Kwashiorkor:
 Edema
◦ bilateral pitting ,painless of the feet and legs in severe
cases may involve the upper extremities and face
Skin lesions are usually present
◦ include Hyperpigmentation, hypopigmentation
desquamation and ulceration (flaky paint dermatosis)
◦ affected site areas of edema, continuous pressure
( buttocks and back), or frequent irritation (perineum
and thighs).

20. The extent of dermatosis can be described in the
following way:
+ mild: discoloration or a few rough patches of skin
+ + moderate: multiple patches on arms and/or
legs
+ + + severe: flaking skin, raw skin, fissures
(openings in the skin)

23. Hair
dry, fine, straight, without its normal sheen, and can
be pulled out easily
Color usually changes to brown, red, or even yellowish
white
 “Flag sign” Alternating periods of poor and relatively
good protein intake can produce alternating bands of
depigmented and normal hair

24. Flag sign

25. Mental status
apathetic and irritable, cry easily, and expression of
misery and sadness
Gastrointestinal
Anorexia, postprandial vomiting, and diarrhea
Hepatomegaly with a soft, round edge caused by
severe fatty infiltration
abdomen protruding because of distended stomach
and intestinal loops

26. Marasmic- kwashiorkor
 combines clinical characteristics of kwashiorkor and
marasmus
 edema of kwashiorkor, with or without its skin lesions,
and the muscle wasting and decreased
subcutaneous fat of marasmus

28. Laboratory studies
Blood glucose
Hgb or HCT
Blood film
Stool microscopy
Urine analysis and culture
Chest x-ray
Tests for tuberculosis

29. Serum concentrations of total proteins specially
albumin
 are markedly reduced in edematous PEM, and they
are normal or moderately low in marasmus
Electrolytes
 intracellular concentrations of potassium and
magnesium decrease, and that of sodium increases

30. The ratio of nonessential to essential amino
acids in plasma is elevated in kwashiorkor
Serum free fatty acids are elevated particularly
in kwashiorkor
Urinary creatinine excretions markedly reduced
particularly in kwashiorkor

31. Management
severe acute malnutrition(SAM) -6month to
5years
 W/H or W/L < 70% or
 MUAC < 110 mm with a Length > 65 cm
or
 Presence of bilateral pitting edema

32. Admission to in patient
SAM plus
Medical complication or
Failed appetite test or
Edema +++ or
Wt/ht< 70% with edema or

33. Medical complications
Unable to breast feed drink or feed or vomiting
everything
 Convulsions
Very Weak, Lethargic or unconscious
Pneumonia
Hypothermia or Fever >39 0C
Shock, Severe DHN, Hypoglycaemia
Severe anemia, Jaundice, Bleeding Tendencies
Dermatosis +++
Dysentery, Persistent diarrhoea

34. Treatment at a outpatient treating program
WFL/H < 70% of median or
MUAC <11cm or
Edema of both feet (+, ++)
AND
No medical complication AND pass appetite test

35. SAM for Infants less than 6 months
WFL < 70% of median or
OR
 Visible severe wasting,
OR
 Edema of both feet
 Admit for inpatient treatment

36. Phase 1 nutritional management
Principles of phase 1 treatment
Feed the patient F- 75
Routine medications
Monitor the patient
Prevent, diagnose and treat complications

37. 1. F75 =75 kcal per 100ml
Has less Na, proteins, fats, lower
osmolarity and renal solute load
Less energy dense
75kcal/100ml and 0.9gprotein /
100ml
Is given 8 times per day

38. Use NG tube when
Taking less than 75% of prescribed diet per 24 hours
in Phase 1
Pneumonia with a rapid respiration rate
Painful lesions of the mouth
Cleft palate or other physical deformity
Disturbances of consciousness

39. 2. Routine medicines
 Vitamin A for all children except those with
edema or those who received vitamin A in the
past 6 months
 On the day of admission and on the day of
discharge
6-11months 100,000IU
>12months 200,000IU

40. Folic acid single dose of folic acid 5mg to
children with clinical signs of anaemia
Antibiotics:
First line : amoxicillin
Second line :chloramphenicol or gentamycin
Measles vaccine: all children > 9 months
without a vaccination card on admission and
discharge after Phase 2

41. 3. Surveillance (monitoring)
Weight each day
degree of edema each day
Body temperature twice per day
stool, vomiting, dehydration, cough, respiration
and liver size assessed each day
 MUAC is taken each week
 Length or Height is taken after 21 days

42. 4. Complications
Dehydration
-All signs of dehydration in normal child are
present in severe malnourished children with no
dehydration
-History of significant recent fluid loss and history
of a recent change in the child’s appearance
- Rx resomal -5ml/kg every 30 minute for the
first 2hrs then 5-10 ml /kg/hr for the next 4-10
hrs.

