ALERT Comprehensive Specialized Hospital

Department of Pediatrics

Clinical Year I

Case Report 1

Prepared By: Nazerawit Wondimu

Submitted to: Dr Abiyu
October 13, 2024 G.C
Identification

This is Fenet Getachew a 1 year and 7month old toddler who is from zenebewerk, Addis ababa.
She was admitted to ACSH pediatrics ward 7 bed number 7/2 on Hidar 6 / 2017. Her mother is
W/ro Kenene Gadisa a 23 years old housewife married to the child's father. She has a grade 6
education and is a Christian. Her father is Ato Getachew Tsegaye 26 years old, works in
construction and a Christian. The mother and father provided the history and there appeared to be
no language barrier. Date of clerking was on Hidar 11/ 2017

Previous admission- no history of previous admission

Chief compliant- Generalized body swelling of 3days duration

History of present illness

This is 1 year and 7 month old female toddler who was relatively healthy until 1 week ago, when
she started to have generalized body swelling which started in her lower extremities that
progressively involved the abdomen , upper extremities and face. Associated to this she also had
loss of appetite and vomiting of ingested matter of 2 days duration which is non-projectile, non-
blood tinged, non-foul smelling, and non-bilious occurring 3-4 times a day. Additionally, she
developed diarrhea, passing a loose stools about 4 times per day, with no blood or mucus.
Following these symptoms, she was taken to koshe health center and subsequently referred to
ACSH for better management on Hidar 6/2017.

She is born to a a para 1 mother who had all ANC visit and gave birth after 9 months of
pregnancy to twins by SVD , the birth weight was 2.5 kg and the baby cried immediately after
birth. There is no history of maternal smoking, alcohol use, medication, or infections during
pregnancy.

She is fully vaccinated. She was not breast fed and was started on formula milk from birth. The
formula is prepared with 1 scoop per 30 mL of water, consumes 150 mL per feed, 5 feeds per
day, feeding takes approximately 20 minutes per session. At 6 months of age, she transitioned to
diluted cow milk (half milk and half water) and began complementary feeding with cereals
(bulla, atmit, cerefam) 4times per day. After a week she started to eat mashed potato, fruits and
vegetables. Before she gets sick she was able to eat solid food like shiro with injera in which she
eats 3 times per day with the family and she share meal with her siblings. Her protein intake is
minimal with no animal source foods. The mother reported that she often refuses food and has
poor appetite.

The formula and the cow milk are prepared fresh for each feeding using tap water. The water is
not boiled before use. The mother washes her hand before preparing and feeding her babies. The
bottle is stored in a clean area after washing.
She has been exposed to sunlight after 2 months of her birth every day for 10-15 minutes starting
from 2 o’clock without clothes but with the application of ointment.

She was able to support her head at 5 months of age and sit unsupported at 8 months, she began
to stand supported at 1 year and 3 months. Currently she can crawl which she started 7 months
back , stand supported and only say mama and baba.

The mother is housewife and the father works in construction and he doesn’t have a stable
income.

She lives with her family in a 3 room house with separated kitchen which has 1 functional
window. They use tap water for drinking and cleaning purpose. They dispose the waste 1 times a
week.

Otherwise,

 She has no history of fever, fast breathing, cough

 She has no history of Yellowish discoloration of eye or skin or contact with jaundiced
person or stool color change
 She has no history of Reddish discoloration of urine, foamy urine or reduced urine output
 She has no history of Feeding interruption, excessive sweating, recurrent respiratory
infection
 She has no history of Bluish discoloration of the body
 She has no history of medication use prior to developing the diarrhea([Link])
 She has no history of Loss of consciousness or abnormal body movement
 She has no history of recent watery diarrhea, weight loss and sunken
eyeball(dehydration)
 She has no previous history of tonsillitis, pharyngitis and skin infections
 There is no history of similar illness in the family
 There is no family history of DM , HTN, stroke

Birth history

Immunization history

Nutritional history

Developmental history

Past medical and surgical history- There is no past medical illnesses, surgeries or known
allergies.

