Malnutrition in children

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 Malnutrition

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«Hidden» death due to malnutrition in Ethiopia

80% of the death due to malnutrition is contributed

by Mild and moderate malnutrition

Mild &
moderate

Sévère
Only 1 in 5 malnutrition-related deaths is
due to severe malnutrition
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 Overview of malnutrition
Nutrition is the provision of adequate energy
and nutrients to the cells to enable them to
perform their physiological function (of
growth, reproduction, defense, repair, etc).
WHO
defines malnutrition as
"the cellular imbalance between supply of nutrients &
energy and the body's demand for them to ensure
growth, maintenance, and specific functions”.

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 Malnutrition includes:

Malnutrition is the result of a lack or an excess in the

provision of energy and/or nutrients to the body
(under nutrition or overweight/obesity)
• Macronutrient deficiency
• Micronutrient deficiency (Hidden Hunger)
• Over nutrition- Overweight and obesity
􀃆Best assessed by weight & height

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 Cont’d

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 Cont’d

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 Understanding malnutrition
Wasting: means that the infant/child is thin:
she/he has lost fat and muscle mass
Stunting: means that the infant/child is short in
stature: she/he did not grow in length/height
has he/she should have
Underweight: means that she/he weighs less
than she/he should. A child can be both wasted
and stunted

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 Cont’d
Wasting is usually due to a recent lack of food or
illness (infections) that prevents the child from
eating or absorbing nutrients of foods
Stunting is a long term process, often starting in
utero which is due to the mother’s malnutrition,
to food intake lacking quality.
Overweight and obesity are due to excessive
energy intake and lack of physical activity

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 TYPES OF UNDERNUTRITION

UNDERNUTRITION

ACUTE CHRONIC
UNDERNUTRITION UNDERNUTRITION

• Marasmus
• kwashiorkor
• Marasmic- • Stunting
• Underweight
kwashiorkor
• Wasting
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 Definition of terms
Protein-energy-malnutrition (PEM): A clinical syndrome
present in infants and children as a result of deficient
intake and/or utilization of food(mainly protein).
Marasmus: form of acute malnutrition that is characterized
by wasting of body tissues. Marasmic children are
extremely thin
Kwashiorkor: form of acute malnutrition characterized by
bilateral edema and weight-for-height of less or equal to -
2 SD
Marasmic-Kwashiorkor: form of acute malnutrition
characterized by bilateral edema and weight-for-height of
less than -2 SD
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 PROTEIN-ENERGY MALNUTRITION

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 EPIDEMIOLOGY

• The majority of world’s children live in developing

countries
• Highly prevalent in developing countries
• All children with PEM have micronutrient deficiency.

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 Which countries are home to the stunted children ?

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Determinants of child malnutrition
No Single cause:
❖Primary due to inadequate food availability
❖Secondary to many causes
Other disease lead to low food ingestion,
inadequate nutrient absorption or utilization,
increased nutritional requirements, increased
nutrient losses

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 Etiology…..
Social and Economic Factors
✔ Poverty
✔Ignorance
Cultural problems
Biological factors
✔ Maternal malnutrition
✔ Infection
✔Dietary factor bulky foods with low nutritional
value
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 Cont’d
Environmental factors
⮚ Overcrowded and/or unsanitary living
conditions
⮚ Agricultural patterns, droughts, floods, wars,
Age of the host
⮚ More frequent among infants and young
children

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1/12/2022 DETERMINANATS OF MALNUTRITION 20
 Classification of PEM
A . Community (Gomez)
– Parameter: weight for age
– Reference standard (50th percentile) WHO
chart
– Grades:
I (Mild) : 90-70
II (Moderate): 70-60
III (Severe) : < 60

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 Classification of PEM
B. Welcome system:
- Parameter: weight for age
- Reference standard Harvard curve
Weight for age Edema- Edema +

60-80% Underweight Kwashiorkor

<60% Marasmus Marasmic-kwash

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 Cont’d
C. Water low classification asses severity of
wasting and stunting

Grade of Wt/ht (Wasting ) Ht /age (Stunting )

malnutrition
Normal > or=90% > or=95%

Mild 80-89% 90-94%

Moderate 70-79% 85-89%

severe <70% <85%

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Abnormal Physiology in Malnutrition

• The malnourished child has abnormal

physiology that has implications for case
management.
• With severe malnutrition, the physiological
systems slow down or ‘shut down’ and do
less to allow for survival on limited nutrients.
• This slowing down of the systems is called
reductive adaptation.

