Case Study Presentation.pptx

TABLE OF CONTENTS
• OVERVIEW (INTRODUCTION)
• EPIDEMIOLOGY
• AETIOLOGY
• PATHOGENESIS AND PATHOPHYSIOLOGY
• SIGNS AND SYMPTOMS
• DIAGNOSIS
• TREATMENT
• PREVENTION
• DIETARY RECOMMENDATIONS
• CASE STUDY PRESENTATION
• REFERENCES

INTRODUCTION TO SEVERE ACUTE
MALNUTRITION
According to World Health Organization, in broad terms, Malnutrition refers to an
impaired development linked to both deficient and excessive nutrient intake which
could be overnutrition and undernutrition.
a) Undernutrition: This is an insufficient nutrition supply to the body, either due
to lack of food , or the inability of the body to absorb its nutrients.
b) Overnutrition: This is a form of malnutrition arising from excessive intake of
nutrients, leading to the accumulation of body fats that impairs health.

INDICATORS FOR MEASURING
MALNUTRITION
INDEX CLASSIFICATION
WEIGHT-FOR-HEIGHT ACUTE MALNUTRITION (WASTING)
HEIGHT-FOR-AGE CHRONIC MALNUTRITION (STUNTING)
WEIGHT-FOR-AGE ANY PROTEIN ENERGY MALNUTRITION
INCLUDING UNDERWEIGHT

WHAT IS SEVERE ACUTE MALNUTRITION
(SAM)?
Severe Acute Malnutrition (SAM) is defined by; very low weight for height/length (z score below -3 SD
of the median WHO child growth standards) or a Mid Upper Arm Circumference less than 115mm or
11.5cm, or by the presence of nutritional oedema. Severe Acute Malnutrition is both a medical and social
disorder.
There are two principal forms of SAM and they are;
1) Marasmus: evidenced by significant loss of muscle mass and subcutaneous fat, resulting in a skeletal
appearance.
2) Kwashiorkor: characterized by bilateral oedema of the lower limbs and oedema of the face, often
associated with cutaneous signs (shiny or cracked skin, burn-like appearance, discoloured and brittle
hair).
The two forms may be associated (Marasmic-Kwashiorkor).

EPIDEMIOLOGY
According to WHO, Severe Acute Malnutrition is a contributor present in half of all cases of
malnutrition. Six million children die of hunger everyday; underweight births and intrauterine growth
restrictions cause 2.2 million deaths a year. Poor or non existent breastfeeding causes another 1.4
million deaths. Other deficiencies such as lack of Vitamin A or Zinc, for example, accounts for 1
million deaths.
According to UNICEF, Nigeria has the second highest burden of stunted children in the world with a
national prevalence rate of 32 percent of children under five. An estimated ten million children in
Nigeria suffer from SAM, but only two out of every ten children affected is currently reached with
treatment.
In 2010, Protein Energy Malnutrition resulted in 600,000 deaths down from 883,000 deaths in 1990,
that is, in a space of twenty years.

AETIOLOGY OF SEVERE ACUTE
MALNUTRITION
1) Not having enough nutrition or having too little food.
2) Consuming too much of one nutrient and not enough of another.
3) Digestive problems and issues with nutrient absorption.
4) Poor sanitation and hygiene.
5) Poor breastfeeding practices causing infant not to get adequate feeding.
6) Inadequate support and nutrition during pregnancy and in a child’s early years.
7) In developed countries, severe acute malnutrition (marasmus) can occur due to
the eating disorder, anorexia nervosa.

U N I C E F C o n c e p t u a l F r a m e w o r k o n t h e C a u s e s o f M a l n u t r i t i o n

PATHOGENESIS
• Better understanding the pathogenesis of severe acute malnutrition may help to explain the high mortality of
children both during and after hospitalization and identify new targets for interventions to supplement existing
treatment strategies.
• Consistent evidence shows that immune mediators are altered in malnutrition and that systemic and intestinal
inflammation are associated with poor outcomes in SAM. This studies suggest that immune dysfunction
contributes to infectious susceptibility.
• Malnutrition is also characterized by complex derangement in gut microbial, metabolic, immune and
hormonal pathways, organ dysfunction and micronutrient deficiencies in the context of co-infections,
enteropathy, and chronic inflammation.