Family and social history

 Physical Examination
General Appearance
The patient is well looking but with no signs of cardiorespiratory distress. He has no gross
dysmorphic features and looks malnourished. She is alert and not irritable

Vital Signs
Pulse rate: 100 bpm measured from Right radial artery, regular, full in volume… normal

Respiratory rate: 25 breaths per min, regular…normal

Blood Pressure: not measured due to unavailability of appropriate BP cuff

Temperature: 35.3oC, axillary in the afternoon…normal

SaPO2: 96% with atm oxygen

Anthropometery

Weight: 7.2 kg

Length : 70 cms

HC: 45 cms

MUAC: 11cm( severely wasted)

Interpretation (using WHO chart)

Weight For Age: < -3 (severely underweight)

Length For Age: Between >3 (Normal)

HC For Age: at -1 (Normal)

Weight For Length: Between -1 & -2 (Normal)

H.E.E.N.T

Head: anterior fontanel is flat and measure 1*1, normal shape and size. No gross deformities,
swellings, scars or tenderness. No area of tenderness or scalp infections. Brown colored hair and
easily pluck able. No craniotabes, frontal bossing.

Ears: Normal set ears normal shape and size of pinnae, no discharge, no tenderness over the mastoid
process

Eyes: pink conjunctiva, non-icteric sclera, no lesions on the eye(bitot spot, corneal ulcerations),no
discharge, no periorbital edema, no nystagmus or strabismus.

Nose: no discharge. central septum, no tenderness over the maxillary and frontal sinuses

Mouth and Throat: dry mouth and buccal mucosa, No cyanosis or ulceration of lip(angular
cheliosis,glossitis). No cleft lip. No papillary atrophy, thrush, or dryness. No gum hypertrophy. No
hyperemia or swelling of the tonsils.

Lymphoglandular system

Lymph nodes are not palpable over the occipital, post auricular, pre auricular, submandibular,
submental, cervical, supraclavicular, axillary, epitrochlear, or inguinal regions.

Respiratory system:

Inspection: No nasal flaring, peripheral or central cyanosis, mass or deformities. No scar. No

subcostal and intercostal retractions. no audible wheeze or stridor. Ribs are not prominent. No
Harrison groove, costochondral bedding

Palpation: central trachea, no superficial mass or tenderness, symmetric chest expansion. tactile
fremitus was done while baby was crying and was comparable.

Percussion: there is resonant percussion tone over the chest wall. (Diaphragmatic excursion is not
done.)

Auscultation: Vesicular breath sounds heard over the lung fields. Equal and good air entry on both
sides. No wheezing, stridor, crepitation, rhonchi, or pleural friction rub.
Cardiovascular system:

General: no pallor, cyanosis or clubbing.

Arteries: Pulse is palpable over, carotid, brachial, radial, popliteal, anterior tibialis, and dorsalis
pedis bilaterally. No radio femoral delay.

Veins: No distended neck, chest, abdomen, and leg veins. JVP is not done.

Precordium:

Inspection: The precordium is quiet. There is no bulging or abnormality in shape. Apical beat is not
visible.

Palpation: No tenderness. The PMI is palpable in the left 5th interspace, slightly lateral to the mid-
clavicular line. It is localized and tapping. There are no palpable heart sounds. no thrills or heaves.

Auscultation: S1 and S2 are well heard. They are not muffled or accentuated. no added sounds or
murmur and gallop were appreciated.

Abdomen:

Inspection: The abdomen is distended. It is symmetric and moves with respiration. The umbilicus
is inverted with horizontal slit. There are no scars. No visible veins, peristalsis or pulsations.

Auscultation: No bruit over the abdominal aorta, renal arteries, or iliac arteries. Normal bowel
sound were heard ( 12 per minute)

Percussion: tympanic percussion tone over the abdomen. Signs of fluid collection (shifting dullness
and fluid thrill) are negative.

Palpation:

Superficial – No tenderness, guarding, rigidity or superficial mass

Deep – No deep tenderness, organ enlargement

Genitourinary system: No suprapubic mass and tenderness

Integumentary system:

Skin: dry skin , hypo and hyperpigmented skin lesions on the buttock area and thigh(grade 1
dermititis), no palmar pallor, jaundice, cyanosis.

Hair: Normal distribution, brown color, pluck able

Nails: Pink, no cyanosis, koilonychia, clubbing and capillary refill is 2 sec(normal)

Musculoskeletal system:

Look: grade 2 bilateral pttting edema, extra digit on right hand, Comparable muscle bulk. No
spine deformities.

Feel: There is no tenderness, warmth, crepitations, or swelling over the joints. .

Move: There is no asymmetry and limitation in movement of limbs

Nervous System:

General: she is conscious and GCS score = 15/15

Cranial nerves:

CN I- Not assessed due to age

CN II- Intact Direct and indirect pupillary light reflexes. Visually acuity and fundoscopy not done.

