SEVERE ACUTE MALNUTRITION

PRESENTED BY: MORACHA KEVIN (MOI UNIVERSITY-KENYA)

MODERATED BY: DR. MARETE (CONSULTANT PEDIATRICIAN)

INTRODUCTION

• Presence of bilateral edema or severe wasting (weight for height/length <-3SD) or MUAC <115mm.

• Both Kwashiorkor and Marasmus are managed similarly.

• Children who are <-3SD weight for age may be stunted but not severely wasted. They don’t require hosp adm unless with serious illness.

Formerly PEM:

• WHO: "the cellular imbalance between supply of nutrients and energy and the body's demand for them to ensure growth, maintenance, and specific functions."

• Forms: Kwashiorkor, marasmus, marasmic kwashiorkor, underweight.

• Marasmus involves inadequate intake of protein and calories, whereas a child with kwashiorkor has fair-to-normal calorie intake with inadequate protein intake.

EPIDEMIOLOGY

• Worldwide, SAM is among leading causes of death among children <5Yrs

• More common in the developing states

• Malnutrition causes abt 5.6 to 10 million deaths/yr, with sever malnutrition contributing to abt 1.5 million of these deaths ( Heinkens et al. 2008)

Cont..

• Prevalence of SAM in developing counties is 40% while in developing countries is 2- 10%

• Factors found to predispose in high income countries : chronic diseases and congenital disorders

• In developing countries: Socioeconomic status

– EA journal Vol 81 No. 8 Aug 2004

Kenya’s Epidemiology• 2009, MoH : National figure for acute

malnutrition of under 5’s is approx. 6%

• Variations exist in diff parts of the country: arid and semi arid areas- 15-20%

• It has been noticed that most of the malnourished children in Kenyan hospitals have hx of: – poverty

– single mothers,

– single parents,

– displacement by clashes,

– birth out of wedlock,

– mother and child staying separate from father due to working conditions,

– and sharing of income with extended families

• (EA journal Vol 81 No. 8 Aug 2004)

Study at MTRH on risk factors for PEM June 2001 to June 2002 by Prof. Ayaya, Prof. Esamai et al

concluded that poverty, social conditions under which the child was living, sex of the child and incomplete immunizations were risk factors for the severe protein energy malnutrition.

ETIOLOGY

• Primary - when the otherwise healthyindividual's needs for protein, energy, or both are not met by an adequate diet. (most common cause worldwide)

• Secondary - result of disease states that may lead to sub-optimal intake, inadequate nutrient absorption or use, and/or increased requirements because of nutrient losses or increased energy expenditure.

PRECIPITATING FACTORS

Lack of food (famine, poverty)

Inadequate breast feeding

Wrong concepts about nutrition

Diarrhoea & malabsorption

Infections (worms, measles, T.B)

WHO classification

Acute malnutrition(severity)

MUAC (cm) WHZ

None >13.5 >-1

At risk 12.5 to 13.4 -2 to -1

Moderate 11.5 to 12.4 -3 to -2

Severe <11.5 <-3

Kwashiorkor

• Former classifications include: Welcome classification, Gomez and Seo anne and Lathams.

Wellcome working party.

NB: If WT >80% with oedema– Kwashiorkor. Parameter: weight for

age + oedema

Weight Oedema

Underweight 80% - 60% -

Kwashiorkor 80% - 60% +

Marasmus <60% -

Marasmus-Kwashiorkor.

<60% +

SAM Pathogenesis- Theories

1. Dietetic Hypothesis (classical)

– Kwashiorkor : Predominantly protein deficiency

– Marasmus : Energy deficiency

2. Adaptation Hypothesis (Gopalan’s )

– Marasmus : Extreme case of adaptation

– Kwashiorkor : A stage of adaptation failure• Continued prolongation of stress• Sudden precipitation or aggravation by a fulminant infection like measles, whooping cough, diarrhoea or pneumonia

3. Free Radical Hypothesis (Golden’s) • Kwashiorkor from over production of free radicals and breakdown of protective mechanisms. Low serum iron causes increased production of free O2 radicals These oxides (free O2 radicals) are normally buffered by protein and mopped up by anti-oxidants such as

• Vitamins A,C,E• Glutathione:-Defc causes toxic accum of free O2

radicals• Zinc.• Selenium

4. Jelliffe’s Hypothesis• A mixture of interactions and sequelae of dietary imbalances, infections and infestations, emotional trauma and toxins

5. Aflatoxin Hypothesis• Contamination of food. • In kwash, free O2 radicals potentially toxic to cell

membrane are produced during infections or as a result of ingesting aflatoxin from aspergillus flavus fungi growing in moist grains and ground nuts.