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 Assignment
Physiologic changes in malnutrition
• Liver function
• CVS
• GIT
• GUS
• Skin, muscle and bone
• Immune system
• Brain development

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 Infection-Malnutrition Synergism

Weight loss
Growth faltering
Immunity lowered

Disease Incidence
Inadequate dietary
Severity
intake
Duration

Appetite loss
Nutrient loss
Malabsorption
Altered Metabolism
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Pathophysiology of Severe Acute Malnutrition

•Severe acute malnutrition can result in

profound metabolic, physiological and
anatomical changes.

•Virtually all physiological processes are

altered due to severe acute malnutrition.

• Every organs and systems are involved in

reductive adaptation.
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 FOUR FUNCTIONAL CONSEQUENCES OF MALNUTRITION

▪ Illness – via increasing susceptibility to

infection
▪ Intelligence loss
▪ Reduced productivity
▪ Mortality

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Kwashiorkor

FLAKY PAINT DERMATITIS

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 Kwashiorkor

FLAKY PAINT DERMATITIS

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 KWASHIORKOR

• Cecilly Williams, a British nurse, had introduced the word

Kwashiorkor to the medical literature in 1933.
• The word is taken from the Ga language in Ghana & used
to describe :
- ‘’The sickness of weaning’’
- “The sickness the older child gets when the next baby is
born”
- Disease when child is displaced from breast
(Cicely Williams, 1935, Gold Coast, W Africa)
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 Etiology
• Lack of knowledge about diet
• Poverty
• Natural calamities like drought, earthquakes, etc
• Repeated infections like diarrhoea, measles, etc
• Religious customs (people of certain religions
avoid non-vegetarian diet which has high-quality
proteins)

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 Kwashiorkor ...
• Incidence is more in:
⮚ Low birth weight
⮚ Broken families
⮚ In children with whose parents are
unemployed
⮚ Large families

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 Kwashiorkor ...
• Kwashiorkor is lack of physiological adaptation to
unbalanced deficiency where the body utilized
proteins
• Edema: decrease oncotic pressure,
– Recent: greater Increase Renin activity, Na and
fluid retention.
• Amino aciduria due to proximal tubular dysfunction
• Hepatomegaly due to fatty infiltration from
lipogenesis of excess CHO
• Dermatitis
• Skin lesion
• Loss of Appetite

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 MARASMUS

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 Marasmus…

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 Cont’d

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 Marasmus
• The term marasmus is derived from the Greek
marasmos, which means wasting.
• A nutritional disorder due to deficiency of protein
and calories, particularly calories, characterized
by:
⮚Growth failure
⮚Gross wasting
⮚Absence of oedema

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 Marasmus…
• Marasmus represents the end result of
starvation where both proteins and calories
are deficient.
• Affects all age but common < 1 year.
• In Marasmus the body utilizes all fat stores
before using muscles.

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 Causes
Cause: The same as PEM.
but Primary causes
• Lactation failure – the commonest cause
Lactation failure -------🡪introduction of dilute &
dirty formula -------🡪 infections (diarrhoea) 🡪
starvation therapy due to diarrhoea
-------🡪 Marasmus
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 Causes …
2. Secondary causes
a. Birth weight: common in premature & LBW
b. Cardiovascular diseases like VSD, ASD, and
PDA due to:
– Recurrent respiratory infections
– Feeding and growth failure
– Cough & breathlessness