CN III, IV &VI - The eyes can move in all directions, no nystagmus and strabismus. No ptosis.

CN V- The has good sucking of the breast.

CN VII- Face is symmetrical at rest and upon voluntary movements like smiling, and no mouth
deviation.

CN VIII- Responds to noises like finger snapping

CN IX & X- Not done due to age

CN XI- Symmetric shoulders with no shoulder drop

CN XII- Good tongue thrusting during cry.

Motor: Normootonic limbs. Bilaterally comparable muscle bulk, no spontaneous fasciculation.

Reflexes

Superficial: the plantar reflexes are intact

Sensory: Responds to pinching of the extremity.

Co-ordination: not done due to age

Meningeal signs: Not assessed due to age

Subjective summary

This is a 1 year and 7month old female patient that presented with generalized body swelling of 3
days duration which started in her lower extremities that progressively involved the abdomen , upper
extremities and face. She also had loss of appetite and vomiting of ingested matter of 2 days
duration which is non-projectile, non-blood tinged, non-foul smelling, and non-bilious occurring 3-4
times a day. Additionally, she developed diarrhea, passing a loose stools about 4 times per day, with
no blood or mucus. She was not breast fed and was started on formula milk from [Link] has gross
developmental delay. Her protein intake is minimal with no animal source foods. She often refuses
food and has poor appetite.

Objective summary

The patient is well looking , alert and awake. The vital signs are in a normal range. She is severely
underweight, severely wasted with MUAC of 11 but the other anthropometric measurements are in a
normal range. She has open flat anterior fontanel measuring 1*1and brownish discoloration of hair
which is easily pluck able. She has dry mouth and buccal mucosa, dry skin , hypo and
hyperpigmented skin lesions on the buttock area and thigh(grade 1 dermititis) and grade 2 bilateral
pitting edema
Differential diagnosis

 SAM
 Congestive heart failure
 Nephrotic syndrome
 Liver cirrhosis
 Protein losing enteropathy
 Poststreptococcal Glomerulonephritis (PSGN)

Discussion of differentials

Severe acute malnutrition

Severe Acute Malnutrition (SAM) is a critical form of undernutrition, characterized by severe

wasting or bilateral pitting edema. The primary cause is inadequate food intake, while secondary
causes include conditions like malabsorption, increased nutritional needs, and increased nutrient
losses (e.g., chronic diarrhea). SAM affects multiple organs, including the liver, which produces
less glucose and transport proteins, leading to hypoalbuminemia and edema, and the kidneys,
which contribute to fluid retention. The heart’s reduced size and output increase the risk of heart
failure with fluid overload, while impaired gut function increases the risk of bacterial
translocation. SAM also leads to immune suppression, raising the risk of infections. Clinical
manifestations vary by form: marasmus presents as severe wasting with a "skin and bones"
appearance, while kwashiorkor shows bilateral pitting edema, a moon face, and fatty liver. The
mixed form, marasmic kwashiorkor, includes both wasting and edema. Common signs include
dull, sparse hair with a "flag sign," skin hyperpigmentation, abdominal distension with
hepatomegaly, developmental delays, lethargy, bradycardia, and hypotension. SAM develops
gradually over weeks or months, allowing the body to adjust metabolically and behaviorally,
leading to a lower level of cellular nutrient availability Additionally, SAM impacts the central
nervous system, leading to delayed development, irritability, and cognitive impairment.
Complications of SAM include hypoglycemia, infections, intractable vomiting, persistent
diarrhea, electrolyte imbalances, dehydration, severe anemia and hypothermia.
Criteria of admission for infants less than 6 months include recent weight loss or failure to gain,
WFL < -3 z score, Ineffective feeding, Any grade of bilateral pitting edema and Presence of any
of the medical complications. For children 6month-59 month include Sever wasting (MUAC
<11.5cm or WFH<-3 z score) or bilateral pitting edema +++ with any Medical complications and
failed appetite test.

Management involves a two-phase approach: the stabilization phase, where repair cellular
function, correct fluid and electrolyte imbalance, restore homeostasis, and prevent death from the
interlinked triad of hypoglycemia, hypothermia, and infection, followed by the rehabilitation
phase, where the child’s nutritional intake is gradually increased to promote recovery. Proper
monitoring and supportive care are critical to prevent complications and ensure successful
treatment.

