_Complications of a breastfed infant of a vegetarian mother_ by sofiaie

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									Growth and Nutrition 3/2/09

Question 4
During a prenatal visit with expectant parents, they report that they are strict vegans. They ask you to
advise them on a healthy diet and any required supplements. The mother plans to breastfeed the newborn
exclusively for the first 6 months.

Of the following, you are MOST likely to tell them that their newborn may require supplemental:
    A. Calcium
    B. Folate
    C. Iron
    D. Vitamin B6
    E. Vitamin B12

A vegan diet, by definition, excludes all foods derived from animal products. A lacto-ovo-vegetarian diet
may include milk and eggs. Although a vegan diet may be healthy, there is a risk for vitamin B12
deficiency because vitamin B12 is only found in foods of animal origin. Breastfeeding vegan mothers may
produce milk that is deficient in this vitamin and require supplementation that generally is achieved by
continuing the consumption of prenatal vitamins containing vitamin B12.

During pregnancy, vitamin B12 is concentrated in the fetus and stored in the liver. Infants born to vitamin
B12-replete mothers have stores of vitamin B12 that are adequate to sustain them for the first several
months postpartum. Vitamin B12 deficiency rarely occurs before 4 months of age. Infants of vitamin B12-
deficient breastfeeding mothers, or infants receiving low amounts of animal-source foods, may be
vulnerable to vitamin B12 deficiency.

The recommended supplementation for breastfed vegan infants to prevent vitamin B12 deficiency is 0.4
mcg/day during the first 6 postnatal months and 0.5 mcg/day from 7 months to 1 year of age. Vegan
infants who are not breastfed should receive iron-fortified soy infant formula until 1 year of age to avoid
deficiencies in iron. Vegan infants require no other mineral or vitamin supplementation.

Vegan diets in older children and adolescents may be low in calcium (similar to the typical American
"teenage diet" that contains less than the recommended intake of dairy products), and the zinc
consumption may be relatively low due to the absence of phytate, which renders zinc more bioavailable.
Children who follow vegan diets may have relatively diminished overall energy intake because such diets
commonly are low in fat and high in fiber.

Review of nutrient intake and energy intake in conjunction with growth curves of children eating vegan
diets in both the United States and the United Kingdom demonstrate no significant health issues. Height
and weight measured in vegan populations may be slightly lower than average but not in the range of
failure to thrive or short stature. Adolescents eating vegan diets are more likely than adolescents eating a
typical American diet to meet nutritional goals, including recommended intake of fruits and vegetables.
Vegan adolescents are less likely to be obese because they consume fewer foods high in fat. However,
they remain at risk for vitamin B12 deficiency and should consume at least a daily multivitamin. They are
less likely to have anemia but just as likely to have low calcium intake as their non-vegan peers.

Folate and vitamin B6 are not likely to be deficient in persons who consume vegan diets because those
nutrients are found in many legumes, fruits, and vegetables that are the mainstays of the diet

Growth and Nutrition 3/2/09

Topic Area: Clinical features of vitamin deficiencies
A 16-year-old boy in your practice has cystic fibrosis. As a complication of his illness, he has developed
cirrhosis and cholestasis. He now complains of shaky hands. Neurologic examination demonstrates
hyporeflexia and tremor with hands outstretched.

Of the following, the patient's symptoms are MOST consistent with deficiency of:
    A. Vitamin A
    B. Vitamin B1 (thiamine)
    C. Vitamin C
    D. Vitamin D
    E. Vitamin E

Because the young man described in the vignette has chronic cholestasis, he is at risk for developing
deficiency of any of the fat-soluble vitamins, including vitamins A, D, E, and K. His neurologic
symptoms of tremor and hyporeflexia most strongly suggest vitamin E deficiency.

Vitamin E (tocopherol) is an important factor in stabilizing the lipid membrane of the red blood cell and
the lipids in the myelin sheath of neurons. Therefore, the most common presenting features of
hypovitaminosis E are hemolysis (primarily reported in preterm infants) and peripheral neuropathy
(identified in infants and children who have chronic cholestasis, pancreatic insufficiency, or

Supplementation of formulas and parenteral nutrition with vitamin E has reduced substantially the
incidence of hemolysis in the vitamin E-deficient preterm infant. However, patients who have cystic
fibrosis or cholestatic liver disease require both monitoring of vitamin E concentrations and
supplementation with vitamin E. Because vitamin E is a fat-soluble vitamin, those who have cholestasis
may have difficulty absorbing alpha-tocopherol, the form of vitamin E available in most dietary
supplements. For this reason, d-alpha-tocopheryl polyethylene glycol 1,000 succinate, a water-soluble
form of vitamin E, should be given to patients who have significant cholestatic liver disease. The
recommended dose for a patient who has cholestatic liver disease is 15 to 25 IU/kg per day.

