Protein-Calorie Malnutrition (PCM) Professor Ali Shaltout.

Protein-Calorie MalnutritionProtein-Calorie Malnutrition(PCM)(PCM)

Professor Ali ShaltoutProfessor Ali Shaltout

Wellcome ClassificationWellcome Classification

Wt. 60 – 80 % < 60 %

No edema Under weight Marasmus

Edema Kwashiorkor (Kwo)

Marasmic Kwo

Kwashiorkor (KWO)Kwashiorkor (KWO)

Etiology:Etiology:

Severe deficiency of protein intake 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 yearsAge: 6 months - 2 years

Inadaquate breast feeding without supplementation Inadaquate breast feeding without supplementation

Dietetic errors (dilutional formula)Dietetic errors (dilutional formula)

Pathology of KWOPathology of KWO

1.1. Fatty infiltration of the liver Fatty infiltration of the liver

2.2. Atrophy of the intestinal villi (Brush border)Atrophy of the intestinal villi (Brush border)

3.3. Atrophy of pancreatic acini (selective) Atrophy of pancreatic acini (selective)

4.4. In severe cases: Heart,kidney and brain are In severe cases: Heart,kidney and brain are

affected.affected.

Clinical Manifestations of KWOClinical Manifestations of KWOConstant Features Variable Features

1- Growth Failure 1- Hair changes

2- Edema 2- skin changes

3- Muscle wasting 3- Hepatomegaly

4- Mental changes 4- Infections

5- GE

6- Anemias

7- Vitamin def.

8- Hypothermia

9- Hypoglycemia

10- Hypoclacemia

Constant Features Constant Features

1- Growth Failure:1- Growth Failure:

Failure to gain wt, followed by loss of wt.Failure to gain wt, followed by loss of wt.

Wt: is first affected, then height. Wt: is first affected, then height.

2- Edema:2- Edema:

Puffy eye lids, edema of the face Puffy eye lids, edema of the face early sign early sign

then edema of the extremities (pitting edema)then edema of the extremities (pitting edema)

No ascitis or pleural effusion (very rare)No ascitis or pleural effusion (very rare)

Constant featuresConstant features ContinueContinue

3- Muscle wasting:3- Muscle wasting: Estimated by midarm circumferenceEstimated by midarm circumference

why? 1. Not affected by edemawhy? 1. Not affected by edema 2. Constant between 1-5 years.2. Constant between 1-5 years. 3. Ms. wasting is proximal3. Ms. wasting is proximal

> 13.5 cm Normal> 13.5 cm Normal 12.5-13.05 cm Prekwo12.5-13.05 cm Prekwo < 12.5 cm Severe KWO< 12.5 cm Severe KWO

4- Mental changes:4- Mental changes: Apathy, miserable lookApathy, miserable look

lack of interest to the surroundinglack of interest to the surrounding failure to smilefailure to smile

Due to:Due to: Disturbed metabolism of aromatic aminoacidsDisturbed metabolism of aromatic aminoacids

Hair Changes in KWOHair Changes in KWO

Sparse, easily pickable, dyspigmentedSparse, easily pickable, dyspigmented Flag sign (bands of dark and light coloured zones Flag sign (bands of dark and light coloured zones

along the length of hairs)along the length of hairs) A/E:A/E:

1- Sulphar - containing aminoacids 1- Sulphar - containing aminoacids 2- 2- Pantethonic acid Pantethonic acid 3- Cupper 3- Cupper

Skin Changes In KWOSkin Changes In KWO

Dermatitis is common (in flexure sites)Dermatitis is common (in flexure sites) Hyperpigmentation, desquamation, ulcerations Hyperpigmentation, desquamation, ulcerations

and secondary infectionand secondary infection A/EA/E::

1- Protein 1- Protein 22- - Essential FA Essential FA 3- Vitamin A 3- Vitamin A 4- Niacin 4- Niacin 5- Zinc 5- Zinc 6- Suprarenal disturbance6- Suprarenal disturbance

Hepatomegaly in KWOHepatomegaly in KWO

Caused by fatty infiltrationCaused by fatty infiltration

( due to ( due to liporotein and lipotropic factors) liporotein and lipotropic factors) Return to normal on recoveryReturn to normal on recovery No cirrhotic changes 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 :Ascitis in KWO may be due to :

• TB peritonitisTB peritonitis• Toxic hepatitis & cirrhosisToxic hepatitis & cirrhosis

KWO and Vitamin D DeficiencyKWO and Vitamin D Deficiency

Patient with KWO has vit. DPatient with KWO has vit. D Atrophic rickets Atrophic rickets

(generalized osteoprosis) (generalized osteoprosis)

Manifested rickets (rosaries,….) in patient with Manifested rickets (rosaries,….) in patient with