In the case of this patient she has generalized body swelling which starts from her foot, poor
feeding history,gross developmental delay, dry mouth and buccal mucosa, easily pluck able and
brownish discoloration of hair, kwash demititis,diarrhea, vomiting, bilateral pitting edema,
MUAC =11(severe wasting) which is an evidence for SAM.

Congestive heart failure

Heart failure is a clinical and pathological syndrome that results from ventricular dysfunction,
volume, or pressure overload, alone or in combination. It leads to characteristic signs and
symptoms, such as poor growth, feeding difficulties, respiratory distress, exercise intolerance,
and fatigue, and is associated with circulatory, neurohormonal, and molecular abnormalities. It is
characterized by the heart's inability to effectively pump blood to meet the body's demands.

Pediatric heart failure encompasses a spectrum of etiologies, often influenced by age. Cardiac
dysfunction may arise from intrinsic myocardial pathology, including genetic cardiomyopathies,
inflammatory myocarditis, or structural damage secondary to congenital coronary anomalies or
acquired conditions. Additionally, electrical disturbances within the heart, manifesting as
arrhythmias, can contribute to heart failure. Congenital heart defects, characterized by outflow
tract obstructions, shunts, or valvular dysfunction, represent another significant cause of pediatric
heart failure. Finally, systemic conditions such as severe anemia or large arteriovenous
malformations can also lead to cardiac compromise in children.

Prominent manifestations of heart failure in infants include tachypnea, feeding difficulties,

emesis, poor weight gain, diaphoresis, irritability, weak cry, and labored respirations with
intercostal and subcostal retractions, as well as nasal flaring. Cardiac-induced pulmonary
congestion may mimic bronchiolitis, with wheezing often being a more prominent finding than
rales. Hepatomegaly is generally present, and cardiomegaly is invariably observed. Despite
pronounced tachycardia, a gallop rhythm can frequently be identified. Assessing jugular venous
pressure in infants may be challenging due to the short neck and difficulty in achieving a relaxed
state; palpation of an enlarged liver serves as a more reliable indicator of elevated systemic
venous pressure.

Diagnostic evaluation of pediatric heart failure involves a comprehensive approach incorporating

imaging, electrophysiology, and laboratory testing. Chest radiography (CXR) can assess cardiac
silhouette for enlargement and provides information about pulmonary vascularity, which varies
depending on the underlying cause. Electrocardiography (ECG) is useful for assessing potential
causes but does not establish the diagnosis, while echocardiography remains the standard for
quantifying ventricular function. Cardiac magnetic resonance imaging (CMR) offers detailed
information regarding ventricular function, volume, mass, and tissue characterization. Cardiac
catheterization, an invasive procedure, is helpful for evaluating hemodynamics and structural
heart defects. Laboratory testing evaluates end-organ function and systemic perfusion, including
renal function, liver function, lactate levels, and electrolytes. Elevated B-type natriuretic peptide
(BNP) levels are a marker of heart failure.

Management of pediatric heart failure focuses on addressing the underlying cause, maintaining
adequate cardiac output, and reducing volume overload. If surgically correctable congenital heart
defects are present, medical therapy aims to optimize the patient for surgery. For irreversible
cardiac dysfunction, such as cardiomyopathy, medical management provides symptomatic relief
and may allow for recovery if the insult is reversible. Long-term therapies include reverse
remodeling agents like beta-blockers, angiotensin-blockers, combination angiotensin
receptor/neprilysin inhibitors, and aldosterone antagonists to improve myocardial function.
Adequate blood pressure control is crucial to reduce afterload. In advanced heart failure or
cardiogenic shock, inotropic agents and mechanical circulatory support may be required.
Nutritional support is crucial, particularly in infants, who may require increased caloric intake
and may benefit from nasogastric feedings. Iron supplementation is recommended for iron
deficiency.

In the case of this patient even if the swelling started from foot, she exhibits no evidence of
tachypnea, tachycardia, cardiomegaly, hepatomegaly, murmurs, or gallops, feeding interruption
and recurrent infection. Based on these findings, heart failure can be excluded at this time.