Deficiency of vitamin A, B1, C, or D would not be expected to cause such a clinical presentation. Vitamin
A deficiency causes impaired vision ("night blindness") and corneal ulcers; vitamin B1 deficiency can
cause myopathy and heart failure ("beriberi"); vitamin C deficiency causes irritability, bone lesions, and
bruising (scurvy); and vitamin D deficiency causes osteopenia or rickets.

Growth and Nutrition 3/2/09

Question 3
You are evaluating an 8-week-old infant whose birth weight was 1,000 g and who was delivered at 30
weeks' gestation. He experienced early respiratory distress and sepsis, but now these problems have
resolved, and he recently progressed from parenteral nutrition to full enteral feedings.

Of the following, the feeding that will provide the BEST mineral content to ensure healthy bone
development for this infant is:

    A.   Cow milk-based infant formula
    B.   Human milk (unsupplemented)
    C.   Premature formula
    D.   Protein hydrolysate formula
    E.   Soy protein-based formula

Very low-birthweight (VLBW) preterm infants, such as the baby described in the vignette, are at risk for
delayed bone mineralization due to constraints in delivering optimal nutrition to them while in the
neonatal intensive care unit. A key component to bone health, mineralization, and overall nutritional well-
being is the balance of calcium (Ca++) and phosphorous (P). Optimal (Ca++) and (P) delivery that matches
in utero accretion cannot be attained with total parenteral nutrition (TPN). Only after attaining full enteral
nutrition goals can the desired delivery of (Ca++) and (P) be provided and the infant's bone mineralization
approach that of a healthy term infant.

Inadequate (P) delivery in the VLBW preterm infant results in demineralization of bone and metabolic
bone disease (osteopenia, neonatal rickets). Such disease typically presents after 4 weeks of TPN and
often is accompanied by normal serum (P) and (Ca++) concentrations and elevated alkaline phosphatase
activity. Excessive (P) delivery is uncommon in preterm infants, but may result in hypocalcemia, tetany,
and seizure activity. Inadequate nutritional (Ca++) delivery also can result in bone resorption as the body
attempts to maintain normal serum (Ca++) concentrations.

The optimal source of nutrition for the infant in the vignette should provide sufficient energy substrate
(carbohydrate and lipid) and protein to facilitate growth and development as well as the necessary
minerals and vitamins to help make up for delayed bone mineralization. Term infant cow milk-based
formula lacks sufficient calories, protein, (Ca++), (P), and other trace minerals and vitamins, as does
unsupplemented human milk. Term formulas and human milk require supplementation with a fortifier to
meet these goals.

Formulas designed specifically for preterm infants contain higher caloric density; more readily absorbed
lipids; greater protein content; and enriched (Ca++), (P), and other minerals and vitamins. They provide
the best mineral content to ensure healthy bone development in VLBW preterm infants and generally do
so by the time the infant attains a postconceptive age of 44 weeks. Protein hydrolysate formulas and soy
protein-based formulas deliver suboptimal energy, protein, minerals, and vitamins to VLBW preterm
infants and should be used only for a specific indication for a limited period of time.

Growth and Nutrition 3/2/09

Topic Area: Differential features of human and cow milk formulas
A 3-month-old infant who has a history of renal dysplasia associated with obstructive uropathy has
marked polyuria. He is breastfeeding and receiving supplemental cow’s milk-based formula. In an effort
to reduce the high urine output, you consider reducing the renal solute load by changing feedings from the
milk-based formula currently being used.

Of the following, the MOST appropriate change is to:
    A. A hydrolyzed formula containing medium-chain triglycerides
    B. A more concentrated (24-kcal) milk-based formula
    C. Human milk exclusively
    D. Soy milk-based formula
    E. Whole cow milk

The infant described in the vignette has polyuria caused by a urinary concentrating defect. The
concentrating defect is the result of tubular damage due to the obstructive uropathy. The inability to
concentrate the urine causes the kidneys to create an "excessive" volume of urine to excrete the solute
load presented to them.

One strategy to reduce polyuria is to reduce the solute burden placed on the kidneys. Potential renal solute
load is affected by intake of protein, sodium, potassium, chloride, and phosphorus. The protein and
phosphorus content are the most important variables when comparing infant feeding regimens.

