2. Protein-Calorie Malnutrition (PCM) Professor Ali Shaltout

3. Wellcome Classification

4. Kwashiorkor (KWO) Etiology:  Severe deficiency of protein intake Usually occurs after weaning from breast on chate diet. Usually occurs after weaning from breast on chate diet. Age: 6 months - 2 years Inadaquate breast feeding without supplementation Inadaquate breast feeding without supplementation Dietetic errors (dilutional formula) Dietetic errors (dilutional formula)

5. Pathology of KWO 1. Fatty infiltration of the liver 2. Atrophy of the intestinal villi (Brush border) 3. Atrophy of pancreatic acini (selective) 4. In severe cases: Heart,kidney and brain are affected.

6. Clinical Manifestations of KWO

7. Constant Features 1- Growth Failure:  Failure to gain wt, followed by loss of wt.  Wt: is first affected, then height. 2- Edema:  Puffy eye lids, edema of the face  early sign  then edema of the extremities (pitting edema)  No ascitis or pleural effusion (very rare)

8. Constant featuresContinue 3- Muscle wasting:  Estimated by midarm circumference why? 1. Not affected by edema why? 1. Not affected by edema 2. Constant between 1-5 years. 2. Constant between 1-5 years. 3. Ms. wasting is proximal 3. Ms. wasting is proximal  > 13.5 cm Normal  12.5-13.05 cm Prekwo  < 12.5 cm Severe KWO 4- Mental changes:  Apathy, miserable look lack of interest to the surrounding lack of interest to the surrounding failure to smile failure to smile  Due to: Disturbed metabolism of aromatic aminoacids Disturbed metabolism of aromatic aminoacids

9. Hair Changes in KWO  Sparse, easily pickable, dyspigmented  Flag sign (bands of dark and light coloured zones along the length of hairs)  A/E: 1- Sulphar - containing aminoacids  2- Pantethonic acid  3- Cupper 

10. Skin Changes In KWO  Dermatitis is common (in flexure sites)  Hyperpigmentation, desquamation, ulcerations and secondary infection  A/E : 1- Protein  2- Essential FA  3- Vitamin A  4- Niacin  5- Zinc  6- Suprarenal disturbance

11. Hepatomegaly in KWO  Caused by fatty infiltration ( due to  liporotein and lipotropic factors) ( due to  liporotein and lipotropic factors)  Return to normal on recovery  No cirrhotic changes ( cirrhosis occur only if toxic or viral hepatitis) ( cirrhosis occur only if toxic or viral hepatitis)  Ascitis in KWO may be due to : TB peritonitisTB peritonitis Toxic hepatitis & cirrhosisToxic hepatitis & cirrhosis

12. KWO and Vitamin D Deficiency  Patient with KWO has vit. D  Atrophic rickets (generalized osteoprosis)  Manifested rickets (rosaries,….) in patient with KWO=rickets (vit. D  ) developed before occurrence of KWO

13. Anemias in KWO Any type of anemia can occur in KWO 1- Macrocytic anemia (Folic acid and B 12  ) 2- Microcytic hypochromic anemia (iron, cu,Zn  ) 3- Normocytic normochromic anemia (Bone marrow arrest) * Types 1 & 2 are common and are called Dimorphic anemia * Type 3: is rare and occurs only in severe forms of KWO (protein  ).

14. Malnutrition (KWO)  Infection Secondary immune deficiency Due to: 1- Cell- mediated immunity  2- Phogocytic functions  3- Transferrin  4- Local:  secretory IgA  Hcl (TB & HIV infection ++)  Hcl (TB & HIV infection ++) * Chest x ray is important to exclude TB.

15. Malnutrition  Malabsorption Due to: 1-  Salivary amylase 2-  Hcl 3-  pancreatic lipase, amylase 4- Villous atropy 5- Fatty liver 6- Immuno def.

16. Biochemical Changes in KWO 1- S. albumin  (the most characteristic change) 2- Hypoglycemia, Hypocalcemia Hypokalemia, Hypomagnesemia Hypokalemia, Hypomagnesemia 3- BUN / Cr ratio < 8 4- Enzyme def.: Amylase, lipase, Disaccharidases, Transaminases, Alk. Phosphatase. 5- Vitamins and mineral def. 6- Anemias

17. Anthropometric Measures 1- Weight chart (Flat curve) 2- Height (less affected) 3- Mid-Arm C. (< 12.5 cm) 4- Chest / head ratio (<1 after 6 mo.) 5- Bone age (chronic malnutration )

20. Complications of KWO 1- Intercurrent infections (TB& HIV) 2- GE 3- Congestive HF 4-Hypoglycemia 5- Hypothermia The commonest cause of death in KWO: The commonest cause of death in KWO: Chest infection (CXR)Chest infection (CXR) The cause of sudden death in KWO: The cause of sudden death in KWO: Hypoglycemia (Lucine- induced)Hypoglycemia (Lucine- induced)

21. Prevention of KWO  Encourage breast feeding with supplementation.  Proper weaning on high protein and balanced diet.  Immunization against infectious diseases.  Early detection of malnutrition and correction.