KWO=rickets (vit. DKWO=rickets (vit. D) developed before ) developed before

occurrence of KWOoccurrence of KWO

Anemias in KWOAnemias in KWO

Any type of anemia can occur in KWOAny type of anemia can occur in KWO1- Macrocytic anemia (Folic acid and B1- Macrocytic anemia (Folic acid and B1212 ) )

2- Microcytic hypochromic anemia (iron, cu,Zn2- Microcytic hypochromic anemia (iron, cu,Zn))

3- Normocytic normochromic anemia (Bone marrow 3- Normocytic normochromic anemia (Bone marrow arrest)arrest)

* Types 1 & 2 are common and are called Dimorphic * Types 1 & 2 are common and are called Dimorphic anemia anemia

* Type 3: is rare and occurs only in severe forms of * Type 3: is rare and occurs only in severe forms of KWO (protein KWO (protein ).).

Malnutrition (KWO) Malnutrition (KWO) InfectionInfection

Secondary immune deficiency Due to:Secondary immune deficiency Due to: 1- Cell- mediated immunity 1- Cell- mediated immunity 2- Phogocytic functions 2- Phogocytic functions 3- Transferrin 3- Transferrin

4- Local: 4- Local: secretory IgA secretory IgA

Hcl (TB & HIV infection ++)Hcl (TB & HIV infection ++)

* Chest x ray is important to exclude TB.* Chest x ray is important to exclude TB.

Malnutrition Malnutrition Malabsorption Malabsorption

Due to:Due to: 1- 1- Salivary amylase Salivary amylase

2- 2- Hcl Hcl

3- 3- pancreatic lipase, amylase pancreatic lipase, amylase

4- Villous atropy 4- Villous atropy

5- Fatty liver 5- Fatty liver

6- Immuno def. 6- Immuno def.

Biochemical Changes in KWOBiochemical Changes in KWO

1- S. albumin 1- S. albumin (the most characteristic change) (the most characteristic change)

2- Hypoglycemia, Hypocalcemia2- Hypoglycemia, Hypocalcemia

Hypokalemia, Hypomagnesemia Hypokalemia, Hypomagnesemia

3- BUN / Cr ratio < 8 3- BUN / Cr ratio < 8

4- Enzyme def.: Amylase, lipase, Disaccharidases, 4- Enzyme def.: Amylase, lipase, Disaccharidases, Transaminases, Alk. Phosphatase. Transaminases, Alk. Phosphatase.

5- Vitamins and mineral def. 5- Vitamins and mineral def.

6- Anemias 6- Anemias

Anthropometric MeasuresAnthropometric Measures

1- Weight chart (Flat curve)1- Weight chart (Flat curve)

2- Height (less affected)2- Height (less affected)

3- Mid-Arm C. (< 12.5 cm)3- Mid-Arm C. (< 12.5 cm)

4- Chest / head ratio (<1 after 6 mo.)4- Chest / head ratio (<1 after 6 mo.)

5- Bone age (chronic malnutration )5- Bone age (chronic malnutration )

Complications of KWOComplications of KWO

1- Intercurrent infections (TB& HIV)1- Intercurrent infections (TB& HIV)

2- GE2- GE

3- Congestive HF3- Congestive HF

4-Hypoglycemia4-Hypoglycemia

5- Hypothermia5- 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)

Prevention of KWOPrevention of KWO

Encourage breast feeding with supplementation.Encourage breast feeding with supplementation.

Proper weaning on high protein and balanced diet. Proper weaning on high protein and balanced diet.

Immunization against infectious diseases. Immunization against infectious diseases.

Early detection of malnutrition and correction. Early detection of malnutrition and correction.

Treatment of KWOTreatment of KWO

1- Treat the cause.1- Treat the cause.

2- Treatment of dehydration: (Hypotonic dehydration)2- Treatment of dehydration: (Hypotonic dehydration) FluidsFluids electrolytes electrolytes Plasma (shocked)Plasma (shocked)

3- Dietetic management: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-free milk (Al 110, Isomil, Bebelac FL), if there is

lactose intolerencelactose intolerence Protein- rich diet: Meat, eggs, cheese, fish,….Protein- rich diet: Meat, eggs, cheese, fish,….

