Nutritional Problems in Public Health

1. Nutritional Problems in Public
Health
Prof Dr. Sanjev Dave
Assoc Prof Community Medicine
ASMC Hardoi(UP)
Ex-HOD Department of Community Medicine
Soban Singh Jeena Govt Institute of Medical sciences & Research,Almora
(Uttarakhand)

2. • Low Birth weight
• Protein Energy Malnutrition
• Xerophthalmia
• Nutritional Anemia
• Iodidine disorder
• Endemic Flurosis
• Lathyrism

3. •Low Birth Weight

4. Birth weight
• BW is the SINGLE MOST important
determinant for the chance of survival,
healthy growth and development.
• Cut off limit for normal BW is 2.5kg and above
• Any infant with a BW of less than 2.5 kg
regardless of gestational age is considered as
LOW BIRTH WEIGHT baby

5. Grading of LBW
• 2.5kg-2 kg = LBW
• 2kg-1.8 kg = Very LBW
• <1.8 kg = Extremely LBW
2.5 kg -3.5 kg = Normal birth weight
>3.5 Kg = Obese

6. Importance of LBW
1. Reflects inadequate nutrition and ill health
during ANC period
2. Associated with mental retardation
3. High risk of perinatal and infant mortality
IMR is 20 times higher for all LBW than other babies
Lower is the BW- Lower the chance of survival

7. Importance of LBW….
• 4. Most important cause of death in the
critical neonatal period
• 5. Second leading cause of death in under 5
and
• 6. Chance to become victims of PEM

8. LBW: Causes
Maternal factors
• Malnutrition
• Severe anemia
• Heavy physical work
• HTN
• Malaria
• Toxemia
• Smoing
• Low SES
• Very young age
• High parity
Placental causes
•Placental insufficiency
•Placental abnormality
Foetal causes
•Foetal abnormality
•Intrauterine
infection
•Chromosomal
abnormality
•Multiple gestation

9. Prevention
• Direct Intervention:
– Identification of High risk pregnant women and
giving them special care
• ANC mother’s health card
– Increased food intake
– Correction of anemia
– Controlling infection: malaria, UTI, bacterial
vaginosis
– Early detection and treatment of medical disorder

10. Prevention of LBW….
• Indirect Management
–Avoidance of smoking
–Family planning for birth spacing
–Improving health and nutrition of the young
girls
• Supplementary food and
• Iron and folic acid food fortification in various
govt schemes

11. Treatment
• Tt is based on Birth weight. Divided in to three
categories:
• BW <2.5-2 kg: Institutional care for day or two+
Special home care
• BW b/w 1800gm-2kg: Basic Institutional care +
Kangaroo Mother care
• BW <1800: Comprehensive Institutional care

12. PEM

13. What is PEM??
• PEM is a syndrome synonymus with under
nutrition,
• Results from low intake of food (Food gap)
containing sufficient energy and protein and
other nutrients (in quantity and quality)

14. Malnutrition/infection Cycle
Inadequate dietary
intake
Weight Loss
Growth faltering
Lower Immuity
Mucosal damage
Disease: Incidence, Duration,
severity
Appetite Loss
Nutrient loss
Malabsorption
Altered
Metabolism

15. Contributory factors in the web of
causation
• Economic Factors:
Low Income and poor purchasing power
Poor availability of food and health care
Poor and insanitary living condition
Many mouths to feed
Infection and Disease
Frequent illness and infectious diseases like diarrhoea,
respiratory infection, cold cough
Socio cultural factors
Gender bias
Decision making
power
Workload of the care
giver
Family traditions
Composition of the
family
Infrastructural
resources
Faith healers
Environment
Poor safe drinking water
Poor sanitation and hygiene
Housing conditions

16. • Knowledge and Attitude
Low literacy
Lack of understanding for appropriate use of food
Lack of knowledge sign and symptoms for malnutrition
Lack of knowledge where to go in case of problem
Care and Feeding Practice
Misconception about use or restriction of some food
Delayed or inadequate colostrum feeding
High dilution of the formula feeding
Use of unsafe water in food handling
Poor personal Hygiene
Use of more starchy food that is lack of deficient of protein and
other micronutrients

17. Classification of the PEM
Ranges from growth failure to overt marasmus/.Kwashiorkar
Features MARASMUS KWASHIOKAR
Clinical Always Present
Muscles wasting Obvious Hidden by Odema
Fat wasting Severe loss of SC fat Fat –often retained
but not firm
Odema None Present in Lower
Legs
Weight for Height Very low Low but masked by
odema
Mental Changes Sometimes quite and
apathetic
Irritable, moaning,
apathetic