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 Causes …
c. Respiratory causes: TB, etc
d. Gastrointestinal causes
– Congenital hypertrophic pyloric stenosis- vomiting
– Congenital megacolon- diarrhoea
– Cleft lip & palate – inadequate intake of feeds, mainly
breast feeds
e. Infections
– Repeated diarrhoea
– Severe infections like congenital syphilis
– Malabsorption syndrome

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 Causes …
3. CNS causes
• Hydrocephalus and CNS infections like
tuberculosis meningitis, pyogenic meningitis
can cause marasmus due to decreased intake
& chronic vomiting

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 Clinical manifestations

• Growth retardation or growth failure (wt. for age

<60% or wt. for Ht < 70%)
or < -3 SD
• Sunken eye balls
• Mood change (irritable)
• Good appetite
• Diarrhea
• “Old man face” appearance
• Mild skin & hair change (less common sign )
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 Clinical manifestations…

• Abdomen may be large or distended

• Wasting of subcutaneous tissue
Steps – Remove the child’s cloths.
Look for severe wasting of the muscle of buttocks
& legs. The child has no fat & look like bone &
skin.
• When the wasting is extreme there are many fold
of skin on the buttocks & thigh.
• It look as if the child is wearing baggy pants
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 Anthropometric Indicators of Malnutrition

• Anthropometry is the determination of

nutritional status by physical measurements
and comparing them to relevant reference
charts.
• Anthropometric measurements that have
been used include H/A, W/A, W/H,HC,MUAC,
and skin fold thickness.

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 MALNUTRITION INDICATORS

NUTRITION INDICATOR MEASUREMENT CLINICAL INDICATOR

INDICATOR

Acute Malnutrition Weight-for-Height Wasting, kwashiorkor

(SAM & MAM)

Chronic Under nutrition Height-for-Age Stunting

Underweight (composite Weight-for-Age Underweight

indicator)

Over nutrition Body Mass Index Overweight/Obesity

(weight/Height2

Micronutrient Deficiencies Biochemical indicators Hypoalbuminemia,

Xerophthalmia, stomatitis
etc

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 SD Score Method
Which children are underweight?
(Low Weight for Age)
•Children whose weight is <-2 SD score of the
median weight of children of the same age in
the reference population
•Reflects current and past nutritional status

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 Methods…
Which children are stunted?
(Low Height for Age)

•Children in a given population whose height is <-2

SD of the median height of children of the same
age in the reference population

•Reflects past nutritional status (chronic malnutrition)

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 Methods…
Which children are wasted?
(Low Weight for Height)

•Children in a given population whose weight is

<-2 SD of the median weight of children of the
same height in the reference population

•Reflects present nutritional status (acute)

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 Diagnosis
• Malnutrition is usually diagnosed through anthropometry
(weight-for-height, in which the weight and height of the
child is compared to those of an international reference;
MUAC, or other).

• However, the main symptom that reveals the metabolic

status of the child is “lack of appetite”.

• Patients with no appetite usually present a severe

complication -visible or not- that need specialized
treatment.
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 Diagnosis

• Normal: ± 1 SD
• Mild: -1 to -2 SD
• Moderate -2 to -3 SD
• Severe less than -3

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 Investigations
❑Blood
• CBC
• Serum electrolytes, plasma protein estimation
• Blood culture & sensitivity for evaluation of septicaemia
❑Urine
• Albumin, sugar, urine culture & sensitivity
❑Stool
• Ova of parasite, culture & sensitivity if there is
diarrhoea
❑Chest X-ray: to r/o TB & other infections
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 Complications
SAM
• Children with SAM are classified as ‘complicated’
have clinical features of infection or metabolic
disturbance, severe oedema or poor appetite.
• Children with ‘uncomplicated’ SAM are clinically
well, alert and have retained their appetite

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 Direct causes of death:
1. Hypoglycemia