PATHOGENESIS CONTINUED
• SAM has several pathological and clinical features which may explain clinical outcomes in co-occurring
conditions.
i. SAM is characterized by intestinal damages, leading to impairment of the mucosal barrier and
increased intestinal permeability.
ii. SAM has underlying systemic immune activation.
iii. SAM is frequently complicated by persistent diarrhoea, pneumonia and gastroenteritis that may
plausibly arise due to loss of intestinal barrier function.
iv. SAM is accompanied by significant physio-pathological disorders such as metabolic disturbances,
anaemia, compromised immunity leading to susceptibility to infections often difficult to diagnose.

POPULATIONS AT RISK
1) People living in developing countries or areas with limited access to food.
2) People that live in poverty or have low incomes.
3) Individuals with increased nutritional needs, especially children and pregnant or breastfeeding women.
4) Babies born premature or with a low birth weight.
5) Babies who were not exclusively breastfed and did not start up on adequate complementary feeding.
6) Children with Avoidant Restrictive Food Intake Disorder (ARFID)
7) Older adults, particularly those who live alone or have disabilities.

SIGNS AND SYMPTOMS
• Lethargy
• Weight loss
• Dull, sparse, brittle hair
• Loose and wrinkled skin (marasmus)
• Poor wound healing
• Cold hands
• Rapid pulse
• Dehydration
• Severe palmar pallor
• Pitting oedema on dorsum of feet or bilateral
pitting oedema (kwashiorkor)
• Mouth ulcers
• Dry eyes
• Pale conjunctiva
• Bitot spots seen with vitamin A deficiency
• Loss of knee and ankle reflexes
• General pallor
• Apathetic (less active)
• Irritable on handling

DIAGNOSIS OF SEVERE ACUTE
MALNUTRITION
 In severe wasting (marasmus), a child has lost fat and muscle and appears like “skin and bones”. To look for and
diagnose severe wasting, remove the child's clothes and access the front view. Look out for the following
• Is the outline of the child’s ribs easily seen?
• Does the skin of the upper arm look loose?
• Does the skin of the thighs look loose?
• Are the shoulder bones easily seen?
• Is flesh missing from the buttocks?
 In children with kwashiorkor, oedema (swelling fluid on the tissues) is seen. Oedema is usually seen on the feet and
lower legs of arms. In severe cases, it can be seen on the upper limbs and face.
To check for oedema, grasp the foot so that it rests on your hand. With your thumb on the foot, press gently for a few
seconds. The child has oedema if a pit (dent) remains on the foot three seconds after the thumb is lifted.

MALNUTRITION CONTD
To be considered a sign of severe acute malnutrition, oedema must be present on both feet. The extent of
oedema is commonly rated in the following way:
• + : (Mild) oedema on both feet
• ++ : (Moderate) oedema on both feet, lower legs, hands and lower arms
• +++ : (Severe) generalized oedema including both feet, legs, hands, arms and face
Note: oedema is characterized with kwashiorkor and marasmic-kwashiorkor in severe acute malnutrition.
 Expected weight for age calculated using the following formulas based on age of child
• 0 to 12 months = n + 9/2
• 1 to 6 years = 2 (n+5)
• 7 to 12 years = 7n – 5/2

MALNUTRITION CONTD
 Mid Upper Arm Circumference
(MUAC) which measures fat and muscle
in the mid upper arm. MUAC of the left
arm should be measured for children.
• Red indicates severe acute malnutrition
with a MUAC measuring less than
110mm or 11cm.
• Orange indicates moderate acute
malnutrition with a MUAC measuring
less 110mm or 11cm to less than 125mm
or 12.5cm
• Yellow indicates a risk of acute
malnutrition with a MUAC measuring
125mm 0r 12.5cm to 135mm or 13.5cm