18. MARASMUS KWASHIOKAR

19. Classification of PEM…….
Features MARASMUS KWASHIOKAR
Clinical Some times Present
Appetite Usually good Poor
Diarrhoea Often Often
Skin Changes Usually none Diffuse
pigmentation”Flacky
paint dermatosis”
Hair changes Seldome Sparsy, silky, easily
pulled out
Hepatic
Enlargement
None Sometimes, due to
fatty liver

20. Classification of PEM…..Biochemical
Changes
Biochemical
Changes
Marasmus Kwashiokar
Serum Albumin Normal Or slightly
decreased
Low (<3gm/100ml)
Urinary Urea per
g creatinine
Normal or decreased Low
Hydroxyproline/
Creatinine ratio
Low Low
Plasma/Amino
Acids
Normal Elevated

21. IAP Classification
Based for wt for age
• >80 % = normal
• 71-80%= grade I malnutrition
• 61-70% = grade II malnutrition
• 51-60% = grade III malnutrition
• 50% or less= grade IV malnutrition

22. H/A
W/H
M> - 2SD <m-2 SD
M> - 2SD Normal Wasted
<m-2 SD Stunted Wasted and
stunted
1. Children With insufficient BUT well proportionate
growth
2. Normal Height but wasted
Waterlow’s Classification

23. Nutritional Status Stunning Wasting
Normal >95 90
Mildly Impaired 87.5-95 80-90
Moderately Impaired 80-87.5 70-80
Severely Impaired <80 <70
Weight for Height= Weight of the child x100 / Weight of the normal
child at the same height
Height for Age= Height of the child x100 / Height of the normal
child at the same age

24. Severe Acute Malnutrition
(SAM)
• Occurs in young children, 6mths -5 years
• Defined as:
– Very low weight for height <-3SD for median (WHO
growth standard)
– Visible severe wasting
– Bipedal/Bilateral edema
– Mid UAC < 11.5cm
If there is edema, case is always classified as SEVERE

25. Preventive Measures
• Health
Promotion
ANC care
Care during Lactation
Low cost weaning food
Measures to improve
family diet
Nutrition education for
correct feeding
practice
Home economics
Family planning and
Specific Protection
diet rich in P & E:
egg, milk, fresh fruits
Immunization
Food fortification
Early Diagnosis and
treatment
Periodic Survillance for any
lag of growth
E D& T for Infection
Rehydrtion in diahhoea
Deworming of heavily
infested children
Rehabilitation
Nutritional Rehab sr
Hospital tt
Follow up services

26. • Xerophthalmia
• Dry eye

27. Vit A Deficiency
• Ocular manifestation of Vit A def: Xerophthalmia
• Most common and serious nutritional cause of
blindness
• Commonest in age gr 1-3 years…often related to
faulty weaning practices
Totally preventable cause of blindness by correct
feeding practices and early diagnosis

28. Causes of VAD
• Inadequate Breast feeding
• Poor quality of complimentary feeding
• Poor intake of Vit A rich food for long time
• Fat Malabsorption
• Inflammatory conditions
• Frequent Infections like diarrhoea/ measles

29. India
• Rice
eating
States
– AP
– TN
– K
– Bihar
– WB
Acc to WHO (2009): Global VAD is 40%,
mainly among preschool and preg and
lactating women
India: 5.7% children in India suffer from
eye signs of VAD
Acc to NNMB: (2006):
Prevalence of Bitot spot: 0.7%
Prevalence of night Blindness: o.5%

30. WHO Classification of VAD
(Collective form of VAD and blindness)
S
N
Symptoms/ Stage Discription
Night Blindness Early sym, Impairement of dark adaptation,
Esp in sunset and dark light
Conjuctival xerosis Dryness of Conjuctiva, loss of transperancy, wrinkling ,
depigmentation, eyelid: thick, wrinkled, and rough
Bitot spot Dirty white or foamy raised spots , outer side of cornea
Are because of denuded conjuctival epithelial cells
Corneal xerosis Sigh of Severe VAD
Cornea: looses nornal shining, appears dry and rough,
Child tends to keep eyes closed in bright lightdue to
photophobia
Corneal Ulceration(<1/3
cornea)
If become deep..lead to perforation
Corneal
Ulceration(>1/3)
Liquifection of whole cornea
Corneal Scarring Healed cornea: leaves the scar

31. Dry Eye
Bitot Spot
Keratomalacia
Bilateral Blindness

32. Prevention and Control of VAD
• Vit A Supplementation
• Food based approach or dietary diversification
• Nutrition and Health Education
• Fortification

