Pem

child health and pediatrics

1. P.E.M
PROTEIN ENERGY
MALNUTRITION
DR. SHILULI

2. Definition
•Malnutrition -cellular imbalance between supply of
nutrients and energy and the body's demand for them
to ensure growth, maintenance, and specific functions
•PEM: Range of clinico-pathologic condition arising
from lack of varying proportions of protein and
calories,occurring most frequently in infants and
young children usually associated with infection

3. •Studies suggest that marasmus represents an adaptive
response to starvation, whereas kwashiorkor
represents a maladaptive response to starvation.
•It invariably reflects combined deficiencies in protein,
energy and micronutrients.

4. •The distinction between the 2 forms of PEM is based
on the presence (kwashiorkor) or absence (marasmus)
of edema.
•Marasmusinvolves inadequate intake of protein and
calories and is characterized by emaciation.
•Kwashiorkorrefers to an inadequate protein intake
with a fair to normal caloric (energy) intake. Edema
characteristic.

5. Classification
•Malnutrition can be classified as acute versus
chronic.
•Features of chronic malnutrition include
stunted growth
mental apathy
developmental delay
poor weight gain.

6. •Acute malnutitionmanifests itself in two major
forms:
•marasums(the most common form) and
kwashiorkor
•some patients' condition may manifest as a
combination of both forms (marasmic
kwashiorkor).

7. Indicators of PEM

8. •The parameters used in classification include;
oWeight for age
oHeight for age
oWeight for height
Classification

10. WHO CLASSIFICATION

11. •Severe malnutrition is defined as severe stunting or
severe wasting, or edematous malnutrition.
Wasting (indicates acute malnutrition)
Stunting (indicates chronic malnutrition)
•Patients with edematous malnutrition (Kwashiorkor)
should be considered to have severe malnutrition even
if stunting or wasting z-scores are not in the severe
range.

12. •Weight for height
•MUAC
•Body Mass Index
•Indices (Kanawati, Dughdale, Rao & Singh’s)
•Skin fold thickness
Age Independent Indices

13. MUAC–(1 –5 yrs):
Level(severity) MUAC
Severe <11.5 cm
Moderate 11.5-12.4cm
At risk 12.5-13.4cm
Normal : >13.5 cm
13

15. Epidemiology
•Malnutrition implicated as the underlying factor in about
50% of deaths of children <5 yrs in developing countries.
•Children between 12 and 59 months are esp. at risk
because they are the most vulnerable to infections like
gastroenteritis and measles.
•It is estimated that, in developing countries, more than
25% of all children younger than 5 years are malnourished

16. •A study was done on the prevalence of malnutrition in Kenya
using 3 nutritional-status indicators: stunting, wasting and
underweight.
•The overall prevalence was 36%, 6% and 27% respectively.
•Stunting was lowest among the 12-23 month age group and
highest among the 12-23 month age group, w prevalence 15x
higher in boys.
•The most pressing form of malnutrition in Kenya is PEM,
which largely affects infants, pre-school, and school children.

17. •Low birth weight
•Multiple pregnancy
•Closely spaced pregnancies
•Early stoppage of breast feeding
•Too early or too late weaning
•Recurrent infections
•Illiteracy
•Poverty
•Malabsorption
Risk factors

18. Etiology
•Primary -when the otherwise healthy individual's
needs for protein, energy, or both are not met by an
inadequate diet.
•Secondary -as a result of disease states that may lead
to suboptimal intake, inadequate nutrient absorption or
use, and/or increased requirements because of nutrient
losses or increased energy expenditure.

19. Primary Malnutrition
•Protein + energy intake are below requirement for normal
growth
Parents are not giving their child enough food because:
•they can’t afford to (they are poor, unemployed);
•they don’t want to (in cases when parents abuse or
neglect their children);
•they don’t know(they are too young or uneducated).

20. Secondary malnutrition
Impaired absorption /Excessive GI loss of nutrients
•persistent diarrhea,
•vomiting
•malabsorptive conditions,
•heavy helminthic infestation
•Metabolic abnormalities
Increased nutritional requirement due to
•Infections (measles, pertussis, Tb, HIV)
•drugs -antibiotics /anabolic / catabolic drugs

21. Cont….
Increase protein loss e.g
•proteinuria (nephrosis)
•infections
•haemorrhage
•burns
Failure of proteins synthesis e.g
•in chronic liver disease.