MALNUTRITION CONTD
• Green indicates that the child is well
nourished with a MUAC measuring
greater than 135mm or 13.5cm.
 Severe acute malnutrition is principally
diagnosed by Z-score below -3 standard
deviation of the median World Health
Organization’s child growth standard.
S.D. score = Child's weight – Median
reference value/ S.D. for reference
population
 Other laboratory tests such as; blood
tests for general screening (urine and
blood glucose), protein tests (serum
albumin), specific tests for nutrients such
as iron, potassium, etc

MANAGEMENT
Principles of management of SAM are based on three (3) phases:
• Stabilization phase – this phase usually lasts for 1-2 days. The feeding formula (F-75) is used
during this phase as a starter diet which promotes recovery of normal metabolic function and
electrolyte balance. All children in this phase must be carefully monitored for signs of overfeeding
or overhydration.
• Transition phase – this phase is the subsequent part of the stabilization phase and usually lasts for
3-7 days. This phase is intended to ensure that the child is clinically stable and can tolerate an
increased energy and protein intake. There is a change in type of diet in this phase with a gradual
transition from starter diet (F-75) to a catch-up diet (F-100). The quantity of catch up diet given is
equal to the quantity of starter diet given in stabilization phase.
• Rehabilitation phase – the child progresses to rehabilitation phase when; has reasonable appetite,
finishes more than 90% of feed given, there is major reduction or loss of oedema, no other medical
complication. In this phase, the aim is to promote rapid weight gain, stimulate emotional and
physical development and prepare the child for normal feeding at home.

TEN STEP MANAGEMENT OF SEVERE
ACUTE MALNUTRITION ACCORDING TO
WHO
10 STEP MANAGEMENT STABILIZATION PHASE TRANSITION PHASE REHABILITATION PHASE
INDICATORS DAY 1-2 DAY 3-7 WEEK 2-6
HYPOGLYCEMIA YES
HYPOTHERMIA YES
DEHYDRATION YES
ELECTROLYTE IMBALANCE YES YES YES
INFECTIONS YES YES
MICRONUTRIENT NO IRON NO IRON GIVE IRON
INITIATE FEEDING YES YES
CATCH UP GROWTH YES
SENSORY STIMULATION YES YES YES
PREPARE FOR FOLLOW-
UP
YES

TREATMENT
• If a doctor diagnoses severe acute malnutrition, a treatment plan will be made for the patient. The
patient will also be assessed and evaluated by a Registered Dietitian Nutritionist and other health
care providers.
• During the initial phase, frequent but small feeding is important to prevent both hypoglycaemia and
hypothermia. Feeding during the initial phase should be approached cautiously because of the
fragility of the child's physiological state. Breastfed children should be encouraged to continue
breastfeeding throughout the three phases.
• Dehydrated children who are in shock should be rehydrated orally or by nasogastric tube using
ReSoMal or half strength WHO low-osmolarity oral rehydration solution with added potassium
and glucose.
• Infections should be treated routinely upon admission by provision of a broad-spectrum antibiotic.

TREATMENT CONTD
• Micronutrient deficiencies should be treated by giving vitamin A (200,000 IU for children older than age 12
months, 100,000 IU for children ages 6-12 months and 50,000 IU for children ages 0-5 months) coupled with
daily multivitamin, folic acid, zinc and copper supplementation for at least two weeks. Iron supplementation
should only be given once child has begun gaining weight.
• During the rehabilitation phase, if available, children could be transitioned to Ready To Use Therapeutic
Foods (RUTF’s) according to the updated WHO guidelines. Children's respiratory and pulse rates should be
monitored closely. After transitions to RUTF’s, children should receive feedings consisting of 100-200 kcal
per kilogram body weight and 4-6g protein per kilogram body weight every 4 hours. Breastfeeding should
continue to be encouraged.
• After recovery, parents should be taught to feed children frequently with energy and nutrient-dense foods and
to continue to stimulate their children's sensory and emotional development. Parents should be requested to
bring children back for regular follow-up checks.