Poststreptococcal Glomerulonephritis (PSGN) is the most common cause of

glomerulonephritis (GN) in children, typically following infections with nephritogenic strains of
Group A β-hemolytic streptococci. These infections, affecting the throat (pharyngitis) or skin
(pyoderma), often precede the onset of PSGN by 1-2 weeks or 3-6 weeks, respectively. The
disease is characterized by acute nephritic syndrome, presenting with sudden gross hematuria,
edema, hypertension, and renal dysfunction.
 It is more prevalent in children aged 5-12, especially in less developed regions, and has
decreased in industrialized nations due to better hygiene and reduced streptococcal infections.
The pathogenesis involves immune complex formation, molecular mimicry, and complement
activation, leading to glomerular injury. Clinical manifestations range from asymptomatic
microscopic hematuria to acute renal failure, with complications such as hypertensive
encephalopathy, pulmonary edema, and heart failure in severe cases. Diagnosis involves
urinalysis, CBC, complement levels (C3 is typically low), and serologic evidence of recent
streptococcal infection, confirmed by elevated antibody titers like anti-streptolysin O and anti-
DNAse B. Imaging (MRI or CXR) may be needed for complications like encephalopathy or
heart failure. Renal biopsy is reserved for atypical cases or persistent symptoms. Treatment is
largely supportive, with antibiotics to prevent streptococcal spread, antihypertensives, diuretics,
and salt/fluid restriction. Most cases resolve within 6-8 weeks, though microscopic hematuria
may persist for up to two years.

As already mentioned in the history the patient has no previous history of tonsillitis, pharyngitis,
skin infections, urine color and output changes and also the swelling starts from the foot which
makes it unlikely for PSGN.

Liver cirrhosis in children is a chronic liver condition characterized by progressive scarring of the
liver tissue, often resulting from congenital liver diseases, chronic viral hepatitis, metabolic
disorders, or biliary atresia. The clinical presentation includes failure to thrive, jaundice, fatigue, and
abdominal distention. Body swelling, particularly ascites, is a prominent feature of cirrhosis and
typically begins with the development of ascites due to portal hypertension. As liver function
deteriorates and portal pressure rises, fluid accumulates in the abdomen, causing progressive
abdominal distention. Swelling may also occur in the lower limbs due to hypoalbuminemia, where
the liver's reduced ability to produce albumin leads to a decrease in plasma oncotic pressure,
allowing fluid to leak into the tissues. As the disease advances, children may develop hepatomegaly,
splenomegaly, and varices, and their overall condition may worsen with signs of hepatic
encephalopathy or bleeding complications. Diagnosis is made through blood tests (showing elevated
liver enzymes, low albumin, and prolonged prothrombin time), imaging (ultrasound or CT/MRI to
assess liver and spleen size), and liver biopsy for definitive confirmation. Management includes
treating the underlying cause, controlling complications like ascites with diuretics, and considering
liver transplantation in severe cases. Early detection and intervention are crucial to improving
outcomes and preventing further liver damage.
In the case of this patient she has generalized body swelling which started from leg unlike the liver
cirrhosis which starts from abdomen. She also has no evidence of failure to thrive, jaundice, fatigue
and signs of organomegally which makes it unlikely.

Protein-Losing Enteropathy (PLE) is a condition characterized by excessive protein loss from the
gastrointestinal tract, leading to hypoalbuminemia, edema, and malnutrition. It can result from
various underlying causes, including inflammatory bowel diseases (such as Crohn’s disease), celiac
disease, lymphatic disorders like intestinal lymphangiectasia, gastrointestinal tumors, and infections.
Clinical manifestations include generalized edema, abdominal distention, diarrhea, ascites, and
fatigue. Diagnosis involves laboratory tests showing low serum albumin levels, imaging to identify
structural causes, and sometimes endoscopic biopsy for underlying conditions. Treatment focuses on
managing the root cause of PLE, nutritional support, and stabilizing protein levels, often with
intravenous albumin and other supportive therapies.

Nephrotic syndrome is a condition characterized by heavy proteinuria, hypoalbuminemia, edema,

and hyperlipidemia. It affects 1-3 per 100,000 children under 16 years and can lead to severe
complications, including infections and hypercoagulability. Proteinuria is defined by a 24-hour urine
protein excretion of >3.5g or a urine protein:creatinine ratio >2 and dipstick protein >3+. Edema is
the most common symptom, resulting from mechanisms like the underfill or overfill hypothesis.
Hyperlipidemia involves increased cholesterol, triglycerides, and LDL, with de
]creased HDL. Children with nephrotic syndrome are more susceptible to infections, particularly due
to immunoglobulin and complement loss, with pneumococcal infections being a major concern. The
condition also predisposes patients to a hypercoagulable state, increasing the risk of thromboembolic
events. Nephrotic syndrome in children typically responds well to corticosteroid therapy, with 80%
of cases improving. Edema in nephrotic syndrome typically begins in the face and periorbital area,
progressing to generalized body swelling, and is associated with hyperlipidemia, proteinuria, and
possible infections. Additionally, nephrotic syndrome may lead to a hypercoagulable state.

