failure to thrive

2. History
• A 10 months old saudi female present to ER on
2015 with Hx of fever and diarrhea for 2 days .
• HPI:
• The patient was in her usual state of health
before 2 months , when she started to have
constipation for tow months followed by diarrhea
and vomiting food content, non projectile , no
blood, associated with High grade fever 40C .

3. History
• Past neonatal and medical Hx:
• Preterm(30 Weeks) of twin pregnancy, Caesarean section Due
to pre-PROM ( preterm premature rupture of membrane ) .
‐Admitted to NICU for 75 days with:
• o Neonatal respiratory distress syndrome (RDS) .
• o Intraventricular hemorrhage (IVH) of brain
• o Necrotizing Enterocolitis (NEC)
• Sepsis
• Past surgical Hx: -ve
• Allergies : No Known Allergy

4. Pre-premature rupture of membrane
• defined as rupture of membrane (amniotic
sac) (<37 week gestational age) which
contains amniotic fluid, which surrounds and
protects the fetus in the uterus.
• Complication of baby in pre-PROM :
• Sepsis if PPROM cause by vaginal infection .
• Prematurity which risk of (RDS , IVH ,
Necrotizing Enterocolitis (NEC) .

5. History
• Developmental : (delayed?) rolling from side to
side ,social smile, saying mama, moving objects
from hand to hand .
• Immunization : Up To 6 Months .
• Diet : taking orally aptamil formula plus 1 spoon
Of serelac /day .
• Family Hx : positive Consanguinity First Degree
cousins , no multiple abortions, No similar
condition or Chronic disease In the Family

6. Physical examination
• The patient was conscious looked ill ,no signs of dehydrated not pale
jaundiced or cyanosed.
• Vital sign :
• Heart rate:199
• RR: 30
• BP=119/69
• Temp= 40 C
• O2 sat=98%
• ANTHROPOMETRIC MEASURMENT :
• Weight: 4.8 kg
• Height : 55 cm
• Head circumference : unknown

7. Growth parameter
weight–for-age
below 3rd
percentile

8. Growth velocity
• multiple reading more
Important than single
reading.

10. • Growth weight :
• At birth : 1.1kg
• At 2.5 months : 1.6 kg
• At 10 months : 4.8 kg

11. Summary
• A 10 months old Saudi girl , preterm (30
weeks) , was admitted through ER as case of
gastroentritis . The vomiting non progectile ,
food content , yellow , non bloody ,no mucous
, high grade fever . No history in change urine
color .

12. Laboratory investigation
• CBC:
• WBC 11.9 K/UL H (4-11)
• RBC : 5.84 M/UL (4,8-6,4)
• HB : 13.3 g/dl (13-19)
• MCV : 72 FL L (76-92)
• PLT : 147 K/UL L (150-450)
• TFT:
• TSH : 8.17 ulU/L H (0.27-4.2)
• T3 : 1.8 pmol/L L (2.8-7)
• T4 : 8.7 mol/L L (12-22)

13. Laboratory investigation
• U&E :
• Sodium : 129 mmol/L L (136-145)
• Potassium : 4.3 mmol/L (3.5-5.1)
• Creatinine : 27 mmol/L L (53-115)
• Total protein : 37 g/L (64-82)

14. Laboratory investigation
• LDH: 469 UL H (100-240)
• Ferritin: 212.9 ng/mL H (13-150)
• CRP: 41.9 mg/L H (0-3)
• Albumin: 15 g/L L (40-47)
• Amylase: 7 UL L (25-115)
• TTGA: 17,7 unit (0-20)
• Blood culture: normal

15. Differential diagnosis
• 1- Gastroenteritis .
• 2- UTI .
• 3- pyloric stionsis .
• 4- celiac disease .

16. Manegment
weight= 4.8 kg
160 cl/kg =
768 kcl __ (50%CHO=384 kcl/4=96 gm ),
(35%fat=269 kcl/9=30 mg).
(15%protein=115 kcl/4=29 gm)
• Thyroxine 25 mcg/ml

17. Failure to thrive
• Definition :
don’t meet expecting standard of growth
FTT is inadequate physical growth diagnosed by
observation of growth over time using growth
chart

19. Epidemiology
• In developed nations :
• 5-10 % of young children
• 3-5% of children admitted into hospitals
• Prevalence higher in developing countries? Why
• Poverty.
• Malnutrition.
• HIV infection .