22. Treatment of KWO 1- Treat the cause. 2- Treatment of dehydration: (Hypotonic dehydration) Fluids Fluids electrolytes electrolytes Plasma (shocked) Plasma (shocked) 3- Dietetic management: Skimmed milk (initial), few days, gradual Skimmed milk (initial), few days, gradual Half cream milk Half cream milk Full cream milk or protein milk Full cream milk or protein milk Lactose-free milk (Al 110, Isomil, Bebelac FL), if there is lactose intolerence Lactose-free milk (Al 110, Isomil, Bebelac FL), if there is lactose intolerence Protein- rich diet: Meat, eggs, cheese, fish,…. Protein- rich diet: Meat, eggs, cheese, fish,….

23. Treatment of KWOContinue 4- Blood & Plasma transfusion 5- Treatment of Anemias: Folic acid & B 12 Folic acid & B 12 Blood Blood iron postponed 10 days iron postponed 10 days 6- Vitamins A,B,C A,B,C vit. D also postponed 10 days vit. D also postponed 10 days 7- Infection control 8- Treatment of hypoglycemia & hypocalcemia

24. Recovery from KWO  Smile: 4 days  Edema: 10 days  Complete: 1-3 month  Death rate:15 % (of admission)

25. Marasmus (Infantile Atrophy) Etiology: Inadequate caloric intake due to:  Dietetic errors (quantitative or qualitative)  Repeated GE.  Malabsorption ( cystic fibrosis, ceiliac D)  Chronic infections as TB.  Congenital malformations as eleft palate, pyloric stenosis, congenital HD,…  Metabolic disorders: Galactosemia, Pku,...

26. Pathology of Marasmus  The main pathological changes is loss of fat stores  Atrophy of muscles and internal agans  Generalized osteoporosis. * Biochemical changes are few and non specific

27. Clinical Features of Marasmus Constant features 1. Wt. Loss 2. Muscle wasting 3. Lo ss of subcut. fat. Others Others  Infection  Vitamin dif.  Hypothermia  Constipation  Emaciation, atrophy  Hypotonia

28. Degrees of Marasmus  First degree:- Wt. loss 15 - 30 % - Loss of subcut. fat of Abdomen  Second degree:- Wt loss 30 - 49% - Loss of Subcut. fat of thigh, buttocks - Loss of Subcut. fat of thigh, buttocks  Third degree: - Wt loss > 50 % - Loss of buccal pad of fat (senile face) - Loss of buccal pad of fat (senile face) - The last fat to be lost because it contains unsaturated fatty acids - The last fat to be lost because it contains unsaturated fatty acids

29. Treatment of Marasmus 1- Treat the cause 2- High caloric diet: 150-200 kcal / kg 3- Diet: High protein, moderate chate & Fat High protein, moderate chate & Fat Start with skimmed milk followed by ½ cream and then full cream milk Start with skimmed milk followed by ½ cream and then full cream milk Lactose-free milk Lactose-free milk 4- Blood,plasma transfusion 5- Correct vit - def 6- Treat any infection

30. Malnutrition In Children Beyond Infancy Mainly due to psychological disturbances or bad feeding habits: Mainly due to psychological disturbances or bad feeding habits:  No reduction of wt.  Fatigue, irritability  Anorexia, constipation  Pallor   Attention and school performance   Susceptibility to infection

31. Early Detection of Malnutrition 1- History: Early weaning Early weaning Dietetic errors Dietetic errors 2- Subclinical (Pre KWO): Failure to gain wt. Failure to gain wt. Hair changes Hair changes Vitamin def. manifestations Vitamin def. manifestations

32. Early Detection of MalnutritionContinue 3- Anthropometric measures: A- Weight chart: Flat curve B- Mid - arm circumference 12.5 - 13.5 cm  Pre KWO12.5 - 13.5 cm  Pre KWO < 12.5 cm  Severe KWO< 12.5 cm  Severe KWO C- HC / Chest C ratio: (After 6 months): < 1 Normal(After 6 months): < 1 Normal > 1 Pre KWO > 1 Pre KWO

33. Early Detection of MalnutritionContinue 4- Biochemical changes: Serum albumin < 2-8 gm / dl Serum albumin < 2-8 gm / dl (one of the earliest changes)(one of the earliest changes) BUN/ Cr. Ratio: 8-12 Pre KWO BUN/ Cr. Ratio: 8-12 Pre KWO < 8 Severe KWO < 8 Severe KWO Non essential / essential A.A: Non essential / essential A.A: 2-3 Pre KWO2-3 Pre KWO > 3 Severe KWO> 3 Severe KWO Transferrin  Transferrin 