PREVENTION OF SEVERE ACUTE
MALNUTRITION
• The best way to prevent SAM is to have an adequate intake of calories and protein from a healthy
and adequate diet.
• Providing adequate nutrition and disease prevention strategies including appropriate breastfeeding
and complementary feeding practices.
• Adequate household nutrition especially for women and children.
• Promoting the practice of exclusive breastfeeding for six months

PREVENTION OF SEVERE ACUTE
MALNUTRITION CONTD
• Access to appropriate healthcare for the prevention and treatment of disease.
• Special feeding programs including school feeding programs, food fortification and food
enrichment.
• Improved sanitation and hygiene practices to reduce infections.
• Safe food preparation, cooking and storage practices.
• Nutrition education and awareness of severe acute malnutrition and its effects.

INTRODUCTION TO ANAEMIA
• Anaemia is the general name for a range of disorders affecting red blood cells.
• Red blood cells contain haemoglobin, which is responsible for carrying oxygen in
the blood.
• To produce red blood cells, the body needs iron, vitamin B12 and folic acid. If one
or more of these is deficient, anaemia will develop.
• Anaemia is a medical condition in which there is a decrease of red blood cells or
haemoglobin in the blood, or a lowered ability of the blood to carry oxygen.

EPIDEMIOLOGY
• Anaemia is one of the six WHO global nutrition targets for 2025 endorsed by World Health
Assembly in 2012 and 2013.
• Anaemia is the most common blood disorder affecting about a quarter of the global population.
• A moderate degree of iron deficiency anaemia affects approximately 610 million people worldwide
or 8.8% of the population.
• Mild iron deficiency anaemia affects another 375 million.
• In 2013, anaemia due to iron deficiency resulted in about 183,000 deaths.
• It is slightly more common in women (9.9%) than men (7.8%).

AETIOLOGY OF ANAEMIA
• Anaemia primarily arises either due to blood
loss, decreased red blood cell production or
increased red blood cell breakdown
(haemolysis).
• Anaemia manifests in;
i. Iron deficiency
ii. Certain inherited blood diseases (e.g.
Thalassaemia).
iii. Anaemia occurring in chronic disease
iv. Lack of vitamin B12 or folate
v. Chemotherapy drugs
vi. Diseases of the bone marrow
vii. Acute blood loss; heavy periods, internal
bleeding (e.g., from stomach ulcer)
viii. Chronic renal failure
ix. Endocrine disorders
x. Infections

PATHOGENESIS AND PATHOPHYSIOLOGY
• Red blood cells are produced in the bone marrow and circulate in the
blood stream before they are broken down in the spleen.
• Iron not used for erythropoiesis is transferred by transferrin to the
storage pool where iron is stored in two forms; ferritin and
hemosiderin.

PATHOGENESIS AND PATHOPHYSIOLOGY
CONTD
• The most important is ferritin (a heterogenous group of proteins surrounding an
iron core), which is soluble and active storage fraction located in the liver (in
hepatocytes), bone marrow, and spleen (macrophages), red blood cells and in
serum. Iron stored in ferritin is readily available for any body requirement.
• If the level of red blood cells (and therefore haemoglobin), in the blood is
abnormally low, the oxygen-carrying capacity of the blood is reduced and anaemia
develops.
• Iron deficiency develops in stages. In the first stage, iron requirement exceeds
intake, causing progressive depletion of bone marrow iron stores. As stores
decrease, absorption of dietary iron increases in compensation. In later stages,
deficiency impairs red blood cells synthesis, ultimately causing anaemia.

POPULATIONS AT RISK
• Pregnant women
• Women with menorrhagia
• Malnourished individuals
• Consumers of strict vegetarian diet
• Infants and children 2 years and under
• Women of child-bearing age
• Adolescent girls
• Regular blood donors

SIGNS AND SYMPTOMS
• Feelings of weakness and fatigue.
• Poor concentration
• Shortness of breath
• Increased cardiac output
• Pallor
• Jaundice
• Restless leg syndrome

DIAGNOSES
Anaemia can be diagnosed by carrying out several laboratory investigations such as;
• Full blood count (FBC) which determines the number, size, volume, and haemoglobin
content of red blood cells.
• Packed cell volume (PCV) to measure the proportion of blood that is made up of cells.
• Blood iron level. Serum and ferritin levels to determine total body iron stores.
• Levels of vitamin B12 and folate (vitamins necessary for red blood cell production).
• Reticulocyte count, bilirubin levels and other blood and urine test.