2. Hypothermia

3. Dehydration

4. Infection

5. Severe anemia

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Time Magazine, August, 2008
 MANAGEMENT OF MEDICAL COMPLICATIONS
❑ Hypoglycemia
• Hypoglycemia is a low level of glucose in the
blood.
• In severely malnourished children, the level
considered low is <54 mg/dl (< 3 mmol/litre).
• The hypoglycemic child is usually hypothermic
(low temperature) as well.
• Other signs of hypoglycemia include lethargy,
limpness, and loss of consciousness.
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 Hypoglycemia mgt
• 5 to 10 ml/kg of sugar water ‘PO’ for
conscious pt. 5 to 10 ml/kg of sugar water by
NG-tube or 5 ml/k.g a single injection of 10%
glucose solution for unconscious pt.
All malnourished patients with suspected
hypoglycemia should be treated with second-
line antibiotics

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 Hypothermia
• A severely malnourished child is hypothermic if the
rectal temperature is below 35.5 0C or if the
auxiliary temperature is below 35 0C.

• Severely malnourished children are at greater risk of

hypothermia than other children and need to be
kept warm.

• The hypothermic child has not had enough calories

to warm the body.
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 Hypothermia….
• If the child is hypothermic, he is probably also
hypoglycemic.
• Both hypothermia and hypoglycemia are signs
that the child has a serious systemic infection

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 Mgt Hypothermia
-Use kangaroo care technique with care taker

• put a hat on child

• Wrap the mother & child together.
• Keep the room warm.
• Treat hypoglycemia
• Treat by antibiotic

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KMC 61
 Cont …
• Dehydration (DHN) - Taker over load of
&septic shock. fluid solutes
- use ReSoMal solution
to rehydrate SAM.
• Anemia - give 10ml/kg of packed
RBC or whole blood
• Infection Antibiotics

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 ReSoMal
• ReSoMal is available commercially.
• However, ReSoMal can also be made by
diluting one packet of the standard WHO-
recommended ORS in 2 liters of water, and
adding 50 g of sucrose (25 g/l) and 40 ml (20
ml/l) of mineral mix solution

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 Amount of ReSoMal to give

• Starting with 5 ml/kg every 30 minutes for the

first 2 hours orally or by NG tube, and then 5–
10 ml/kg per hour/for 10 hours, totally 12
hours is required.
• This rate is slower than for children who are
not severely malnourished.
• Reassess the child at least every hour.

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 Calculate amount of ReSoMal to give

• For a child who has dehydration but no sign of

shock, give ReSoMal as follows, in amounts
based on the child’s weight:

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Assessment and Classification of Acute Malnutrition

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 Management of SAM
CASE MANAGEMENT OF SAM

• The principles of management of severe acute

malnutrition, whatever the programme
setting, are based on 3 phases.

Phase I
Transition Phase
Phase II

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 Phase 1 (Stabilization phase)
❑children with complicated SAM are initially
admitted to an inpatient facility for stabilization.
❑These children are admitted to phase 1 room.
During this phase:
• Life-threatening medical complications are treated
• Routine drugs are given to correct specific
deficiencies
• Feeding with F-75 milk (low caloric and sodium) is
begun

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 Phase 1…
• The children in Phase 1 should be together in
a separate room or section of the ward and
not mixed with other patients
• Routine drugs has to be started immediately
after they are admitted
❖Amoxacilline
❖Vitamin A
❖Follic acid

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 Transition phase
Transition phase is started with F-100 or RUTF
When
❑The child appetite recovers
❑ The main medical complications are under control and
❑ Oedema start to reduce

This phase is important for slow transition as the

introduction of large amounts of RUTF or F100 could lead
to imbalance of body fluids and severe medical
complications. In this phase:
– Routine drugs are continued
– Feeding with RUTF or F100 is started
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Criteria to move back from transition phase to phase1

❑Move the child back to Phase 1:

• If the patient gains weight more rapidly than
10g/kg/d (this indicates excess fluid retention)
• If there is increasing oedema
• If a child who does not have oedema develops
oedema
• If there is a rapid increase in the size of the liver
• If any other signs of fluid overload develop.

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 Move the child back to Phase 1 …

• If tense abdominal distension develops

• If the patient gets significant re-feeding
diarrhea so that there is weight loss.
• If patient develops medical complication
• If NG-tube is needed
• If patient takes less than 75% of the feeds in
Transition Phase

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 Criteria to move from transition phase to phase 2

• Marasmic pt. spends a minimum of 2 days and

if tolerating the new diet with out complication
• Completing the diet with good appetite.
• Complete loss of or radical decreasement of
edema (in kwashiorkor).