33. Vit A Supplementation
• “National Prophylaxis Programme against
nutritional blindness” started in 1970:
Beneficiaries Pre school children(1-5 yr),
operated through AWC
• Modified in 1992: Coverage to children (9mths -3
years)
• Since Tenth Five yr plan: Prog is the part of
NRHM…covers all children upto the age of 5 years

34. 1) Prophylactic dose:
– One lakh: at nine months
– Two lakh IU: every six months upto the age of 5 years
2) For Sick Children:
All children with xerophthalmisa to be treated with massive dose of Vit A
All Cases of measles should be treated with additional dose of Vit A
All children of severe malnutrition should be treated with Vit A
Dose(GoI schedule): 2 lakh IU Immediately and 2 lakh IU repaet dose after
4 weeks
3) Promotion of Vit A rich food by pregnant and lactating women
GLV, yellow/orange vegetables (pumpkin, carrot, papaya, mango,
orange) with cereals pulses to the weaning child

35. Nutritional Anemia

36. Nutritional anemia
• Nutritional anemia is a disease syndrome
caused by malnutrition
• Defined by WHO “a condition in which Hb
content of the blood is lower than normal as a
result of deficiency of one or more nutrients,
redardless of the cause of deficiency”

37. • Iron Def Anemia is the most widespread micronutrient
def irrespective of gender, caste, creed, religion.
• Silent emergency in women (15-49) and children (6-
35mths)
• In adolescents girls educational and economic state
does not have any influence in the prevalence of
anemia….
• …….as they soon will enter in the reproductive
cycle….so imp to screen them for tt and prevention of
anemia.

38. Age group RDA (mg/day)
Adults, males
Adults, females:
Pregnancy
Lactation
28
30
38
30
Requirements of iron for different age groups

39. Etiology
• Low dietary intake of iron rich food
• Poor absorption of Iron from GIT
• Loss of Iron from body
• Increased demand
• Low body store

40. Consequences/Detrimental effect of
anemia
• In main three areas
– 1) Pregnancy:
• Incresed risk of Maternal mortality and Infant mortality
• Abortion, premature births, IUGR, PPH, Low BW
– 2) Infections: Caused and aggrevated by:
• Malaria,
• Intestinal parasites
– 3) Work Capacity:
• Poor performance
• Delayed mental and physical developrment

41. Intervention: prevention and
treatment of anemia
• 1) Iron and Folic acid supplementation:
– National Nutritional Anemia Prophylaxis
programme was launched in 1970
– Beneficiaries: children, pregnant women and
lactating mother

42. –It is now operated as part of the RCH prog
• Expanded targets are:
– Infants :6mth-12 mhts
– School children: 6-10 years
– Adolescents: 11-18 years
– Pregnants
– Lactating women

43. • 6mth-60mth(5years): for 100 days
– 20mg elemental Iron
– 100Microgm folic acid
• School children 6-10 years: for 100 days
– 30 mg elemental Iron
– 250microgm of Folic acid
• Adolescent aged: 11-18 years: for 100 days
– 100 mg elemental Iron
– 500microgm of folic acid

44. • Pregnant women:
• For Prophylaxis:one tab and
• For tt: Two Tabx100 days
– 100 mg elemental Iron
– 500microgm of folic acid
• Lactating women:
– 100 mg elemental Iron
– 500microgm of folic acid

45. (2) Iron Fortification
• WHO recommend strategy where prevalence of
anemia is very high
• Commonest medium to fortify is salt..
– as universally consumed,
– by all segment of population and
– no special delivery system
• Ferric-ortho-phosphate or Ferrous sulphate with
sodium bisulphate is enough to fortify salt

46. Food based approach
• Promotion of breast feeding and timely
complementary feeding
• Increased consumption of Vit C
• Use germination ot fermentation to increase
bioavailability of iron
• Promotion of Kitchen garden for GLV, Vit A
and C rich food like papaya, mango, lemon

47. • Iodine Deficiency Disorder

48. IDD
• It is the most preventable cause of mental
retardation and brain damage in the world
affecting the quality of life
• More of the geographical problem rather than
socioeconomic in nature
• No State in India can be said entirely free from
Goitre, but most commonly present in the goitre
belt….streching from Kashmir to Naga Hills in the
East…2400 km

49. Proposed classification of Goiter (WHO)
Grade Sigh and Symptoms
Grade 0 No palpable and visible goiter
Grade 1 A mass in the neck that is consistent with an
enlarged thyroid that is palpable
But Not visible when neck is in normal position.
It moves upward in the neck as the subject
swallows.
Nodular alteration can occur when thyroid is not
enlarged
Grade 2 A swelling in the neck.
Visible when neck is in normal position and
consistent with an enlarged thyroid when neck is
palpated