MEDICAL TREATMENT OF ANAEMIA
• First, a healthcare provider will find out if the anaemia is being caused by a poor diet or a
more serious health problem. Ways of treating and managing anaemia include:
• Iron supplements taken orally.
• Iron given through an intravenous (IV) infusion.
• Transfusion of red blood cells.
• Most children with severe acute malnutrition are severely anaemic. But it is dangerous to
give oral iron until the child has been treated for infections, regains appetite and starts
gaining weight.

DIETARY INTERVENTIONS OF ANAEMIA
Nutrition specific interventions that address the immediate determinants of anaemia, such as poor diet and
nutrition-sensitive interventions that address the underlying causes of anaemia, such as diseases or infections,
aim to prevent and control nutritional anaemia. This can be achieved by the following ways:
• Fortification: fortification refers to the deliberate addition of nutrients to foods (e.g. in the form of powders
like tombrown). This is a practical way to improve the diet of target population. Fortification of foods with
vitamins and minerals (iron, folate, vitamin B12, zinc, vitamin A, etc).
• Increasing food variety through nutrition education and provision of foods rich in minerals and vitamins such
as fruits, vegetables, and iron-rich foods such as dairy products, red meat, etc.

DIETARY INTERVENTIONS OF ANAEMIA
CONTD
• Nutrition education on the use of iron pots for cooking.
• Increasing ascorbic acid rich foods to improve the absorption of non-
haeme iron.
• Ginger, carrot and beetroot blend for children above six months,
young children, adolescent girls, pregnant women, etc.

PREVENTION OF ANAEMIA
• Eating a diet that provide iron, vitamin B12 and vitamin B9 along with vitamin C
food sources to help with the absorption.
• Good nutrition in pregnancy and after pregnancy to increase mothers iron stores.
• Proper hydration.
• Encouraging exclusive breastfeeding.
• Proper sanitation and hygiene to mitigate the occurrence of infections which could
deplete blood levels.

CASE STUDY PRESENTATION
With this I present to you a six (6) months old female baby admitted
into the Children Medical Ward on the 26th May, 2021 on account of;
• Weight loss × 3/12
• Vomiting × 1/7
• The Dietitians were invited on the 31st May, 2021 for their expertise
management.

MEDICAL NUTRITION THERAPY
• ASSESSMENT
• Social/Family History
• Patient hails from Ogoni, Rivers state but resides
with family in Port Harcourt city.
• Patient is a Christian of the Pentecostal
denomination.
• Patient is the second child in a monogamous family
of two children (two girls).
• Patients older sister is five years old.
• Mother is a registered nurse with a BSc degree.
• Father is a secondary school teacher with a BSc
degree.
• Patients sister never had similar illness.
• Family lives in a two bedroom apartment.
• Toilet facility is a water cistern.
• Source of drinking water for patient is sealed bottled
water. Other members of the family use bore hole.
• Cooking is done using a gas cooker and kerosene
stove on rare occasion.
• Patient sleeps under a treated net but co-sleeps with
parents most times when she gets fussy at night.

PAST MEDICAL HISTORY
• Patient has a history of frequent vomiting, loss of appetite and infection at
four months.
• This was managed at a peripheral hospital with medications and a diet
modification of pap, milk, egg, palm oil and sugar by a doctor.
• Patient was not able to tolerate feed and therefore kept vomiting. This
relapse continued for two months.
• No prior history of blood transfusion.

PRESENT MEDICAL HISTORY
• Infection and vomiting continued which led patient to University of
Port Harcourt Teaching Hospital (UPTH) for expertise management.
• Patient presented to the Paediatric Department four weeks ago with a
complaint of persistent vomiting × 1/7 and weight loss × 3/12.

PRENATAL/ANTENATAL/POSTNATAL
HISTORY
• Pregnancy was planned and desired.
• Antenatal began at four (4) months.
• Pregnancy was properly monitored in a hospital.
• Baby was born through spontaneous vaginal delivery.
• Baby cried immediately after birth.
• Birth weight was 3.2kg.
• No complications with mother or baby after birth.
• Child is not up to date with immunization according to National Program on Immunization (NPI) schedule (stopped
at 10 weeks).