Human milk possesses a lower potential renal solute load than cow milk or cow milk-based formulas.
Accordingly, the most appropriate change in feeding for the infant in the vignette is to recommend that
the mother stop cow milk formula supplementation and exclusively breastfeed. If human milk is not
available, a "low-solute" cow milk-based formula can be used. A low calcium-phosphorus formula has
the next lowest potential renal solute load compared with human milk. Regular cow milk, soy milk-based
formula, hydrolyzed formula with medium-chain triglycerides, and 24-kcal milk-based formula all have
greater renal solute loads than human milk.

Growth and Nutrition 3/2/09

Topic Area: Features of vitamin toxicities
Jason was always the class weakling. He was picked on from early childhood because he was small. He
is currently preoccupied with a desire to ―bulk up‖. Jason is 16 years old and a high school senior.
Jason recently joined a weight club because his buddies encouraged him to use weights. His friends also
suggested that he go on a program of increasing his vitamin/mineral and protein intake. He presents at
your office complaining of headache, nausea, and weakness.

Of the following, the patient's symptoms are MOST consistent with:
    A. Fat soluble vitamin toxicity
    B. Water soluble vitamin toxicity
    C. Iron Deficiency Anemia
    D. Calcium Deficiency
    E. Both A and B

Vitamin toxicity is a condition in which a person develops symptoms as side effects from taking massive
doses of vitamins. Vitamin toxicity, which is also called hypervitaminosis, is becoming more common
because of the popularity of vitamin supplements. Many people treat themselves for minor illnesses (or
try to improve their general health or appearance) with large doses of vitamins. The Recommended Daily
Allowance (RDA) is set at a point where almost all individuals (based on age, gender, and lifestage) have
their metabolic needs met and no toxic effects are found. The Daily Recommended Intakes (DRIs) are
actually a set of four reference values: Estimated Average Requirements (EAR), Recommended Dietary
Allowances (RDA), Adequate Intakes (AI), and Tolerable Upper Intake Levels, (UL). Micronutrient
intakes at high levels (especially with supplement use) should be considered drugs. FDA continues to
struggle with the concept of regulating rather than recommending limits on their use.

Fat-soluble vitamins include vitamins D, E, A (retinol), and K. Water-soluble vitamins include folate
(folic acid), vitamin B12, biotin, vitamin B6, niacin, thiamin, riboflavin, pantothenic acid, and vitamin C
(ascorbic acid). Taking too much of any vitamin can produce a toxic effect. Vitamin A and vitamin D are
the most likely to produce hypervitaminosis in large doses, while riboflavin, pantothenic acid, biotin, and
vitamin C appear to be the least likely to cause problems.

Example of fat soluble vitamin toxicities
VITAMIN A: The symptoms of vitamin A overdosing include accumulation of water in the brain
(hydrocephalus), vomiting, tiredness, constipation, bone pain, sun sensitivity, and severe headaches. The
skin may acquire a rough and dry appearance, with hair loss and brittle nails. Vitamin A toxicity is a
special issue during pregnancy. Expectant mothers who take 10 mg vitamin A or more on a daily basis
may have an infant with birth defects. These birth defects include abnormalities of the face, nervous
system, heart, and thymus gland.

VITAMIN D: The symptoms of vitamin D toxicity are nausea, vomiting, pain in the joints, and loss of
appetite. The patient may experience constipation alternating with diarrhea, or have tingling sensations in
the mouth. The immediate effect of an overdose of vitamin D is abdominal cramps, nausea and vomiting.
Toxic doses of vitamin D taken over a prolonged period of time result in irreversible deposits of calcium
crystals in the soft tissues of the body that may damage the heart, lungs, and kidneys.

Examples of water-soluble vitamin toxicities
Vitamin B1 (Thiamin) toxicity can cause headache, irritability, insomnia, tachycardia, hypotension and
convulsions. Vitamin B3 (Niacin) can cause flushing, wheezing, stomach pain, nausea, vomiting,
diarrhea, blurry vision, and liver damage. Folate toxicities can mask a B12 deficiency.

