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Nutritional Problems in Public Health.pptx
- 1. Nutritional Problems inPublic 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 Birthweight • Protein Energy Malnutrition • Xerophthalmia • Nutritional Anemia • Iodidine disorder • Endemic Flurosis • Lathyrism
- 3.
- 4. Birth weight • BWis 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 isbased 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.
- 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 WeightLoss Growth faltering Lower Immuity Mucosal damage Disease: Incidence, Duration, severity Appetite Loss Nutrient loss Malabsorption Altered Metabolism
- 15. Contributory factors inthe 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 andAttitude 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 thePEM 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
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- 19. Classification of PEM……. FeaturesMARASMUS 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 MarasmusKwashiokar 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 forwt 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 StunningWasting 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 ANCcare 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.
- 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 ofVAD (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.
- 32. Prevention and Controlof 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.
- 36. Nutritional anemia • Nutritionalanemia 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 DefAnemia 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 dietaryintake 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 treatmentof 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 nowoperated 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): for100 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 DeficiencyDisorder
- 48. IDD • It isthe 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 ofGoiter (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 GoiterControl Programme • 4 Essential components – Iodised salt or oil – Monitoring and surveillance – Manpower training – Mass communication
- 51. Iodized salt oroil • 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 • NeonatalHypothyroidism 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 • Allhealth worker • Other involved in the programme – For all aspects of goiter control including legal enforcement
- 54. Mass communication • Nutritioneducation: for creating public awaeness • Legal enforcement
- 55.
- 56. Endemic Flurosis • Occurswhen drinking water more Fluorine (3- 5mg/L) • Toxic manifestations include: – Dental Fluorosis – Skeletal Fluorosis – Genu velgum
- 57. Dental Fluorosis • Excessof 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.
- 59. Skeletal fluorosis • Lifetime 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 • Seenin 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. Changingthe 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.
- 63. • Paralysing dsin human and animal • Occurs in two form: neurolathyrism (Human) and Oseolathyrism (Animal) • Patient develop spastic paralysis of lower limb of gradual onset
- 64. • Commonly seenin 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 isa 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. OneStick 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.