DEVELOPMENTAL MILESTONES
• 6 weeks – turning to the direction of sound.
• 3 months – sitting up with support
• After the third month, no developmental milestone was recorded.

NUTRITION ASSESSMENT
• ANTHROPOMETRY
 Weight – 3.5kg (31/5/2021)
 Length – 59cm
 Expected weight for age – 7.5kg (n+9 ÷ 2)
 % Expected weight for age – 46.7% (-4 SD Zscore)
 MUAC – 10cm

NUTRITION ASSESSMENT CONTD
• BIOCHEMICAL INVESTIGATION
 Na = 108 (135-145) mmol/L low
 K = 5.3 (3.5-5.5) mmol/L normal
 HCO3 = 17 (24-30)mmol/L low
 PCV = 27 (40-54)% low
 RBC = 4.2 (4.5-5.5)×10^12/L low
 WBC = 4.9 (4-10.8) )×10^9/L normal
 Platelets = 286 (90-300)×10^9/L normal

CLINICAL ASSESSMENT
 On examination, patient was seen to be in n respiratory distress, small
for age, afebrile, had flaking dermatitis, wrinkled skin, nil pedal
oedema, prominent ribs, acyanosed, anicteric, pale and wasted

• DIETARY ASSESSMENT
 Patients caregiver (mother) was assessed and revealed the following:
 Patient was put to breast an hour after birth.
 Baby stopped exclusive breastfeeding at 3 months after she fell ill.
 Baby is a picky and fussy eater.
 Mother introduced NAN1 at three months and pap with NAN milk at 4 months.

 Also at 4 months, patient was fed pap, milk, egg, palm oil and sugar (recommended by a
doctor in a peripheral hospital), but vomits everything after ten minutes of feeding.
 Mother removed sugar and palm oil which reduced vomiting.
 Started using homemade tombrown at 5 months.
 Mother used to feed 60mls of pap and two scoops of SMA gold milk.
 Mother later introduced lactogen baby milk and stopped NAN and SMA Gold because
she suspected lactose intolerance.
 Baby later fed 45mls of pap every two hours which she tolerated well.
 At six months before admission, baby was being fed pap and milk only and alternates
with cerelac and feeds expressed breastmilk three times a day.

DIAGNOSIS
• MEDICAL DIAGNOSIS
Severe acute malnutrition (marasmus), sepsis, moderate anaemia, persistent vomiting and electrolyte
derangement.
• NUTRITIONAL DIAGNOSIS
 Inadequate protein and energy intake related to nutritional misconception (mother) and failure to
thrive as evidenced by small weight for age and -4SD Z score
 Reduced blood levels of iron related to inadequate intake of iron rich foods and infection as
evidenced by low PCV (27%) .

MEDICAL INTERVENTION
Professional personnel involved include:
Paediatricians
Dietitians
Nurses
Laboratory scientists
Pharmacists

DRUG INTERVENTION
S/N MEDICATIONS ROLE
1 IV PIPERACILLIN TAZOBACTAM ANTIBIOTIC
2 TAB ZINC VITAMIN SUPPLEMENT
3 SYRUP MULTIVITAMIN VITAMIN SUPPLEMENT
4 SYRUP VITAMIN B COMPLEX VITAMIN SUPPLEMENT
5 CAP VITAMIN A (100,000 IU) VITAMIN SUPPLEMENT
6 ORAL NYSTATIN ANTIFUNGAL
7 SYRUP FOLIC ACID VITAMIN SUPPLEMENT
8 20mls RESOMAL PER VOMITUS ORAL REHYDRATION
9 1% CLOTRIMAZOLE TOPICAL ANTIFUNGAL
10 IV ROCEPHIN ANTIBIOTIC
11 IV CEFTRIAXONE ANTIBIOTIC

NUTRITION INTERVENTION
• Baby was assessed and mother counselled appropriately on adequate diet.
• Mother was encouraged to continue breastfeeding.
• Patient was placed on NGHPHcal fluid diet of 120kcal per kilogram body
weight (420kcal) of fortified pap.
• Fluid diet to come in form of fortified cereal.
• Patient was fed 45mls every two hours, twelve times daily.