6.Role of hormones

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.

Marasmus• High plasma cortisol in marasmus > kwash

• 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.

7.ROLE OF INFECTION

• Kwash 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.

• Why does infection affect nutritional status?– Poor appetite

– Dietary restriction –misconception of low feeds during diarrhoea.

– Malabsorption of nutrients

– Frank protein-losing enteropathy e.g. in measles, HIV.

8. Serum iron status

• Low serum iron increases free oxygen radicals in circulation

• Proteins , vit A,C, and E, Zn, Se, and glutathione help mop up free radicals. These are reduced in Kwash. Thus free radical excess

PATHOPHYSIOLOGY of SYMPTOMS OEDEMA

Cause:

• Protein-deficient, hypoalbuminaemia, reduced plasma oncoticpressure, shift to interstitium

• Free radical damage of cell membrane, Na+/K+ ATPase malfxtn-leaks

• Hypovolemia reduced GFR, activation of RAAS, Na+ and water retention.

• Incr levels of leukotrienes cause uncontrolled vasodilation-hypovolemia-low BP-decr peritubular hydrostatic pressure – incrtubular reabsorption of salt and water.

PATHOPHYSIOLOGY Cont’d

WASTING

• Calorie def – fats and tissue proteins mobilized to supply energy for metabolic processes.

• Recurrent infections coupled with hypoglycemia cause acute stress response-cortisol released- wasting

• Effects of associated infections e.g. HIV wasting syndrome

PATHOPHYSIOLOGY- Cont’d

HAIR CHANGES

• Keratin synthesis impaired coz of cysteine and methionine def , thus brittle hair easily pulled off /breaks

• Pigment melanin formed from tyrosine deficiency in kwash. Hair changes colour to reddish or grey.

• Periods of good nutrition alternating with poor nutrition- flag sign.

• Dullness and lack of lustre due to weathering of the hair cuticle.

• Bleaching effects of H202

PATHOPHYSIOLOGY- Cont’dSKIN CHANGES

•Ulcerations and flaky paint rash due to Zn def.•Atrophy of sweat and sebaceous glands leads to excessive dryness of the skin.•Hyperpigmentation, erythema, duskiness of exposed areas – niacin def•Cracking and fissuring of hyper pigmented •Generalized hypopigmentation due to stretching of the skin by the edema.

PATHOPHYSIOLOGY- Cont’d

HEPATOMEGALY/ FATTY LIVER

– Free radicals damage mitochondrial enzymes in the liver causing reduced synthesis of proteins.

– Beta LP def – accumulation of TG in the liver – fatty liver –Hepatomegally.

POT BELLY

– Hypotonic muscles of abdominal wall resulting in muscle wasting.

– Overgrowth of bacteria in the gut due to reduced immunity-

– Paralytic ileus due to hypokalemia

– Hepatomegally coz of fatty liver

PATHOPHYSIOLOGY- Cont’d

DIARRHOEA

• Caused by recurrent infxns due to reduced immunity- low sIgA and reduced secretion of acid in stomach.

• Malabsorption – deficiency of pancreatic enzymes resulting from pancreatic atrophy/protein deficiency.

• Villous atrophy- reduced absorptive surface

PATHOPHYSIOLOGY- Cont’d

Recurrent infections• Atrophy of thymo-lymphatic glands cause

depletion of T lymphocytes and depressed CMI thus infxns like Herpes, candidiasis common.

• Reduced phagocytic and bactericidal activity of leucocytes- NADPH oxidase and lysozyme def

• C3,C5, and factor b levels reduced – opsonizationand phagocytosis reduced.

• Immune response reduced due to inability to synthesis IL-1,IL-6.TNF alpha due to lack of supply of essential AA.