43. Replace ongoing loss with 30 ml of ReSoMal per
watery stool for oedematous children and with
50-100 ml for non-oedematous children under 2
years
If the child has already received IV fluids for
shock and is switching to ReSoMal, omit the first
2-hour treatment and start with the amount for
the next period of up to 10 hours.

44. Congestive heart failure
C/F weight gain, tachycardia, tachypenia, engorged
neck veins, gallop rhythm, increase in lived size and
tender, creptation
Stop all fluids and feeds, small sugar in water solution
orally
Furosemide 1mg/kg
Digoxin in small doses 5microgram/kg
Even if severely anemic don’t transfuse manage heart
failure first

45. Anemia
Hgb <4g/dl or HCT <12% during the first 48hrs of
admission
Give 10ml/kg of whole blood or packed RBC over 3 hr

46. HypoglycemiaIn severely malnourished children,
the level considered low is less than
<54 mg/dl
Clinical signs that occur in normal
person doesn’t occur in malnourished
children
Eye lead retraction is one important
sign

47. If conscious -50 ml of 10%sugar in water
or F75 diet by mouth
 If loosing consciousness -give 50 ml of
10% sugar- water by naso-gastric tube
If unconscious - 5ml/kg of 10% glucose
solution IV, followed by 50 ml of 10%
sugar by NG tube

48. Hypothermia
Rectal temperature below 35.5oC or under arm
temperature below 35oC
Commonest cause is due to environmental or lack of
cover
-Use the “kangaroo technique” for children with a
caretaker
-Put a hat on the child and wrap mother and child
together

49. -The room should be kept warm, especially at night
thermo-neutral temperature range for malnourished
patients is 28oC to 32oC
-Treat for hypoglycemia and give second-line
antibiotic treatment

50. Transition phase
The criteria to progress from Phase 1 to
Transition Phase are :
- Return of appetite and
-Beginning of loss of edema and
-No IV line, no NGT
F100(100kcal/100ml) is given same amount as
phase 1, 8times per day
Expected wt gain is 6g/Kg/day

51. Criteria to move back from Transition phase to
Phase 1
Rapid weight gain greater than 10g/kg/d
Edema increasing or development of
edema
Rapid increase in the size of the liver
Any signs of fluid overload develop
Tense abdominal distension

52. Cont….
significant re-feeding diarrhea resulting
weight loss
Naso-Gastric Tube is needed
If patient takes less than 75% of the
feeds in Transition Phase

53. Criteria to progress from Transition phase to Phase
2
Good appetite
Complete loss of edema
No other medical problems

54. Phase 2
F100 (100ml = 100 kcal): five feeds per day or
Ready to use therapeutic feeding(RUTF)
One porridge may be given for patients who are
more than 8kg
Phase 2 management can be done as out patient at
home or in therapeutic feeding center
Wt gain 8g/kg/day

55. Routine medications during phase 2
Iron: is added to the F100 in Phase 2
De-worming: Albendazole or
Mebendazole is given at the start of the
Phase 2

56. Failure to respond to treatment

57. Causes of treatment failure
Problems with the treatment facility
Poor environment for malnourished children
Poorly trained staff
Inaccurate weighing machines
 Food prepared or given incorrectly

58. Problems of individual children
Insufficient food given
Malabsorption
Infection, especially: Diarrhoea, dysentery,
pneumonia, tuberculosis, urinary infection
Other serious underlying disease: congenital
abnormalities (e.g. Down’s syndrome)

59. Discharge criteria
W/L>=85% or W/H>=85% =(Two days for in-
patients, two weeks for out-patients)
and
No edema for 10 days (In-patient)
Vaccination updated
Education to the mother is given

60. Follow-up after discharge
The patients should be enrolled in a Supplementary
Feeding Program and given nutritional
support for another 4 months

61. Poor prognostic factors for PEM
Age <6 mon
Signs of circulatory collapse
Altered mental status
Infections
Bleeding tendencies
Dehydration and electrolyte disturbances

62. Congestive heart failure
Total serum proteins <30 g/L
Severe anemia
Clinical jaundice or elevated serum bilirubin
Extensive exudative or exfoliative
cutaneous lesions or deep decubitus
ulcerations
Hypoglycemia or Hypothermia

63. References
Nelson text book of pediatric 19th
edition
Modern malnutrition in health and disease
Protocol for management of severe malnutrition
Ethiopia Federal Ministry of health 2011
(MODFIED FROM DR MAHLET’S PPT)

64.  thank you!!!