Nutrition

Question 1

What are the consequences of malnutrition?

Answer 1

• Malnutrition can make other concurrent illnesses much worse
• Affect child’s intellectual development

Question 2

How do you assess a childs nutritional status?

Answer 2

-HISTORY
-FOOD DIARY (what they were given, and what they actually ate)
-ANTHROPOMETRY
○ weight for height (severe malnutrition=-3 standard deviations away from the mean)
○ height for age
○ mid upper arm circumference (MUAC shows skeletal muscle mass. <115mm=severe malnutrition)

-can also do skin fold thickness over triceps muscle (fat reserves)

Question 3

What nutritional support can we give children who are malnourished?

Answer 3

-If there are no problems with absorption then ENTERAL should be first line
○ maintains gut function
○ NG tube or gastrostomy (additional feeds throughout night, normal eating in day)

-PARENTERAL FEEDS should be given if the gut is not functioning/absorption issues
○ a nutritionally complete feed in IV fluid
○ can be delivered at home
○ long term must be delivered via central venous catheter

Question 4

What is marasmus?

How does it present?

Answer 4

-Marasmus is severe energy intake deficiency (including protein) in children causing:
○Weight for height more than −3 standard deviations below the median, (corresponding to <70% weight for height)
○Oedema is not present.
○Skinfold thickness and mid­arm circumfer­ence are markedly reduced
○Children are often withdrawn and apathetic

Question 5

What is Kwashiorkor?

How does it present?

Answer 5

• Kwashiorkor is a severe protein deficiency
• Generalised oedema (ascitic appearance) and severe distal wasting
• Because of odema, weight may be unchanged

Additional features:
• ‘flaky­paint’ skin rash with hyperkeratosis (thickened skin) and desquamation
• distended abdomen and enlarged liver (usually due to fatty infiltration)
•angular stomatitis
•hair which is sparse and depigmented
•diarrhoea, hypothermia, bradycardia and
hypotension
•low plasma albumin, potassium, glucose and magnesium

Question 6

How do we manage severe malnutrition?

Answer 6

Children with no appetite or medical complications need hospital care (30%) Otherwise care can be community based.

Acute managment:

• Hypoglycaemia - correct urgently
• Hypothermia - wrap up warm, especially at night
• Dehydration - carefully correct
• Electrolytes - correct deficiencies, especially potassium
• Infection - give antibiotics and treat fever and all other signs. Treat oral candida if present
• Micronutrients are really important - give vitamin A and other nutrients
• Initiate feeding - small volumes, frequently, throughout the night (initially food that is low in protein -high protein foods will not be tolerated)

Formula 75 is initially (starter) given followed by Formula 100 (catch up)

Question 7

What causes vitamin D deficiency?

What is pathophysiology?

Answer 7

Vitamin D deficiency
• Usually caused by insufficient intake or defective metabolism of vitamin D

Pathophysiology
• Low vitamin D>low calcium (cant be absorbed by body without vit D > secretion of PTH to normalize calcium but has some other effects:
○ Demineralizes the bone
○ Causes the kidneys to lose phosphate>low serum phosphate (further reducing potential for bone calcification)

Question 8

How can fit D deficiency present?

Answer 8

Vitamin D deficiency

1) Bony deformity and classic rickets picture
2) Symptoms of hypocalcemia (seizures, neuromuscular irritability (tetany), apnea, stridor (decalcification of larynx)

The later presentation is more common in ages where bones are rapidly developing and require more calcium (before 2 years and adolescence)

Question 9

What is rickets?

Answer 9

Rickets signifies a failure in mineralization of the growing bone or osteoid tissue. Failure of mature bone to mineralise is osteomalacia (seen in adults)

Question 10

What is the aitiology of Rickets?

Answer 10

NUTRITIONAL/PRIMARY RICKETS
• Northern latitudes
• Dark skin (reduces ability to produce vita from sun)
• Decreased sunlight exposure (some Asian children)
• Maternal vitamin D deficiency
• Diets in low calcium, phosphorus and vitamin D (e.g. exclusive breast feeding late into infancy, or toddlers on unsupervised dairy free diets)
• Strict vegan diets

INTESTINAL ABSORBTION
• Small bowel problems (e.g. coeliac)
• Pancreatic insufficiency (e.g. cystic fibrosis)
• Cholestatic liver disease (bile unable to get to the gut)

IMPAIRED ACTIVATION of VIT D (hepato/renal disease)
HEREDITORY CAUSES
DRUGS -especially anti­ convulsants such as phenobarbital and phenytoin

Question 11

What foods contain vit D?

Answer 11

Foods that contain vitamin D: egg yolk, fish oil, fatty fish

Question 12

Presentation of Rickets?

Answer 12

Presentation of Rickets
• Pingpong ball sensation of the skull (craniotabes)
○ Elicited by pressing firmly over the occipital/posterior paratial bones
• Wide wrists (crawling child) and ankles (walking child)
• Harrisons sulcus
• Rachitic rosary- palpable ribs and costo-chondral junctions
• Bowed legs
• Short/FTT
• Frontal bossing of skull
• Delayed closure of fontanelle
• Delayed dentition
• Siezures (usually late)
•Hypotonia

Question 13

Diagnosis of Rickets?

Answer 13

Diagnosis
• Dietary history for vitamin and calcium intake
• Blood tests
○ Serum calcium low or normal
○ Phosphorus low
○ Plasma alkaline phosphatase ALP greatly increased (due to anincreasein compensatory osteoblast activity)
○ Parathyroid elevated (due to low calcium)
○ 25­hydroxyvitamin D may be low
• X­ray
○cupping and fraying of the metaphyses and a widened epiphyseal plate