50. Goiter Control
National Goiter Control Programme
• 4 Essential components
– Iodised salt or oil
– Monitoring and surveillance
– Manpower training
– Mass communication

51. Iodized salt or oil
• Iodized salt most widely
used..public health
measures…becos
– Widely used
– Convenient
– Effective means
• Under PFA, India
– 30ppm at production level
and 15ppm at consumer
point
According to NIN Hyderabad:
1 ml xIM inj gives protection
against 4 years
Feasible strategy where
IS is not reachable
IS is short in supply
Disadv:
Expensive
Reaching every person is
difficult

52. Iodine monitoring
• Neonatal Hypothyroidism is the sensitive
indicator for environmental iodine deficiency
and can be effective for monitoring the impact
of a programme
National Labs for monitoring and surveillance
1) Iodine excretion determination
2) Determination of iodine in water and soil and food
3) Detrmination of Iodine in salt for quality control

53. Manpower training
• All health worker
• Other involved in the programme
– For all aspects of goiter control including legal
enforcement

54. Mass communication
• Nutrition education: for creating public
awaeness
• Legal enforcement

55. •Endemic
Flurosis

56. Endemic Flurosis
• Occurs when drinking water more Fluorine (3-
5mg/L)
• Toxic manifestations include:
– Dental Fluorosis
– Skeletal Fluorosis
– Genu velgum

57. Dental Fluorosis
• Excess of Fl when calcification of tooth is occuring
esp in the initial 7 years
• Intake of Fl is 1.5mg/L
• Mottling of teeths: incisors of upper jaw
• Loose shiny appearance
• Later white patch…..yellow….brown
• Loss of enamel

58. Dental Flurosis

59. Skeletal fluorosis
• Life time daily intake b/w 3-6 mg/L
• Seen in older adults
• Heavy fluoride deposition on
skeleton
• Manifested as pain numbness
&tingling sensation of the
extremities, stiffness of neck
• Crippling flurosis can occur

60. Genu valgum
• Seen in population whose
staple is Sorgum (jowar)
…diet based on Sorgum
retain more Fl than rice
based diet
• Seen in some dist of AP
• The lower limbs appear as
knock kneed due to
osteoporosis

61. Interventions
• 1. Changing the water source: if possible
2) Chemical TT: Defluofidisation by chemical
• Tachnique was developed Environmental
Engineering Research Institute, k/a NALGONDA
technique
• Addition of two chemical : lime and alum in
sequence and followed by flocculation,
sedimentation and filteration

62. •Lathyrism

63. • Paralysing ds in human and animal
• Occurs in two form: neurolathyrism (Human)
and Oseolathyrism (Animal)
• Patient develop spastic paralysis of lower limb
of gradual onset

64. • Commonly seen in population having “Khesari
Dal” or Lathyrus Sativus
• Local name: Teora Dal/ Lak Dhal/ Batra/
• Gharas/ Matra
• Characteristic feature: Triangular in shape with
a pit
• Looked like Red gram/bengal gram

65. Lathyrus Sativus
It is a good source of protein
but contains a toxin affecting
the nerves.

66. • Toxin: BOAA: Beta –Oxalyl-Amino-Acid
• Diet containing 30% of this dal , consumed over a
period of 2-6 mths will result in Neurolathyrism.
• N L mainly affect young men b/w the age of 15-
45
• Ds has 5 stages.

67. 5 stages
• 1. Latent Stage: completely reversible stage,
therefore imp for public health point
– Person apparently normal but with stress shows ungainly
gait
– On neurological examination shows characteristic physical
sign
2. No stick Stage:
Pt walks with short jerky steps without any help of stick…
Large no of patient are in this stage

68. • 3. One Stick Stage: Crossed gait, with
tendency to walk on toes…due to muscular
stiffness
• Use of one stick to maintain the balance
Two Stick Stage:
Symptoms are more severe
Gait is slow and clumpsy, get easily tired
Due to excessive bending of knees and
crossed legs …pt needs crutches
Crawler Stage:
Finally Erect posture is impossible
Knees cannot take the support of body weight
Atrophy of the thigh and leg muscles
Crawls by throwing his weight on his hands

69. Interventions
Removal of toxin
 Steeping method
 Soaking the pulse in hot water for about 2 hours and the soaked
water is drained off completely
 Genetic Approach
 Development of low toxin varieties of Lathyrus
 Banning the crop
 The Prevention of food adulteration act in India has banned Lathyrus
in all forms

70. • Thank You…