NUTRITION INTERVENTION CONTD
• Mineral and vitamin supplements were added in fluid preparation.
• The feed was adequate in quantity and quality.
• Mother was advised to use healthy oils in the fluid preparation.
• Mother was counselled on proper hygiene and food handling.
• Mother was advised to stop using Tombrown.
• Mother was educated on recipe and method of fluid preparation to ensure adequate
feeding.

PREPARATION OF HIGH ENERGY MIXTURE
(HEMix)
S/N INGREDIENTS OUANTITY
1 PEAK (0-12MONTHS) 20g (2 Scoops)
2 BOILED EGG 1 whole
3 VEGETABLE OIL 5mls
4 GLUCOSE 10g
5 PAP 200mls
6 VITAMIN C 1 tablet
7 VITAMIN B COMPLEX 1 tablet
TO BE MADE UP TO 540mls MORNING AND EVENING

CALORIE DISTRIBUTION
• CHO = 55% ; 55/100 × 420Kcal = 231
• CHON = 15% ; 15/100 × 420Kcal = 63
• FAT = 30% ; 30/100 × 420Kcal = 126
• Dividing through by Atwater’s Factor
• CHO ; 231/4 = 57.75g
• CHON ; 63/4 = 15.75g
• FAT ; 126/9 = 14g

FOOD ITEMS QUANTITY
(g)(mls)
420Kcal
ENERGY
(g)
57.75g
CHO
(g)
15.75g
CHON
(g)
14g
FAT
(g)
PEAK (0-
12MONTHS) MILK
20 102 11.2 4.12 5.4
BOILED EGG 75 101.25 -------- 10.45 7.13
VEGETABLE OIL 5 45 -------- -------- 5.0
GLUCOSE 10 40 10 -------- --------
PAP 200 182.6 39.53 2.07 1.0
VITAMIN C --------- -------- -------- -------- --------
VITAMIN B
COMPLEX
--------- -------- -------- -------- --------
TOTAL 470.85Kcal 60.73g 16.64g 18.53g

WEIGHT GAIN AND MONITORING CHART
DATE WEIGHT IN KG
31/5 3.5
1/6 3.6
2/6 3.6
4/6 3.7
7/6 3.6
9/6 3.8
11/6 3.85
13/6 4.0
17/6 4.3

NUTRITION MONITORING
• Patient was no longer on nasogastric tube.
• Had a blood transfusion on 12th June, 2021.
• PCV increased to 34% after laboratory investigations were done.
• Patient now tolerates 600mls of feed of 150Kcal per kilogram body weight (75mls) every three
hours, 8 times a day.
• The feed was increased based on acceptability and tolerance.
• Egg was excluded from diet as mother could only lay her hands on a blender for the first four days.
• Was advised to continue giving egg after discharge.

CONCLUSION
• Patient’s state of health improved, which necessitated her discharge.
• Patient was discharged home on the 19th of June, 2021 with
improvement in weight (4.3kg) and PCV of 34%.

REFERENCES
• Jones K.D., Thitiri J., Ngari M, et al.,(2014), Childhood malnutrition: toward understanding of infections,
inflammation and antimicrobial. Food Nutr Bull;35 (2 Suppl):S64-S70
• Progress For Children: A Report Card on Nutrition. UNICEF (2017)
• Ashworth A., Khanum S., et al.,(2003). Guidelines For The Inpatient Treatment Of Severely Malnourished
Children. Geneva: World Health Organization.
• WHO/UNU/UNICEF. (2001). Iron Deficiency Anaemia, Assessment, Prevention And Control; A Guide For
Programme Managers. Geneva.
• Weksler, Babette (2017). Wintrobe’s Atlas Of Clinical Haematology. Lippincott Williams and Wilkens.
P.pt105
• Maakaron, Joseph (2016). Anaemia: Practice Essentials, Pathophysiology, Aetiology. Emedicine.
• West African Food Composition Table.
• Nigerian Food Composition Table (2017)

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