22. PATHOGENESIS
Theories of PEM Pathogenesis
1. Dietetic Hypothesis
•Kwashiorkor: Predominantly protein deficiency
•Marasmus: Energy deficiency

23. Cont…
2. Adaptation Hypothesis (Gopalan’s )
•Marasmus : Extreme case of adaptation
Prolonged exposure to low calorie intake-progressive
wasting
•Kwashiorkor : A stage of adaptation failure
Continued prolongation of stress

24. Cont..
3. Free Radical Hypothesis (Golden’s)
Kwashiokorresults from over production of free
radicals and breakdown of protective
mechanisms

25. Cont…
4.Jelliffe’sHypothesis
•A mixture of interactions and sequel of dietary
imbalances, infections and infestations, emotional trauma
and toxins
5. Aflatoxin Hypothesis
•Contamination of food-cause liver damage-kwashiokor
results

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

27. •Kwashiorkor–Low plasma cortisol–Muscle
protein NOT mobilized –Low plasma A.A –stimulate
the pituitary to secrete high GH –G.H is lypolytic
causing high plasma free fatty acid –low synthesis of
lipoproteins –Fat accumulates in the liver –impaired
hepatic fat metabolism-Fatty liver.
Cont..
27

28. •Kwashiorkor is often preceded by an episode
of infection with diarrhoea and respiratory
infection being the most common precipitating
factors.
•Others –measles, chicken pox, HIV, Whooping
cough, TB, Malaria et.
3. ROLE OF INFECTION

29. PATHOPHYSIOLOGY
Edema
Cause:
•Protein -deficient, hypoalbuminaemia, reduced plasma oncotic pressure, shift to
interstitium
•Free radical damage of cell membrane ,Na+/K+ ATPase malfunction results in fluid
leakage to interstitium
•Damage to CT of the interstitium by free radicals. –vecharge and GAGS lost thus
water flows freely thru’ interstitium.
•Hypovolemia reduced GFR, activation of RAAS, Na and water retention.
•Incrlevels of leukotrienescause uncontrolled vasodilation–hypovolemia-low BP-
decreased peritubularhydrostatic pressure –increased tubular reabsorptionof salt and
water.
29

30. Cont…
Wasting
•Calorie definition –fats and tissue proteins mobilized
to supply energy for metabolic processes.
•Recurrent infections coupled with hypoglycemiacause
acute stress response-cortisolreleased-wasting
•Effects of associated infections e.gHIV wasting
syndrome
30

31. Cont…
Hair changes
•Keratin synthesis impaired coz of cystine and methionine deficiency ,
thus brittle hair easily pulled off /breaks
•Pigment melanin formed from tyrosine. deficient in kwashiokor.
Enzyme tyrosinaserequires copper as a cofactor in melanin synthesis.
Hair changes colour to reddish or grey.
•Dullness and lack of lustre due to weathering of the hair cuticle.
•Bleaching effects of hydrogen peroxide(ROS)
31

32. Cont…
Skin changes
•Ulcerations and flaky paint rash due to zndeficiency
•Atrophy of sweat and sebaceous glands leads to excessive dryness of
the skin.
•Hyperpigmentation, erytherma,duskinessof exposed areas –niacin
def
•Cracking and fissuring of hyperpigmented skin-crazy pavement
dermatosis
•Generalized hypopigmentation due to stretching of the skin by the
edema.
32

33. Cont…
Hepatomegaly/ fatty liver
•Free radicals damage mitochondrial enzymes in the liver causing reduced
synthesis of proteins.
•Beta lpdeficiency –accumulation of tgin the liver –fatty liver –
hepatomegaly.
Pot belly
•Hypotonic muscles of abdominal wall resulting in muscle wasting.-
Increased laxity of skin
•Overgrowth of bacteria in the gut due to reduced immunity-flatulence
•Paralytic ileus due to hypokalemia
•Hepatomegaly -fatty liver
33

34. Cont…
Diarrhoea
•Caused by recurrent infections due to reduced immunity-
low sIgA and reduced secretion of acid in stomach.
•Malabsorption–deficiency of pancreatic enzymes
resulting from pancreatic atrophy/protein deficiency.
•Villusatrophy
34

35. Cont…
Reccurentinfections
•Atrophy of thymolymphaticglands cause depletion of T lymphocytes and
depressed CMI thus infections like Herpes, candidiasiscommon.
•Reduced phagocyticand bactericidal activity of leucocytes-NADPH oxidase
and lysozymedef
•C3,c5, and factor b levels reduced –opsonizationand phagocytosisreduced.
•Acute Phase Reaction(APR) immune response reduced due to inability to
synthesis IL-1,IL-6.TNF alpha due to lack of supply of essential AA.
35

36. Cont…
Anaemia
•Due to dietary deficiency of iron and folate
•Parasitic infections eghookworm.
•Malabsorption due to recurrent diarrhoea.
•Reduced protein synthesis.
36

37. Cont…
Apathy-absence of emotion, feeling, interest
•Hypokalemia-muscle weakness and easy fatigability of
respiratory muscles-child lacks energy
•Lack of stimulation and deprivation causes reduced
growth of brain and nerve thus mental slowing.
•Reduced BMR
•Apathy also attributed to Zinc deficiency.