PATHOPHYSIOLOGY- Cont’d

The “Vicious Cycle”of Undernutrition & Infection

Disease:

. incidence

.severity

.duration

Appetite loss Nutrient loss

Malabsorption

Altered metabolism

Inadequate dietary intake

Weight loss

Growth faltering

Lowered immunity

Mucosal damage

Figure 2. The Synergistic cycle of infection and malnutrition

PATHOPHYSIOLOGY- Cont’d

ANAEMIA

• Due to dietary deficiency of iron and folate

• Parasitic infxtns e.g. hookworm.

• Malabsorption due to recurrent diarrhea.

• Reduced protein intake and synthesis.

APATHY

• Hypokalemia- muscle weakness and easy fatigability of muscles-child lacks in energy

• Lack of stimulation and deprivation causes reduced growth of brain and nerve thus mental slowing.

• Reduced BMR

• Apathy also attributed to Zinc deficiency.

PATHOPHYSIOLOGY- Cont’d

ELECTROLYTE/ MINERAL DEFICIENCIES –Magnesium

• Good evidence that magnesium deficiency is common in severe malnutrition

• Consequences:

– Muscular twitching

– Arrhythmias

– Convulsions

– Predisposes to K+ deficiency

PATHOPHYSIOLOGY- Cont’d

sodium

– Plasma sodium can be low and on occasions is extremely low in children with marasmickwashiorkor.

• However total body sodium is often increased

• So large amounts of additional sodium (fluids and feeds) are poorly tolerated.

PATHOPHYSIOLOGY- Cont’d

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

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.

INITIAL ASSESSMENT

HISTORY

• Assess for danger signs or emergency signs and take history concerning:– Recent intake of food

– Usual diet before current illness: quantity, quality, frequency

– Breastfeeding Hx

– Duration and frequency of diarrhea & vomiting

– Type of diarrhea(watery/bloody)

– Loss of appetite

– Family circumstances: Socioeconomic status i.e.Income, Housing, food &Water supply, Sanitation

– Cough>2wks

– Contact with TB

– Recent contact with measles

– Known or suspected HIV infn or exposure

Further History

1. Birth history: birth weight

2. Immunization history

3. Milestones: achieved/delayed

4. Past medical hx: Resp. infxns, TB, measles, HIV

5. Family history: Parents, Siblings, health status, family occupation, education

PHYSICAL EXAM

• Shock: lethargic or unconscious; with cold peripheries, slow cap refill(>3sc), or weak rapid pulse or low BP

• Signs of deH20

• Severe pallor

• Bilateral pitting edema

• Eye signs of vitamin A def– Dry conjuctival or cornea, Bitot spots

– Corneal ulceration

– keratomalacia

• Vitamin A def: likely to be photophobic – keep eyes closed. Examine eyes gently to avoid corneal rupture.

• Localizing signs of infxn: ear discharge, throat infxns, skin infxns or pneumonia

• Signs of HIV infxn

• Fever : >37.5 c or Hypothermia (rectal: <35.5c)

• Mouth ulcers

• Skin changes

– Hypo/hyperpigmentation

– Desquamation

– Ulceration

– Exudative lesions

• Conduct appetite test: ready to use therapeutic food

Features of Kwashiorkor1.Always present• Generalized edema, Pitting edema over the lower limbs • Growth failure: wasting (may be masked by edema).• Psychomotor changes: apathy, irritability

2.Usually present

• Hair changes: fine but coarse in chronic d’se, easy pluckability, discoloured, light-colored hair streaky red/gray, sparseness (areas of alopecia),Alternate areas of hypo and normal pigmentation-flag sign

• Anemia• Loose stools

3.Occasionaly present

• Hepatomegaly

• Signs of vitamin deficiencies

• Skin changes

A. Diffuse/patchy areas of hypo/hyperpigmentn

B. Thin, shiny, taut skin over edematous areas

C. Moist ulcerations over flexural/pressure points

D. Super infectns e.g.. scabies

Classical lesions– Flaky paint dermatosis: hyper pigmented, desqumation

area(flake) over raw skin.