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 Phase 2 (Rehabilitation Phase)
❑Children that progress through phase 1 and transition
phase enter phase 2 when they have good appetite and
no major medical complication.
❑ During phase 2:
• Routine drugs, deworming tablets and iron, are started
• Feeding with RUTF or F100 is increased in amount
• Child starts gaining weight
❑Whenever possible, phase 2 is implemented as OTP
with RUTF. Otherwise, it can be implemented in in-
patient centers with RUTF or F100.

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 Criteria to move back from phase 2 to phase 1

• Develops any signs of a complication

• Increase/development of oedema
• Development of re-feeding diarrhea sufficient
to lead to weight loss.
• Weight loss for 2 consecutive weighing
• Static weight for 3 consecutive weighing
• Fulfilling any of the criteria of “failure to
respond to treatment”

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 ROUTINE MEDICINES

VITAMIN A
• On the day of admission (day 1), give vitamin
A for all children except those with oedema or
those who received vitamin A in the past 6
months.

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 FOLIC ACID

• On the day of admission, one single dose of

folic acid (5mg) can be given to children with
clinical signs of anaemia.

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 ANTIBIOTICS

• Antibiotics should be given to every severely

malnourished patient, even if they do not
have clinical signs of systemic infection.
• First line treatment: oral amoxicillin (if
amoxicillin not available, use oral ampicillin)
• Second line treatment: Gentamycin (do not
stop amoxicillin)

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• "This recommendation for the use of routine
antibiotics is based on expert opinion and has
not been directly tested in a clinical trial," they
continue, "and observational data suggest that
antibiotics are unnecessary and perhaps even
harmful in children with uncomplicated
severe acute malnutrition (i.e., children with
good appetite and no clinical signs of sepsis)."

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 MALARIA
• Based on national guideline for malaria
treatment Malaria, Diagnosis and Treatment
Guidelies for Health Workers in Ethiopia.
• Never give intravenous infusions of quinine to
a severely malnourished case within the first
two weeks of treatment.

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 MEASLES
• All children from 9 months without a
vaccination card should be given measles
vaccine both on admission and discharge.

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 DEWORMING
• Albendazole or Mebendazole is given at the
start of Phase 2
• Worm medicine is only given to children that
can walk.

IRON
• added to F-100 in phase II

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WARNING: NEVER DO ANY OF THEFOLLOWING:

• Never give diuretics against malnutrition

oedema. The oedema is partially due to
potassuim and magnesium deficiency, that can
easily recover in two weeks.
• Oedema dissapears with appropriate feeding
adding a micronutrient solution.
• Giving diuretics would aggravate the
electrolyte imbalance and would risk death.

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 Cont’d

• Do not give Iron in the first days of treatment

(until Phase 2 or Rehabilitation phase).
• It risks having toxic effects and reduce defense
against infections.

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 Cont’d

• Do not give preparations rich in proteins (more

than 1.5 g of protein per kg/day).
• Any excess in the first days can be dangerous,
because the severely malnourished child is not
able to assume the metabolic effort needed to
deal with them.
• An excess of proteins can overload the liver, the
heart and kidneys and provoke death.

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 Cont’d

• Do not give liquids in perfusion. In the child

with severe malnutrition liquids in perfusion
can easily produce cardiac overload.
• These are only given when there is a diagnosis
of septic shock.