38. Electrolyte/ mineral deficiencies
Magnesium
•Good evidence that magnesium deficiency is common in severe
malnutrition
•Consequences:
–Muscular twitching
–Arrhythmias
–Convulsions
–Predisposes to K
+
deficiency
38

39. Cont…
sodium
•Plasma sodium can be low and on occasions is extremely
low in children with marasmickwashiorkor.
•However total body sodium is often increased
oExpansion of extracellular fluid volume
oLeakage of sodium into cells –sick cell syndrome
•One reason why large amounts of additional sodium (fluids and
feeds) are poorly tolerated.
39

40. Cont…
Micronutrients / Trace Elements
•Zinc
•Copper
•Selenium
Consequences of Zinc deficiency
•Reduced appetite
•Reduced immunity
•Reduced gastrointestinal function –longer period of diarrhoea
•Reduced ability to gain weight even when there is adequate feeding

41. Consequences of Copper and
Selenium deficiency
•Copper is required for adequate tissue growth
and repair, anaemia and poor bone growth may
particularly be associated with inadequate
copper (there is very little in milk).
•Selenium deficiency may be associated with
reduced cardiac muscle function.

42. Complications
•Hypoglycemia
•Hypothermia
•Hypokalemia
•Hyponatremia
•Heart failure
•Dehydration & shock
•Infections (bacterial, viral & thrush)(GI, RTI, UTI;
ooften don’t show classical symptoms and signs)
•Anemia(severe cardiac failure)
•Cardiomyopathy-heart failure

43. Complications
•Diarrhea & vomiting dehydration, electrolyte imbalance, metabolic acidosis
•Hypovolemia(impaired cardiac and renal function
•Refeeding syndrome
•Mortality
•Small stature
•Poor performance in school (IQ)
•Obstructed labour
•Low birth wgtinfants

44. Clinical Presentation
History
•Poor weight gain-birth weight, current weight(assess appropriateness for age)
•Poor feeding/loss of appetite
•Slowed linear growth
•Loose motions, vomiting
•Behavioural changes: irritability,↓ social responsiveness, apathy, anxiety, attention
deficits
•Facial puffiness
•Generalized swelling

45. Clinical Presentation
•Delayed milestones
•Cough –establish hx of contact with person with chronic cough
•Dehydration symptoms-AMS, ↓ urine output
•Hotness of body
•Birth history
•Nutritional history -breastfeeding duration, weaning, usual diet
before current illness: quality, quantity, frequency, 24hr recall(food
& drink in last 24hr), care giver

46. Clinical Presentation
•Immunization
•Family socio-economic history
–Parents/ care givers
–Parents’ income/ occupation
–Expenditure on food
–Education level
–Family size
–Living conditions, water source
–Water source/ sanitation

47. Clinical Presentation
Physicalexamination
General exam:
•Appearance: apathy, puffy, facies, wasting signs
•Hair changes: color, distribution, texture, pluckability
•Dehydration: dry mucous membranes, sunken eyes, sunken fontanelle,
↓ skin turgor/ tenting, cold extremities, temperature gradient, delayed
cap. refill, weak pulse, (in)ability to drink, altered consciousness)
•Pallor, Jaundice, Cyanosis, Lymphadenopathy, Edema

48. Clinical Presentation
•Eye changes-Corneal ulceration, Bitotspots
•Lips-angular cheilitis, stomatitis
•Mouth-oral thrush, gums, teeth;noma-chronic necrotizing
ulceration of the gingiva & cheek
•ENT-signs of infection
•Nail changes-fissured, ridged
•Skin-appearance: flaky vs. shiny, pigmentation, dermatosis
•Subcutaneous fat-↓ in legs, arms; buttocks >>“baggy pants”

49. Clinical Presentation
Systemic exam
•CNS-consciousness, signs of meningitis
•CVS-signs of heart failure
•RESP-rachitic changes, added sounds
•GIT-distension hepatomegaly

50. Clinical Presentation
Anthropometry
•Body weight, Height/ Length
–Weight for age:
>90%(Gomez) >80%(IAP) of expected considered Normal
–Height for age:
ABN= Stunting, chronic
–Weight for height:
ABN= Wasting, acute
–BMI