20. Risk Factors

21. Etiology of FTT

22. Failure to thriveCasesofFTT
Primary
Secondary
organic
Non organic

23. Primary causes of FTT
prematurity:
Intrauterine growth
retardation
All parameters (weight ,height ,and head circumference) will be affected.
A) hypoplasia :(problem In The Fetus itself)
Ex : congenital anomalies , chromosomal disorders .
B) Dysmaturty : ( problem in the placenta circulation )
Ex : Placental defect , abruptio placenta

24. Secondary causes of FTT
2- organic causes (congenital or chronic disease) :
Main Organic Causes of FTT
Inadequate caloric intake/ Excessive
loss of nutrients
Cleft lip or Cleft Palate, Oromotor
Dysfunction, Cerebral Palsy, Parasites,
Gastroesophageal Reflux, Irritable Bowel
Syndrome
Inadequate absorption
Food intolerance and allergy, Celiac
Disease, Inflammatory Bowel Disease,
Inborn errors of metabolism, Cystic
Fibrosis
Increased energy requirements
Chronic infection or immunodeficiency,
Chronic pulmonary disease, Malignancy,
Cystic Fibrosis,
Defective utilization of calories
Trisomies 21, 18, and 13, Diabetes
Mellitus,

25. Secondary causes of FTT
1- Non-‐organic causes :

27. Approach
to history and physical examination

28. Physical examination :
The four main goals of physical examination include :
1- identification of dysmorphic features suggestive of
genetic disorder .
2- detection of an underlying disease .
3- assessment for signs of child abuse .
4- assessment of possible effects of malnutrition.

31. Investigation
What is investigation can do it

32. • Laboratory :
• CBC
• Serum ferritin
• LFT
• TFT
• Urine culture
• Stool culture
• Sweat test
• Serum Creatinine urea , electrolytes, Acid Base status , calcium, Phosphate
• Immunoglobulins
• IgA Tissue Transglutaminase antibodies .
• Radiological:
• X-ray

34. Management

35. prevention
• 1- family Education :
-Encourage Breast feeding
-Advice Mother About Proper weaning
-Proper Way For Sterilization Of bottle.
-Vaccination.
• 2-community Education :
‐ safe Water supply.
-Safe Sewage Disposal system.
-Safe Food supply.
-Health Education Through media.

36. • Hospitalization: phases of treatment include :
• stabilization phase (1stweek) emergency treatment and slow
feeding.
• Rehabilitation phase (2nd. 6th week) supportive treatment
and advancement feeding.
• Follow-up phase (7th-26th week).

38. • Dietetic treatment
• Route:
- oral is preferable.
- Nasogastric tube for the cases with sever anorexia, sever
stomatitis or vomiting
• Amount:
-catch-up growth requirement (kcal/kg/d) = [calories required for age
(kcal/kg/d) x ideal weight for age (kg)]/[actual weight (kg)] .
Supportive treatment
- vitamins vit.( A, D and B complex).
- Minerals ( Zinc, cooper, iron)

39. criteria for transfer to Rehabilitation phase
• Eating well
• Mental state has improved: smiles, responds to stimuli,
interested in surroundings .
• sits, crawls, stands or walks (depending on age) .
• Normal temperature (36.s -37.5 degree c) .
• No vomiting or diarrhea
• No edema .
• Gaining weight: >5 g/kg of body wt per day for 3 successive
days

40.  Diets used in Nutrition Rehabilitation
Milk based diet:
• High energy liquid diet .
• Good in hospital rehabilitation .
• Clean water required .
• Water content support bacterial growth
• Immediate utilization
Ready to Use Food (RUTF) powder:
• Good in home rehabilitation .
• Oil based No water
• Does not support bacterial growth

41.  Types of Nutritional Rehabilitation
• Hospital based Nutritional Rehabilitation
• center based Nutritional Rehabilitation .
Day Nutritional Rehabilitation center .
Residential Nutritional Rehabilitation center .
• Community based Nutritional Rehabilitation

42.  Hospital based Nutritional Rehabilitation :
• During rehabilitation phase:
rapid catch-up growth in weight needs to be attained
facilitates early discharge & prevents secondary infections.
• Caloric intake of 170-220 Kcal/kg/day required for rapid catch
up growth (WHO guideline).
• Rapid catch up growth more than 10 g/kg/day.
• Poor catch up growth -less than 5 g/kg/day (WHO guideline)
• Vitamin A and minerals to be supplemented

43.  2- Centre based Nutritional Rehabilitation
Type A Day Nutritional Rehabilitation center :
• For milder forms of protein energy malnutrition .
• 3 daily meals .
• Mothers help prepare the meals. .
Type B Residential Nutritional Rehabilitation center:
• For severe malnutrition after treated in a hospital for complications .
• Mothers help to prepare the meals & receive suitable instruction on child
feeding .
• Proper education and training to mothers can prevent relapses & prevent
other children in same family from getting affected

44.  3- Community based Nutritional Rehabilitation
(CBNR)
• Goal :
To restore to near normal the nutritional status of the
undernourished child and to have a sustained improved physical
& mental growth, performance of the child.