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 Vitamin A deficiency

• More common between 6 months to 3 years of age

• 50 to 80% of severe protein malnutrition patients are
associated with vitamin A deficiency
 Functions of vitamin A
• Functioning of retina
• Growth and differentiation of epithelial tissue
• Growth of bone
• Reproduction and embryonic development
• Enhances immune function, reduces the
incidence of infectious diseases
 Cont’d
• Infants and young children under 5 year of
age are at highest risk because
- poor stores at birth
- milk and supplementary food(
low vit.A)
- infection including diarrheal
disease and
- growth sets requirement high
 Etiology of vitamin A deficiency
• At birth, the liver has a low vitamin A content that
can be augmented by colostrum and breast milk
• Loss of vitamin A is present by cooking, canning and
freezing of food stuffs, oxidizing agents etc
• Vitamin A deficiency is seen in fat malabsorption or
chronic intestinal disorders
• Low intake of vitamin A
• Increased excretion of vitamin A present in cancer,
urinary tract disease and chronic diseases
• Low protein intake can cause decrease of vitamin A
concentration
 Clinical features
Parameter Features
Eyes •Night blindness is the earliest
manifestation
•Bitot spots: dry, silvery-gray plaques may
appear on the bulbar conjunctivae
•Conjunctival xerosis: drying of conjunctiva
•Corneal xerosis: drying of cornea
•Xerophthalmia: cornification of the
epithelium of the conjunctiva and
disappearance of the mucus cells
•Keratomalacia: desiccation, ulceration and
xerosis of the cornea & conjunctiva
 Clinical features ...
Parameter Features
Respiratory Increased risk of respiratory tract infections
tract
Skin Keratinization & drying of the epidermis
occurred and papular eruptions involving
the pilosebaceous follicles may be found
especially on the extremities

Genitourinary Epithelium is damaged. The patient can

system develop pyuria & hematuria
GI system Reduction of goblet cells; diarrhoea
 Clinical features ...
Parameter Features
CNS •Mental retardation can occur
•Increased ICP with wide separation of
cranial bones may occur
•Hydrocephalus with or without paralysis of
the cranial nerves may occur
Bone Associated with faulty modelling of bone,
with production of thick, cancellous bone
instead of thinner more compact bone
Miscellaneou •Taste and smell are impaired
s •Hearing may be impaired
•It can interfere with erythropoiesis
Bitot’s spot
 Management strategies
1. Breast feeding
2. Food diversification
3. Vitamin A supplementation
4. Food fortification
 Therapy

• Vitamin A capsule on two consecutive days

immediately and another dose within 1-4
weeks
Dose -200,000IU above one year
-100,000IU 6 – 12 month
-50,000IU less than 6 months
 Prevention
• Increase consumption of dark green leafy
vegetables. Egg, livers, fat of fish and meat and
cod liver oil can be provided
• Vitamin A should be supplemented in
malnutrition, diarrhea, measles and acute
respiratory infection.
• Distribution of vitamin A capsule should be given
to the community.
– One capsule every 6 months up to 6 year of
age
• One drop of vitamin A (25,000IU) for every child
with immunization schedule
 Rickets (Nutritional)
• Bone consists of a protein matrix called osteoid and a
mineral phase, principally composed of calcium and
phosphate.
• Rickets, a disease of growing bone, occurs in children
only before fusion of the epiphyses, and is due to
unmineralized matrix at the growth plates.
• Common among children aged 6-36 months
 Rickets ...
• Because growth plate cartilage and osteoid
continue to expand, but mineralization is
inadequate, the growth plate thickens.
• There is also an increase in the circumference
of the growth plate and the metaphysis.
• This increases bone width at the location of
the growth plates, causing some of the classic
clinical manifestations, such as widening of
the wrists and ankles
 Etiology of rickets in general
❑There are many causes of rickets including
• Vitamin D disorders,
• Calcium deficiency,
• Phosphorous deficiency
 Vitamin D disorders

• Nutritional vitamin D deficiency

• Congenital vitamin D deficiency
• Secondary vitamin D deficiency
• Malabsorption
 Metabolism of vitamin D
• Vitamin D is available in two forms:
1. Vitamin D2 Calciferol is an ergosterol
2. Vitamin D3 is available synthetically. It is
present in skin as 7-dehydrocholesterol. It
will be converted to cholecalciferol on
irradiation of skin by ultraviolet rays in the
range of 296-310 nm.
 Etiology of Nutritional vitamin D deficiency