51. Clinical Presentation
•Head circumference
•Mid-upper arm circumference
–Left upper arm
–Midpoint from acromion(shoulder) to olecranon(elbow) with
arm bent at right angle (N= >13.5cm, severe= <11.5cm)
•Skin fold thickness (N= 9-11mm)
•Chest circumference
•Waist hip ratio

52. WHO Classification
Evidence of
Malnutrition
Moderate Severe
Symmetricedema No Yes (edematous PEM)
Weight forheight WHZ <-2 & >-3 (70-
90%)
Z score <-3 (<70%)
Heightfor age WHZ <-2 & >-3 (85-
89%)
Z score <-3(<85%)

53. Kwashiorkor vs. Marasmus
Kwashiorkor Marasmus
1. Generalized edema, pitting edema
over feet & legs, facial edemai.e“moon
facies”, shiny skin
1. Marked muscle wasting; shrivelled
face i.e“little old man/monkey-like”,
wrinkled skin, baggy pants
2. Growth failure-wasting masked by
edema
2.Extreme growth failure
3.Apathy, irritability 3. Alert
4. Poor appetite 4. Good appetite
5. Some subcutaneous fat present 5.Loss of subcutaneous fat
6. Hair changes -fine, sparse, easily
pluckable, flag sign
6.Hair changes less common
7.Hepatomegaly 7. Hepatomegaly absent

54. Kwashiorkor vs. Marasmus
Kwashiokor Marasmus

55. Investigations
1.CBC/ RBC indices-find anemiacause
2.PBF
3.CRP
4.RBS
5.LFTs-albumin
6.Serum pre-albumin
7.Ferritin/TIBC
8.Vitamins & minerals-B12,folate, vit. D, vit. K, Ca2+, Mg2+

56. Investigations
8. Septic screen
–BS for MPS
–Blood cx.
–Urinalysis
–Stool for O/C
–Mantouxtest
–PITC
–CXR

57. Treatment-Whom to Admit?
•Outpatient
Clinically well
Alert
With appetite (passed the
appetite test)
•Inpatient
Medical complications
≥1 IMCI danger signs
–unable to drink or breastfeed
–convulsions
–lethargic or unconscious
Severe oedema
Poor appetite (fails the
appetite test)

58. Treatment-Phases
Phase I (initial
Stabilization)
Day 1-7
Phase II (Rehabilitation)
Week 2-6
Phase III (follow Up)
Week 7-26
1.Tx. oflife threatening
problems
2.Correction of metabolic
abnormalities
3.Correction ofspecific
micronutrient
deficiencies
4.Feeding is begun
1.Intensive feeding to
recover most of lost
weight (“catch-up
growth”)
2.Emotionaland physical
stimulation
3.Mother/ care giver
trained to continue care
at home
4.Preparation for
discharge
1.Intensive feeding to
recover most of lost
weight (“catch-up
growth”)
2.Emotionaland physical
stimulation
DONE AT HOME
3.Nutrition clinic visits:
planned & regular
If risk of relapse TCA in
1/52, 2/52, 1/12, 3/12
After 6mo. Yearly visits
until 3yrs

59. Treatment-10 step Approach
1. Treat Hypoglycemia
•RBS <3mmol/L; if unavailable treat as
hypoglycaemia if not alert
•Give 5mls/kg D10
•Start P.O or NGT glucose or feeds as soon as
possible(not >30min after admission)
•Monitor glucose every 30min

60. 2. Manage Hypothermia
•Axillary temp. < 35.0⁰C, Rectal temp. <35.5 ⁰C
•Treatment:
–Feeding/controlling hypoglycemia
–Keep dry
–KMC
–Blankets
–Warm bags of fluid
–Heaters/Lamps
•Monitor temp. 2hrly until rectal temp. up to 36.5⁰C

61. 3. Manage Dehydration
•Check for dehydration if diarrhoea present
If in shock i.e. AVPU <A with absent/weak pulse, cap
refill >3s, cold extremities with temp. gradient
•20mls/kg RL with D5 (450mls RL + 50mls 50%
Dextrose)in 2hrs
If severe anaemia Hb <4g/dL
•Transfuse whole blood 10mls/kg in 3hrs+
Furosemide 1mg/kg

62. If not in shock/ after txshock
•I.VRL in D5 4mls/kg/h
OR
•P.Oor NGReSoMal10mls/kg/hrfor 2hrs
Then
•ReSoMal7.5mls/kg over 1hrthen introduce first feed with F75
•Alternate ReSoMal& F75 each hrat7.5mls/kg/h for 10hrs
•↑/↓hrlyas tolerated by 5-10mls/kg/h
•At 12hrs, switch to 3hrly oral/ng feeds with F75