Growth and Nutrition 3/2/09

Topic Area: Relationship of phytates to iron absorption
You are seeing a 12-month-old boy for a routine well child care visit. Which of the following scenarios
would suggest that he should have a blood test screen for iron deficiency anemia?
   A. He started whole milk last week
   B. He has been on a low iron cow’s milk based formula since age 7 months
   C. He was born at 37 weeks gestation
   D. He has Sickle Cell Trait
   E. All of the above

Dietary factors known to impair non-heme iron absorption from the gut include all the following except:
    A. Tea
    B. Milk
    C. Bran
    D. Ascorbic acid
    E. Calcium

The following scenario can lead to inadequate iron intake in infants between 6-12 months of age:
   A. Low iron formula
   B. Early introduction (before age 1 yr) of cow’s milk into the diet
   C. Exclusive breastfeeding past 6 months without additional sources of iron- such as
        meat, iron fortified cereal, or iron supplementation.
   D. More than 24 ounces of milk per day
   E. All of the above.

Factors that place infants and toddlers at increased risk for iron deficiency are 1) rapid growth; 2) poor
dietary intake/absorption; and 2) iron storage.

Rapid Growth: There is an increased need for dietary iron during times of rapid growth, including
infancy and early childhood. Healthy infants should double their birth weight by 4 months, triple by a
year, and quadruple by 2 years. Some infants have the need for even faster growth than normal and are
born with low iron stores- including infants that were born preterm, were growth retarded or born to
diabetic mothers. Iron is transferred across the placenta in the last trimester of pregnancy and is
proportional to body weight.

Dietary Intake: Groups that are growing rapidly are often the same groups that have poor dietary intakes
– infants/toddlers and adolescent women. In general, turnover and loss of iron is mostly from the
formation and destruction of RBC. In adult men, 95% of all iron for RBC production is from recycled
iron and 5% is from the diet. In babies only 70% of all iron come from recycled sources and 30% must
come from the diet.

Iron Absorption: Iron intake and absorption are regulated in the GI tract by a number of factors. The
gut absorption of iron increases when body iron stores are low and when red blood cell production is
increased. Absorption decreases when iron stores are high. The amount and kind of iron in the diet also
impacts absorption. The amount of iron absorbed in the gut ranges from <1% to as high as 50%, with
plant based foods and iron fortifiers (non-heme iron) at the lowest end of the range, dairy products in the
middle and meat, poultry and fish (heme iron) and breast milk at the high end. About 50% of iron is
absorbed from breast milk, 10 % from fortified formula, and 4% from cow milk and unfortified formula.
The iron content of human breast milk is similar to cow’s milk, but due to a variety of complementary
components in breastmilk, such as lactoferrin, up to 50% of iron in breast milk is absorbed. Iron
absorption is increased in the presence of enhancer in the diet, such as ascorbic acid. It decreases in the
presence of inhibitors (phytates) in the diet, such as some vegetables, tea, bran and calcium. Calcium is

Growth and Nutrition 3/2/09

now added to many brands of orange juice- so this may not be a good juice to drink at the same time you
are taking iron.

Iron Storage: Men store about 1-1.4 g of iron, women 0.2-0.4 g and children even less. Full-term
healthy babies are born with about 75 mg/kg or iron. This is usually adequate to meet the needs of full-
term infants until 4 to 6 months. Preterm and low birth weight babies have the same ratio of total of total
body iron to weight, but because they start at a lower weight, they have less total iron. They also grow
faster than full term infants to achieve ―catch-up‖ growth. Their iron stores may be used by 2 to 3

Growth and Nutrition 3/2/09

Topic area: Evaluation of pediatric obesity
A healthy 5 ½ year-old boy presents for his annual physical. He weighs 41.5 lbs and measures at 40.5
inches. His mother and father accompany him. They are both clearly obese and the child appears to be
overweight. Explain what you would do during this visit to address his weight status including
assessment and counseling.

Of the following, which anthropometric indices would BEST determine risk of obesity?
    A. Weight-for-age
    B. Height-for-age
    C. Weight-for-height
    D. BMI-for–age
    E. None of the above

Using the growth chart attached, how would you classify his weight status?
   A. Normal
   B. Underweight
   C. At risk for overweight
   D. Overweight
   E. Obese

Step 1: Calculate the child’s BMI using the formula kg/m2 or [(Weight in Pounds) / (Height in inches) x
(Height in inches)] x 703
        Answer: 17.8 kg/ m2

Step 2: Plot the child’s information on a gender-specific BMI-for-age growth chart (see Appendix B
        Answer: Between the 90th and 95th percentile

Step 3: Interpret your findings
     ―underweight‖ BMI-for-age percentile<5th
     ―healthy weight‖: BMI-for-age percentile > 5th and 85th
     “Overweight”: BMI-for-age percentile > 85th and 95th
     ―Obese‖: BMI-for-age percentile>95th

Differential Diagnosis
Rarely, the cause of overweight/ obesity among children is of an endocrine or genetic origin. The most
common genetic disorder is Prader-Willi syndrome (due to an alteration of chromosome 15 of paternal
origin). If this is suspected, the methilation test should be ordered to confirm the clinical suspicion.
Endocrine alterations are rare, but do exist. Such conditions include hypothyroidism, hypothalamic-
pituitary diseases, and pseudohypoparathyroidism. Most children with excess body weight do not have
an established diagnosis.