– Crazy pavement dermatosis: dry, hyperkeratotic ,fissured skin with alternate areas of hyper/hypo pigmentation

– Mosaic dermatosis: mixed lesions in mosaic form

Features of Marasmus1.Always present• Extreme growth failure,<60% WA• Marked muscle wasting, loss of subcut fat• Alert, with good appetite• Face is shriveled like ‘little old man, monkey like- Relatively larger

head, wrinkled skin, loose skin folds over buttocks, thighs, axilla2.Occasionaly present• Anemia• Diarrhea with signs of dehydration• Vit deficiencies: cheilosis,dermatosis,rickets• Infxns: resp,TB,measles

• Mosaic

dermatosis ↓

Flaky paint dermatosis

• Flag sign

Organization of care

• Those who pass appetite test: Rx as O/Ps for uncomplicated SAM

• Those with Edema +++, lack of appetite, one or more danger signs or with medical conditions requiring admission- Rx as I/Ps

• Separate I/Ps from infectious children and keep them warm (25-30⁰c). Special nutrition unit if available

Out patients

• Respond rapidly to therapy unless have other infections.

• Mainstay is enough fresh affordable balanced food.

• Milk alone is adequate for an infant 4-6mths

• Nutritional education to the caretaker.

• Weight monitoring as a follow-up measure.

• Their daily requirements:

– Calories 120cal/kg/day

– Protein 2-3g/kg/day

– Vit. A 1500 I.U/day.

INVESTIGATIONSa)For general screening and monitoring

Hematological

FHG, PBF, Blood glucose profile, LFT:albumin

Septic screening

BS for MPS, Blood culture, Stool MCS,CXR

Mantoux test, PITC, Urine: urinalysis, M/C/S

Biochemical

Electrolytes: rarely helpful, may lead to inappropriate therapy, LFTs

Iron tests: serum Fe, TIBC, ferritin

Vitamins and minerals:B12,folate,D,K,calcium,magnesium

DIFFERENTIALSKWASHIORKOR

• Nephrotic syndrome

• Liver disease

• Protein losing enteropathy

• Angio-neurotic edema

• CCF

MARASMUS

• Malignancies

• HIV wasting syndrome

• TB, Other chronic illnesses

KWASH DERMATITIS

• Acrodermatitis Enteropathica -zinc deficiency.

• Scurvy

• Pellagra

10 step mgt of malnutrition

1. Hypoglycemia

2. Hypothermia

3. Dehydration

4. Electrolyte imbalance

5. Infections

6. Micronutrient def.s

7. Initial feeding

8. Catch up growth

9. Sensory stimulation

10. Follow up

10 step approach

STABILIZATION REHABILITATION

DAY 1-2 DAY 3-7 WEEKS 2-6

Hypoglycemia -------------

Hypothermia -------------

Dehydration -------------

Electrolyte imbalance ---------------------------------------------------------------------

Infections ----------------------------------

Micronutrient ------NO IRON-----------------------WITH IRON------------

Initiate feeding -----------------------------------

Catch up growth ---------------------------

Sensory stimulation --------------------------------------------------------------------

Prepare for follow-up ---------------------------

Hypoglycemia

Dx: blood glucose < 3mmol/l

• Rx: – 50mls of 10% glucose or sucrose sol (1 rounded

teaspoon of sugar in 3 tablespoons of water) orally or by NGT, followed by 1st feed ASAP

– Give 1st feed of F75 therapeutic milk if available and then CT with feeds 2hrly for 24hrs; then CT feeds 2 or 3hrly day and night

– If unconscious: Rx with IV 10% glucose at 5mls/kg or if no IV access then 10% glucose by NGT

– Start on appropriate IV or IM Abx

• Monitoring: after 30 mins. If BG still <3mmol/L-repeat

• Check for abd distension.

• If Deh2o rehydrate 1st

Hypothermia

• Often indicates coexisting hypoglycemia or serious infxn

• Dx: Axillary temp <35oc rectal <35.5oc• Rx:

– Feed immediately and then 2hrly unless with abd distension

– Dress warmly-cover with a warmed blanket– Keep dry, away from draught– Heaters or lamp– Put child on mothers bare chest or abdomen– Avoid exposure to cold during procedures, bathing

• Monitoring:– Monitor temp 2hrly- rectal till rises to 36.5oc,half

hourly if heater is being used.– Ensure child is covered at all times– Check for hypoglycemia

• Prevention– Feed 2-3hrly– Kangaroo technique– Avoid child exposure to cold– Don’t use hot water bottle of fluorescent lamp– Change wet nappies

Dehydration• Dx: assume that all children with watery

diarrhea or reduced urine output have some dehydration

• Rx:

– No IV route unless in shock

– Resomal 5ml/kg oral every 30 mins for first 2 hours. Then 5 – 10 mls/kg each for the next 4-10 hrs on alternate hrs, with F75 formula. (the exact amt depends on how much the child wants, vol of stool loss and whether the child is vomiting.)