45. Abnormal
Nutrition
Undernutrition
marasmus
Malnutrition
Kwashiorkor
Overnutrition
obesity

46. Protein Calorie Malnutrition
(PCM)
Classifications
1- Wellcome classification : Depends on weight for age & presence of edema.

47. PCM Kwashiorkor (oedmatous PCM) Marasmus (non oedmatous PCM)
Definition: Type of malnutrition in which there's:
1. Acute protein deficiency.
2. Normal or even high caloric intake.
Chronic under nutrition in which there's deficiency of
both proteins & calories.
AGE: 6 months - 2 years Secondary may occur in older children
Causes:
Breast fed
Artificial fed
Weaning child
1- Primary (dietetic)
Prolonged breast feeding supplement
With sweeten food
Diluted formula in artificially fed With
supplement sweeten food
starchy, carbohydrate diet.
1-Primary (Dietetic)
- Prolonged breast feeding
without supplementation
-Diluted formula in artificially fed
-Decrease in all kind of food

48. PCM Kwashiorkor (oedmatous PCM) Marasmus (non oedmatous PCM)
Causes:
2-Secondary (Non dietetic)
1. Infant unable to feed: due to e.g.:
- Premature -Mental retardation(e.g.cerebral palSy)-Severe problems of the nipple or breast.
2. Gastrointestinal causes: Malabsorption syndrome
3. Chronic infections
4. Preterms and twins due to :
- Higher rate of growth-Susceptibility to infection - Weak suckling power
- Limited capacity for digestion and absorption
5. Congenital anomalies & malformations: pyloric stenosis -Bilateral cleft palate
pyloric stenosis.
6. Metabolic disorders
- Lactose intolerance – Galactosaemia .
7. Endocrinal
-Hyperthyroidism (due to hypercatabolism & diarrhea).- Hypothyroidism (due to poor feeding).
9. Malignancies : due to anorexia, hypercatabolic state
Clinical
picture
Hand and foot Edema
-Facial edema produce moon face
appearance.
Due to:
- Hypoalbuminemia
- Salt & water retention due to decreased
inactivation of aldosterone by the fatty liver
No edema
Cachexia
hungry : irritable, Crying & sucking fingers.
Constipation

49. PCM Kwashiorkor (oedmatous PCM) Marasmus (non oedmatous PCM)
Clinical picture
Mentality changes
- The baby looks apathetic, with
anorexia
Due to: -Reduced aromatic amino acids
(phenylalanine, tyrosine & tryptophan)
reduced serotonine, nicotinic acid
Growth retardation
Weight loss may be masked by:-
Oedema.
-Preserved subcutaneous fat
Muscle wasting
Decreased mid arm circumference
Hair changes
Hair is dry, brittle, lightening of hair
- Flag sign: - Alternating bands of light
color & normal color
Occurs in long haired with multiple
relapses.
-Due to tyrosine and Copper deficiency
due to decreased ceruloplasmin.
(Both are essential for melanin
synthesis).
Caloric deficiency manifestation:
Loss of subcutaneus fat
- Loss of fat from the Abdominal wall ~ 1st degree
marasmus.
- Loss of fat from the Buttocks & limbs ~ 2"d degree
marasmus.
-Loss of fat from the Cheeks (senile face)~ 3rd degree
marasmus Outcome:
-Skin becomes thin, loose, wrinkled
• Loss of subcutaneous fat~ prominent normal
costochondral junctions : called false rosaries.
Muscle wasting: muscle are sacrified to keep
normal plasma proteins
Hypoglycemia

50. PCM Kwashiorkor (oedmatous PCM) Marasmus (non oedmatous PCM)
Clinical picture
Skin changes
dry scaling erythematous skin
- Skin infection is common due to: -
Oedema fluid favours infection.
- Fissuring provides portal for organisms.
- Due to: - Vitamin A deficiency
-Zinc deficiency
GIT manifestations
i- Hepatomegaly
- Hepatomegaly is reversible with
treatment.
-Usually there is no cirrhosis
- Hepatomegaly is due to fatty infiltration
due to:
- Decreased lipotropic factors.
- Increased fat synthesis due to high
carbohydrate diet .
ii- Diarrhea due to:
- Infectious : due to destruction of villi lead
to lactose intolerance
-Non infectious : malabsorption due to
decrease amylase and lipase enzymes
iii- Abdominal distension due to:
-Hypokalemia.
- Malabsorption.
-Toxic ileus (with infections).
Hupothermia
due to
- Loss of subcutaneous fat excess heat loss.
- Hypoglycemia decreased heat production.
Vitamin deficiency, anemia, hair & skin
changes are less common than in KWO
No Hepatomegaly