Most Likely Diagnosis:
This child’s BMI-for-age percentile was between the 90th and 95th percentile, making him ―overweight‖.
Careful attention should be paid to his prior growth trajectory to determine if his BMI-for-age percentile
has increased overtime (rapid weight gain). This child should continue to be closely monitored to ensure
that his growth does not accelerate over time. Given that both of his parents are obese, family-based
pediatric obesity prevention strategies should be employed.

Growth and Nutrition 3/2/09

What counseling strategies would BEST address his weight status?
  A. Encourage parents to model healthy eating behaviors
  B. Encourage a low-carbohydrate diet
  C. Discuss the possibility of future bariatric surgery
  D. Encourage his parents to remove the TV from the child’s bedroom and model healthy physical
       activity patterns.
  E. Answers A and D

Counseling: The number one predictor of a child’s weight status is the weight status of the parent.
Because of this, a family-centered behavior change approach may be most effective. Encouraging
families to make small changes such as these may have an impact on the health of the child and the
overall health of the family. Additionally, if the resources are available, it would be helpful to
recommend that the family meet with a dietician for assistance with family menu planning.

Establish healthy family meal/snack-time routines:

       Parents should model healthy eating behaviors
       Provide the child with healthy snacks that are readily available (ex: fresh fruit, cheese and
        crackers, carrot or celery sticks, graham crackers, etc.)—prepare these ahead of time to prevent
        reliance on convenient, high calorie snacks
       Meals should include a protein and at least 2 fruits and/or vegetable
       Exclude high-sugar drinks (i.e. soft drinks, sports drinks, (Gatorade, PowerAde), juice drinks
        (like kool-aid, sunny delight, high C, etc.)
       Limit fast foods
       Keep only healthy foods in the house
       No TV while eating

Encourage healthy physical activity patterns/ discourage sedentary behaviors:
    Parents should model healthy physical activity patterns
    Remove TVs from bedrooms
    Limit screen time to less than 2 hours per day (TV, video games, computer use)
    Find an activity the family enjoys doing together (i.e.: walks, outdoor games, swimming, etc.)
    Play active/ interactive games with your child
    Adults should engage in 30 minutes of moderate-vigorous activities each day/ Children and
       adolescents should engage in 1 hour of moderate-vigorous activities each day

Growth and Nutrition 3/2/09

Topic Area: Recognition and Prognosis of Kwashiorkor and Marasmus in infants/toddlers
A 16-month old girl whose family has recently emigrated from Uganda is referred to you by the WIC
program (at the time of WIC enrollment) for evaluation of failure to thrive. The girl has a twin bother.
At 12 months of age the infant was weaned to primarily carbohydrates and tea. Starting at about 14
months of age the mother reported that the young girl experienced multiple infections (indicative of
respiratory infections and diarrhea). It was noted that the toddler currently had significant edema and that
the child had little appetite, appeared apathetic, and had dry brittle hair and a lesion on her skin.

Of the following, the patient’s symptoms are MOST consistent with:
    A. Vitamin A Deficiency
    B. Marasmas
    C. Kwashiorkor
    D. Folate Deficiency

Protein Energy Malnutrition (PEM) refers to malnutrition states other than those caused primarily by
specific nutrients. However, it invariably reflects combined deficiencies in:
     Protein (amino acids needed for cell structure)
     Energy (protein, fat, and carbohydrates)
     Micronutrients (Vitamin A, iron, zinc, iodine, etc.)

Severe forms of PEM include (see Appendix A for list of major characteristics) :
    Marasmus
           o Lack of protein and calories
           o Extreme growth failure
           o Wasting of muscle and subcutaneous fat (old man’s face)

       Kwashiorkor
          o Lack of protein and some calories
          o Growth failure
          o Psychological changes (irritable, lethargic, poor appetite)
          o Edema
          o Dermatosis
          o Hair changes

Growth and Nutrition 3/2/09

Appendix A:

 Appendix B:
Growth and Nutrition 3/2/09


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