❑Decreased intake
• Lack of vitamin D in the diet
• Lack of exposure to UV irradiation
• Black children are susceptible to rickets owing to
pigmentation of their skin or inadequate
penetration of sunlight
❑GIT causes
• Decreased absorption in the following conditions
a. Coeliac disease, steatorrhoea, pancreatitis, or cystic
fibrosis
b. Glucocorticoids may antagonise vitamin D in
calcium transport
 Etiology ...
❑Liver
• Neonatal hepatitis, and liver cell failure may
decrease absorption of vitamin D
• Anticonvulsants like phenobarbitone and
phenytoin may convert 25(OH)D3 in to more
polar vitamin D3 by P450 enzyme, which is an
inactive form
❑Kidney: chronic renal failure, tubular acidosis,
etc
 Incidence
• The incidence is more during the period of
rapid growth, particularly between 4 months
to 2 years of age
• Equal in both sexes, but it is more in male
children due to rapid growth
 Diagnosis
• Mainly physical examination
• Blood test for Calcium and phosphorus
• Blood test for 25-hydroxy vitamin D
• X- ray to check bone deformity

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 Clinical Manifestations

• Most manifestations of rickets are due to

skeletal changes.
• Craniotabes, a softening of the cranial bones,
can be detected by applying pressure at the
occiput or over the parietal bones. The
sensation is similar to the feel of pressing into a
Ping-Pong ball and then releasing.
• It is a normal finding in many newborns,
especially near the suture lines, but it typically
disappears within a few months of birth.
 Clinical …
• Widening of the costochondral junctions results in a
rachitic rosary; this feels like the beads of a rosary as
the examiner's fingers move along the costochondral
junctions from rib to rib.
• Growth plate widening is also responsible for the
enlargement at the wrists and ankles.
• The horizontal depression along the lower anterior
chest known as Harrison groove occurs due to
pulling of the softened ribs by the diaphragm during
inspiration.
 Clinical …
• Softening of the ribs also impairs air
movement and predisposes patients to
atelectasis.
• The risk of pneumonia appears to be elevated
in children with rickets; in Ethiopia, there may
be a 13-fold higher incidence of rickets among
children with pneumonia.
 Summary of clinical features
❑GENERAL
• Failure to thrive
• Listlessness
• Protruding abdomen
• Muscle weakness (especially proximal)
• Fractures
• Tenderness
❑HEAD
• Craniotabes
• Delayed fontanelle closure
• Delayed dentition; caries
 Summary of ...
• CHEST
• Rachitic rosary
• Harrison groove
• Respiratory infections and atelectasis
• BACK
• Scoliosis
• Kyphosis
• Lordosis
 Summary of ...
EXTREMITIES
• Enlargement of wrists and ankles
• Valgus(outward) or varus(inward) deformities
• Windswept deformity (combination of valgus
deformity of 1 leg with varus deformity of the
other leg)
• Anterior bowing of the tibia and femur
• Leg pain
 Valgus and varus deformity

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Harrison groove
Growth palate widening
Rachitic Rosary
 Differential diagnoses
❑Craniotabes
• Hydrocephalus
• osteogenesis imperfecta, genetics
❑Costochondrial junction enlargement
• Scurvy
• Chondrodystrophy
• Congenital epiphysel dysplasia
• Cytomegalic inclusion disease
• Syphilis
• Copper deficiency
• Vitamin D resistant reckets
 Treatment
• Children with nutritional vitamin D deficiency
should receive vitamin D and adequate
nutritional intake of calcium and phosphorus.
• Vitamin D intake of 400 IU/day, typically given
as a multivitamin.
• It is important to ensure that children receive
adequate dietary calcium and phosphorus; this
is usually provided by milk, formula, and other
dairy products.
 Complications
• Bronchitis
• Bronchopneumonia
• Pulmonary atelectasis
• Anemia
 Prevention
• Exposure to sunlight
• Oral administration of vitamin D
• Daily requirement of vitamin D is 10
microgram or 400IU/day
• Milk fortified with vitamin D can be given
 THANK YOU

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