51. PCM Kwashiorkor (oedmatous PCM) Marasmus (non oedmatous PCM)
picture Clinical
Anemia May be due to: -
Iron deficiency
Prothrombin deficiency ~
hemorrhagic anemia
Vitamin deficiency :
Vitamin A and K deficiency
Vitamin D deficiency

54. PCM Kwashiorkor (oedmatous PCM) Marasmus (non oedmatous PCM)
Complications
death
Dehydration: Due to gastroenteritis &
anorexia.
rercurrent infection:
Due to : - Defective immune system
Septic shock
Electrolyte disturbances:
- Dilutional hyponatremia
- Hypokalemia due to loss in diarrhea
reduced intake & aldosterone effect
-Hypocalcemia & hypomagnesemia may
lead to tetany.
Heart failure due to:
- Severe anemia.
- Volume overload.
-Weak myocardium
Hemorrhage (bleeding tendency) due to:
- Vitamin K deficiency.
Dehydration
rercurrent infection:
Septic shock
Hypothermia
Hypoglycemia
Atrophic ulcers occur over bony prominences .
The most common cause of death is bronchopneumonia
Then electrolyte disturbance

55. PCM Kwashiorkor (oedmatous PCM) Marasmus (non oedmatous PCM)
Investigat
ions
1- Confirm diagnosis:
- Plasma proteins:
-Decreased total plasma proteins (normal6-8
gm/dl).
- Decreased albumin< 2.5 gm/dl (normal 3.5-
5 gm/dl).
-Decreased carrier proteins e.g ceruloplasmin,
transferrin
-Decreased enzymes e.g amylase, lipase
- Low urinary urea to creatinine ratio.
2- For effect :
I. On fat metabolism:
-Increased free fatty acids (due to excess
carbohydrate intake)
2. On CHO metabolism:
- Fasting hypoglycemia due to deficient
glycogen stores in the liver.
3. Mineral metabolism: Copper and zinc
deficiencies are frequent
3- For complication:
- CBC for anemias.
- Sepsis workup in suspected cases
Electrolytes: Na, K, Ca, Mg.
1- Biochemical changes in marasmus
Blood:
- Fasting hypoglycemia (due to reduced glycogen
stores in the liver).
- Plasma proteins slightly reduced.( due to chronic
degradation of muscles to keep plasma proteins)
-Urine: -Ketonuria (due to fat hypercatabolism).
-Increased creatinine (due to muscles
hypercatabolism)
2- For complication:
- CBC for anemias.
- Sepsis workup in suspected cases Electrolytes: Na,
K, Ca, Mg.
3- Search for the cause (if2ry marasmus is
suspected)
1- Stool analysis
2- Urine analysis

56. PCM Kwashiorkor (oedmatous PCM) Marasmus (non oedmatous PCM)
treatment
I. Emergency treatment (In the 1st 24-48 hours) for:
Hypoglycemia:
- Glucose infusion
Dehydration
Anemia: blood transfusion
Hypothermia
- Keep with warmed blankets
- Treat hypoglycemia .
Electrolytes correction
Dietetic treatment
1- Route:
- Oral is preferable.
2- Amount:
- Start with 80-100 cal./kg/day then
- Increase gradually up to 150-220 cal/Kg/day for severely malnourished
3- Protein intake:
-Start with 1 gm/kg/d increased gradually to reach 4 gm/kg/d.
4- Frequency:
- Small frequent feeds every 2-3 hours increased gradually over 1-2 weeks.

57. PCM Kwashiorkor (oedmatous PCM) Marasmus (non oedmatous PCM)
Complicat
ion of
treatment
Hypokalemia :
Hypokalemia is already present aggravated
by glucose infusion
Circulatory overload:
There's already salt & water retention with
infusion of large doses of blood or
plasma volume overload and even heart
failure.
Nutritional recovery syndrome due to :
A- Excess caloric intake excess glycogen
deposition in the liver before
getting rid of excess fat ~ hepatomegaly may
increase at the start of
treatment ,then regress gradually.
B- Excess protein intake liver is exhausted
by protein metabolism lead to
excess ammonia load on the liver leads to:
Hepatic encephalopathy with lethargy,
convulsions & coma.

58. reference
• Nelson Essentials of Pediatrics 7th
• illustrated textbook of paediatrics
• Medscape

59. DONE BY
• Abdulmageed alomer
• Mohamad almaliki
• Abdulrahman alzahrani