63. 4. Treat Electrolyte Imbalance
•Commercial F75
OR
•Mineral mix + 4mmol/kg/day K
+

64. 5. Treat Infection
All children with SAM should get:
•I.V Penicillin 50,000IU/kg QID (or I.V Ampicillin 50mg/kg TDS)
+ Amikacin 15mg/kg for 5/7
•If improved after 48hrs, change Penicillin to Amoxicillin
Add:
•Nystatin/ Clotrimazole-oral thrush
•Albendazoleafter 7 days of treatment-dewormer
•TEO +Atropine-pus/ulcerations in eye

65. 6. Correct Micronutrient Deficiencies
•Vit. A if eye signs on days 0,2,14
•Multivitaminsfor at least 2/52
•Folic acid 2.5 mg on alternate days
•IronONLYif child gaining weight

66. 7. Prescribe feeding needed
•Frequent, small feeds of low osmolarity, low lactulose
•Oral/NG, never parenteral!
•Monitor:
–Amount of feeds
–Vomiting
–Diarrhoea
–Daily weight

67. 8. Catch up growth feeding
•With F100 or RUTF on day 3-7usually after
return of appetite & resolution of oedema
9. Sensory Stimulation
•Caring environment for child
•Cheerful stimulating environment: physical
activity, age appropriate play & toys

68. 10. Preparation for Discharge
•Criteria for discharge:
After tx. of all infections and medical conditions
Good appetite & gaining weight (90% of expected)
Resolution of oedema
Available support at home from family/community
Mother/caregiver should be available, understand and capable of
supplying child’s needs
Follow up

69. 1) Shock
2) Hypoglycemia
3) Hypothermia
4) Metabolic disturbances: hypoNa
+
hypoCa
2+
hypoK
+
5) Infections
6) Convulsions
7) Severe anemia-protein & Fe def.
8) Heart failure
9) Malabsorption
10)RefeedingSyndrome
11)Developmental delays
12)Jaundice
13)Bleeding tendencies
14)Sudden death
Complications

70. Refeeding Syndrome
•Severe electrolyte and fluid shifts associated with
metabolic abnormalities in malnourished patients
undergoing refeeding orally, enterally, or parenterally &
includes hypophosphatemia, hypomagnesemia
hypokalemia
•Hallmark: development of severe hypophosphatemia
after cellular uptake of phosphate during the 1st week
of starting to refeed.

71. RefeedingSyndrome
•At Risk:
Kwashiorkor or marasmus
Anorexia nervosa
Chronic malnutrition, e.g., from carcinoma or in the elderly
Chronic alcoholism
Prolonged fasting
Duodenal switch operation for obesity
Hunger strikers
Oncology patients
Postoperative patients

72. RefeedingSyndrome

73. RefeedingSyndrome
•Manifestations: (serum PO
4
-
≤0.5 mmol/L)
–weakness
–rhabdomyolysis
–neutrophil dysfunction
–cardiorespiratory failure 2⁰to cardiomyopathy/impair eddiaphragmatic contractility
–arrhythmias
–altered level of consciousness
–seizures
–sudden death
•Monitor during refeeding& if low, administer phosphate

74. Prevention of Malnutrition
i. Nutritional Planning:
1.Land reforms-ownership
2.Agricultural improvements-good practices,
application of appropriate technology
3.Affordable food prices-staples
4.Elimination of poverty

75. Prevention of Malnutrition
ii. Direct Nutrition & Health Interventions:
1.Immunization
2.Early dx. & proper tx. of common illnesses
3.Regular deworming
4.Nutritional education
– Nutritional quality and importance of common foods
– Importance of EBF
– Proper supplementation & weaning
– Irrational beliefs and practices
5.Early detection of malnutrition & intervention-growth charts, anthropometric measurments
6.Fortification of foods e.gflour-VitA, Fe, Zn
7.Proper sanitation, water supply & proper hygiene practices

76. References
1.Nelson’s Textbook of Pediatrics, 18
th
ed.
2.Basic Paediatric Protocols January 2016, 4
th
ed.
3.Slideshare
4.WHO MCCI Guidelines ,2
nd
ed. 2013
5.https://www.who.int/elena/titles/full_recommendations/sam_mana
gement/en/
6.http://vikaspedia.in/health/nutrition/malnutrition/strategies-to-
prevent-malnutrition-and-improve-nutrition