Treatment of KWOTreatment of KWO ContinueContinue

4- Blood & Plasma transfusion 4- Blood & Plasma transfusion

5- Treatment of Anemias:5- Treatment of Anemias: Folic acid & BFolic acid & B1212 BloodBlood iron postponed 10 daysiron postponed 10 days

6- Vitamins6- Vitamins A,B,CA,B,C vit. D also postponed 10 daysvit. D also postponed 10 days

7- Infection control 7- Infection control

8- Treatment of hypoglycemia & hypocalcemia 8- Treatment of hypoglycemia & hypocalcemia

Recovery from KWORecovery from KWO

Smile: Smile: 4 days4 days

Edema: Edema: 10 days10 days

Complete: Complete: 1-3 month 1-3 month

Death rate:Death rate: 15 % (of admission)15 % (of admission)

Marasmus (Infantile Atrophy)Marasmus (Infantile Atrophy)

Etiology: Inadequate caloric intake due to:Etiology: Inadequate caloric intake due to: Dietetic errors (quantitative or qualitative)Dietetic errors (quantitative or qualitative)

Repeated GE.Repeated GE.

Malabsorption ( cystic fibrosis, ceiliac D)Malabsorption ( cystic fibrosis, ceiliac D)

Chronic infections as TB.Chronic infections as TB.

Congenital malformations as eleft palate, pyloric Congenital malformations as eleft palate, pyloric

stenosis, congenital HD,…stenosis, congenital HD,…

Metabolic disorders: Galactosemia, Pku,...Metabolic disorders: Galactosemia, Pku,...

Pathology of MarasmusPathology of Marasmus

The main pathological changes is loss of fat The main pathological changes is loss of fat

storesstores

Atrophy of muscles and internal agansAtrophy of muscles and internal agans

Generalized osteoporosis.Generalized osteoporosis.

* Biochemical changes are few and non * Biochemical changes are few and non

specificspecific

Clinical Features of MarasmusClinical Features of Marasmus

Constant featuresConstant features1.1. Wt. LossWt. Loss

2.2. Muscle wastingMuscle wasting

3.3. LoLoss of subcut. fat. ss of subcut. fat.

OthersOthers InfectionInfection Vitamin dif.Vitamin dif. HypothermiaHypothermia ConstipationConstipation Emaciation, atrophyEmaciation, atrophy HypotoniaHypotonia

Degrees of MarasmusDegrees of Marasmus

First degree:First degree: - Wt. loss 15 - 30 %- Wt. loss 15 - 30 %

- Loss of subcut. fat of Abdomen- Loss of subcut. fat of Abdomen

Second degree:Second degree: - Wt loss 30 - 49%- Wt loss 30 - 49%

- Loss of Subcut. fat of thigh, buttocks- Loss of Subcut. fat of thigh, buttocks

Third degree:Third degree: - Wt loss - Wt loss >> 50 % 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 - The last fat to be lost because it

contains unsaturated fatty acids contains unsaturated fatty acids

Treatment of MarasmusTreatment of Marasmus

1- Treat the cause 1- Treat the cause

2- High caloric diet: 150-200 kcal / kg 2- High caloric diet: 150-200 kcal / kg

3- Diet:3- Diet:

High protein, moderate chate & Fat High protein, moderate chate & Fat

Start with skimmed milk followed by ½ cream and then full Start with skimmed milk followed by ½ cream and then full

cream milk cream milk

Lactose-free milkLactose-free milk

4- Blood,plasma transfusion 4- Blood,plasma transfusion

5- Correct vit - def 5- Correct vit - def

6- Treat any infection 6- Treat any infection

Malnutrition In Children Beyond Malnutrition In Children Beyond Infancy Infancy

Mainly due to psychological disturbances or bad Mainly due to psychological disturbances or bad

feeding habits: feeding habits:

No reduction of wt.No reduction of wt.

Fatigue, irritability Fatigue, irritability

Anorexia, constipation Anorexia, constipation

Pallor Pallor

Attention and school performance Attention and school performance

Susceptibility to infection Susceptibility to infection

Early Detection of Malnutrition Early Detection of Malnutrition

1- History:1- History:

Early weaningEarly weaning

Dietetic errors Dietetic errors

2- Subclinical (Pre KWO):2- Subclinical (Pre KWO):

Failure to gain wt.Failure to gain wt.

Hair changes Hair changes

Vitamin def. manifestations Vitamin def. manifestations

Early Detection of MalnutritionEarly Detection of Malnutrition ContinueContinue

3- Anthropometric measures:3- Anthropometric measures:

A- Weight chart: Flat curve A- Weight chart: Flat curve

B- Mid - arm circumferenceB- Mid - arm circumference

• 12.5 - 13.5 cm 12.5 - 13.5 cm Pre Pre KWOKWO

• < 12.5 cm < 12.5 cm Severe Severe KWOKWO

C- HC / Chest C ratio:C- HC / Chest C ratio:

• (After 6 months): < 1 Normal (After 6 months): < 1 Normal

> 1 Pre KWO > 1 Pre KWO

Early Detection of MalnutritionEarly Detection of Malnutrition ContinueContinue

4- Biochemical changes: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 KWOBUN/ 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