– If not available: ½ strength standard WHO ORS with added k+ and glucose.

– If rehydration is still required at 10hrs, give starter F75 instead of Resomal, at the same times. Use same vol of F75 as of Resomal

– If in shock or severe deH20 bt cannot be rehydrated orally or by NGT, give IVF, either RL/ ½ strength darrows with D5W. If neither is available, 0.45%saline with D5W is used

• Monitoring: expect RR, PR to fall and urine to be passed. Return of tears, moist mouth, less sunken eyes and frontanelle and improved skin tugor

– Monitor every 30 mins for 2hrs then hrly for the next 4-10 hrs

• Prevention:

– CT breastfeeding

– Initiate re-feeding with starter F75

– Give 50-100mls Resomal per loose motion

Na+

Mmol/l

K+

Mmol/l

Lactate*

(HCO3-)

Glucose

Mmol/l

ORS 75 20 10 111

ReSoMal 37.5 40 5 ~ 200

INGREDIENT AMOUNT

Water 2LTRS

WHO-ORS ONE 1LTR PACKET

Sucrose 50g

Electrolyte/mineral soln 40ml

Electrolyte imbalance

• All severely malnourished children have deficiencies in K+ & Mg2+

• May take 2 weeks to correct

• Ideally should receive Mg, Zn, Cu and Se as part of mineral mix – added to milk feed.

• Rx:

– Extra K+ 3- 4 mmol/kg daily

– Extra Mg2+ 0.4 – 0.6mmol/daily

Infection • Signs like fever may be absent but still infxn

present, assume all malnourished children have an infection

• Rx:– Start BS abx, measles vaccine if >6mths unimmunized

or vaccinated before 9mo age, albendazole

– No complications: PO amoxicillin(50mg/kg/d BD) X5 days

– Complications(hypogly,hypotherm,lethargy):Im/iv xpen (50000IU QID) or ampicillin(50mg/kg BD) X2 days, then oral amoxicillin( 25-40 mg/kg TID) X 5 days

– Plus Genta(7.5mg/kg OD) X7 days.

• NB: metronidazole 7.5mg/kg TID X7 days may be added to the BS Abx but its efficacy has not been established in clinical trials.

• Rx other infxns as appropriate: meningitis, pneumonia, dysentery, skin infxns, malaria and TB)– Parasitic worms: delay until rehab period. Give

ABZ STAT or MBZ 100mg PO BD X 3/7

– Also do PITC

Micronutrients

• Give daily for at least two weeks

• Vitamin A- < 6/12- 50,000 iu, 6/12-1yr-100,000 iu ,>1 yr- 200,000 iu)on day 1, 2 and 14 – only if child has signs of def eg corneal ulceration or Hx of measles

• Multivitamins supplement if not on RUTF– Folic acid- 5 mg on day 1 then 1 mg/day

– Zinc – 2mg/kg/day

– Copper - 0.3 mg/kg/day

• NB: Vit A, folic acid , Zn and Cu present in F75, F100 and RUTF

• Once gaining weight and good appetite, ferrous sulphate 3mg/kg/day. From the second week

Initial feedingEssential features

• Frequent small 2-3 hrly feeds of low osmolality ,low lactose

• Oral/NGT feeds, never parenteral

• 100 kcal/kg/d

• Protein @ 1-1.5g/kg/d

• Liquid @ 130ml/kg/d(100 if with severe edema)

• If child is breastfeeding continue but still give feeds

• Starter F75(75kcal/100ml and 0.9g protein/100ml)

• Monitoring: amt of feed and left over, vomiting ,diarrhea, daily body wt.