In the case of this patient her swelling starts from the leg unlike nephroic syndrome which starts
from periorbital area and face. She also has no history of urine color change, frothy or foamy urine
and urine output change.
Final assessment Edematous SAM + kwash dermatitis + AGE with no dehydration

Investigation

 Blood glucose level- to check for hypoglycemia, a common complication in SAM

 Serum protein/Albumin- to assess protein deficiency and hypoalbuminemia
 CBC- detect anemia(low Hb and Hct), infection ( leukocytosis)
 CRP- elevated in case of inflammation and infection (N=<10mg/dl)
 Serum electrolyte – to identify electrolyte imbalance like hypokalemia an hyponatremia
 Stool exam (microscopy and culture) - to detect parasitic, bacterial infections and
malabsorption.
 HIV test – mandatory for patients with malnutrition
 Urinalysis – to detect proteinurea,infections(UTI),
 Organ function test- to evaluate organ function and detect complications such as AKI

Management

Principle of management

o Management of complication
Shock
• Diagnosis :
 Lethargic or unconscious and Cold hands Plus either:
 Slow capillary refill (>3 sec) or Weak fast pulse
• The treatment is different in malnourished patient
 Different fluid, less rapid and smaller volume
 Treatment
1.INO2
2. Give IV fluid at 15 mL/kg over 1 hr, using:
• RL with 5% dextrose or
• Half N/S with 5% dextrose or
• If all the above are unavailable, Ringer lactate
3. Measure and record pulse and respirations at the start and every 10 min.
Dehydration
• Difficult to diagnose in patient
[Link] ReSoMal 5 mL/kg every 30 min for 1st 2 hr orally or NG tube.
2. Then give 5-10 mL/kg in alternate hours for up to 10hr
 Hypoglycemia
Blood glucose <3 mmol/L(54mg /dl)
If conscious:
• Give 10% glucose (50 mL), or a feed or 1 tsp sugar under tongue, whichever is quickest
• Then feed F-75 every 30mnt for 2hrs then 2hrly ,day and night
If unconscious:
[Link] give sterile 10% glucose (5 mL/kg)
rapidly by IV.
2. Feed every 2 hr for at least 1st day. Initially give
of feed every 30 min for 2 hr.
Hypothermia
Axillary T°<35°C(95°F); rectal<35.5°C (95.9°F)
• actively rewarm, Feed the child
• dress warmly, including head a and cover with blanket
• keep room hot; Change wet clothes and bedding.
• do not bathe if very ill
• monitor temperature hourly (or every 30 min if using heater)
• stop rewarming when rectal temperature is 36.5°C
Severe anemia
• Hgb <4 g/dL
• If very severe anemia (or Hgb 4-6 g/dL and respiratory distress):
1. Give whole blood 10 mL/kg slowly over 3 hr
2. If signs of heart failure, give 5-7 mL/kg packed cells rather than whole blood
Give furosemide 1 mL/kg IV at the start of the transfusion
Correct electrolyte disturbance
Treat and prevent infection
• no medical complication- Amoxacillin
• medical complication- Ampicillin+gentamycin--> ceftriaxone
Dermatosis
• handle skin gently, prevent furter damage
• cleaning
• dressing
• topical antibiotics
o Correct micronutrient deficiency
• iron- dont give on stabilization phase
• vitamin A-not routinly
• if eye signs of vit A def.(corneal clouding, ulceration, bitots spot) or recent measels now
or in the past 3 month give on day 1, 2 and 15
• Folic acid- dont give routinly
 o Nutrient management –

Stabilization phase:

• life threatening problems are identified and treated

• F-75 contains 75 kcal and 0.9 g of protein per 100 ml , give required amount every
2hr

Transitional phase:

• prepares the patient for rehabilitation phase

• Transition Using RUTF

• During this period, introduce RUTF gradually alongside F-75.

Rehabilitation phase:

• restore wasted tissues (i.e., catch-up growth)

• rapid weight gain

• 200kcal/kg/day

• RUTF or F100 are used

o Follow up