Catch up growth

• Signs that a child has reached this phase:

– return of appetite,

–edema gone and

–no episodes of hypoglycemia

• Treatment:– Gradual transition from starter to catch up – Replace F75 with an equal amnt of

F100(100kcal/100ml and 2.9g protein/100ml) or RUTF for 2-3 days

– On day 3 increase each successive feed by 10ml till some remains uneaten at abt 200ml/kg/d

– Aft gradual transition give frequent feeds unlimited amts, 150-220kcal/kg/d, 4-6g of protein/d

–If on RUTF: start with small but regular meals and encourage child to eat often 8 meals/day. If child cannot take > ½ of RUTF in 12hrs stop and give F75. reintroduce again in 1-2 days

–Monitor for signs of heart failure due to fluid overload.

–Assess progress: daily wt gain

Sensory stimulation

• Tender, loving care• Structured play therapy for 15- 30 mins/d• Physical activity as soon as the child is well

enough.• A cheerful, stimulating environment.• Encourage mother’s involvement e.g.

comforting, feeding, bathing, play• Provide suitable toys for the children.

Associated conditions

Eye problems

• vitamin A, days 1,2,14

• Signs of corneal clouding/ulceration– Caf/tetracycline eye drops qid for 7-10 days

– Atropine eyedrops 1 drops tid 3-5 days

– Cover with saline soaked pads

– Bandage eyes

Severe Anaemia

• Transfuse: Hb < 4gldl,4-6g/dl in resp distress

• Whole blood – 10 ml/kg slowly for 3hrs + frusemide 1mg/kg iv at the start of transfusion

• Packed cells – 10 ml/kg if in CCF

Dermatitis of kwashiokor

• Due to zinc deficiency – replace.

• Soak/bathe areas in 0.01% potassium permanganate sol. For 10min/day

• Apply barrier cream zinc and castor oil ointments, petroleum jelly to raw areas, GV or nystatin cream toskin sores

• Omit nappies/diapers, perineum can stay dry.

Continuing diarrhoea

• Replacement fluids CT

• Stool m/c/s and treat accordingly. giardia; flagyl 7.5mg/kg TID x 7d

• Osmotic diarrhoea: Diarrhea worsens with hyperosmolar F75 and ceases when sugar content and osmolarity are reduced.Rx-lower osmolar feeds

Rehabilitation

• Appetite has returned

• Principles: encourage child to eat as much as possible, breastfeeding, emotional care, prepare mum for continued care

• Criteria 4 Discharge : eating well, improved mental status, normal temp, no vomiting/diarrhea/edema, gaining weight >5g/kg/d for 3consecutive days.

• Continue monitoring progress.

Discharge and follow-upDischarge Criteria

• All infections, other conditions have been

treated

• Good appetite and gaining weight (90%

expected WH )

• Lost any oedema

• Appropriate support in the community or

home

• Mother/carer: available, understands child’s

needs, able to supply needs

Follow up

• Planned and regular, nutrition clinic

• Risk of relapse greatest aft discharge then

should be seen aft 1wk,2wks,1mth,3mths

• If a problem is identified more frequent visits

• Aft 6mths,do yearly visits till 3yrs of age.

PROGNOSIS

• Good if picked early before complications have set in.

• Long-term effects include

• failure to thrive,

• behavioral and cognitive dysfunction,

• Small stature,

• Obstructed labour,

• Low birth wgt infants

PREVENTION

• Appropriate nutrition policies programmes• Improving food security• Protection and promotion of good health• Appropriate care practices for good nutrition• SUMMARY- GOBIFFF the UNICEF adaptation

– Growth monitoring– Oral rehydration– Breast feeding– Immunization– Feeds (supplements)– Female education– Family spacing

REFERENCES

• EA journal Vol. 81 No. 8 Aug 2004

• WHO Guidelines for the management of common childhood illnesses

• EA medical journal on PEM – Aug 2004

ABBREVIATIONS

• WHO: World Health Organization

• I/P: In Patient

• O/P: Out Patient

• GV: Gentian Violet

• AA: Amino Acids

• EA: East Africa

• PEM: Protein Energy Malnutrition

• CT: Continue

ABBREVIATIONS

• RUTF: Ready To Use Therapeutic Feeds• ABZ: Albendazole• MBZ: Mebendazole• ORS: Oral Rehydration Solution• CCF: Congestive Cardiac Failure• AA: Amino Acids• TG: Triglycerides• SAM: Severe Acute Malnutrition• BS: Broad Spectrum• Abx: Antibiotics• LP: Lipoproteins

THANK YOU