case presentation

Micronutrient Deficiencies in Children Younger Than 5 Years

Lillian Nalwoga, MD

Pediatric attending, Children’s Hospital of The King’s Daughters, Norfolk, VA  

John W. Harrington, MD
Director, Division of General Academic Pediatrics, Children’s Hospital of The King’s Daughters, Norfolk, VA

Nalwoga L, Harrington JW. Micronutrient deficiencies in children younger than 5 years. Consultant360. Published online March 23, 2022.


Case Presentation: Chronic Arthralgia and Ecchymoses in a 5-Year-Old Boy
A 5-year-old boy presented to your pediatrician office with painful joints and difficulty walking for the past 2 to 4 days. The patient reported tiredness and joint pains for approximately 1 to 2 months, which progressively worsened to the point where he had difficulty walking and sometimes refused to walk. His mother reported that he bruised and bled more easily than normal and that he sometimes experienced gum bleeding when brushing his teeth.

The patient had a prior diagnosis of autism. Your patient’s mother said your patient was a picky eater, and he only ate pasta, rice, and Cheetos. Physical examination findings included bilateral lower extremity ecchymoses and petechiae and tender joints without obvious swelling and gingivitis.

The differential diagnosis of a child presenting with arthralgia, ecchymosis, petechiae, and gum bleeding is broad and includes leukemia, vasculitis (Henoch-Schonlein Purpura), infection, reactive arthritis, immune thrombocytopenia, child abuse, bleeding disorders, such as hemophilia, and platelet disorders, among other causes. Scurvy is a rare but possible cause in this case.

Actual Diagnosis:
Your patient’s work-up included complete blood count and inflammatory markers, which were normal, except for slightly low hemoglobin of 10 mg/dL. Ascorbic serum level was very low at less than 0.1 mg/dL. The diagnosis of scurvy was made based on the history of restrictive diet and the serum low ascorbic acid level. Your patient was started on daily ascorbic acid (vitamin C) supplementation with rapid improvement and resolution of all symptoms. He received 300 mg/day divided into 3 doses for 1 week followed by 100 mg/day for a duration of 3 months to ensure replenishment and normalization of tissue saturation.  

Scurvy is a rare condition that is caused by a dietary deficiency of vitamin C. Affected children usually have a restricted diet because of an underlying condition, such as anorexia, oral aversion, or neurodevelopmental disorders, such as autism spectrum disorder (ASD).1 Vitamin C deficiency can cause impaired collagen synthesis in the skin, cartilage, and blood vessels. Patients with scurvy often present with gum bleeding, petechiae/ecchymosis, arthralgia, poor wound healing, anemia, prominent hair follicles, perifollicular petechiae, and corkscrew hairs.

Treatment for scurvy is vitamin C supplementation with 100 to 300 mg/day in divided doses for 1 week followed by 100 mg/day for approximately 1 to 3 months, which results in rapid resolution of the symptoms and replenishment.2 To prevent a recurrence, the patient’s diet must contain vitamin C-rich foods, such as a variety of fruits and green leafy vegetables.

Patients with ASD or other neurodevelopmental disorders may have repetitive and restrictive behavior patterns resulting in selective and restrictive eating. The prevalence of selective eating among children with neurodevelopmental disorders ranges from 10% to 35%, while among children with ASD, prevalence estimates range from 46% to 89%.3 Selective eating makes expanding diet variety and the introduction of new foods very difficult for many parents/guardians and pediatricians. Without appropriate interventions, selective eating can result in macronutrient and/or micronutrient deficiency, like the case previously presented.

Pediatricians recommend that parents/guardians should try the following measures to improve diet variety:

  • Repeat presentation of new foods in small amounts, with a gradual increase in food portions as the child gets used to eating the new food.
  • Give positive reinforcement for accepted new food in the form of verbal praise and reward with a preferred toy or activity.
  • Schedule regular mealtimes and keep a record of foods eaten.

The most common micronutrient deficiency is iron deficiency (ID), which if left untreated may lead to iron deficiency anemia (IDA). ID occurs in 6.6% to 15.2% of toddlers while IDA occurs in 0.9% to 4.4% of toddlers.4 Ethnic, racial, and socioeconomic status can play a role in the occurrence of both ID and IDA.4 The occurrence of both ID and IDA varies depending on ethnic, racial, and socioeconomic status.4 ID occurs as a result of decreased enteral iron intake, absorption of iron in the gastrointestinal tract (GI), or if there is increased GI iron loss. ID is defined as a state of insufficient iron levels to meet the body’s growth demands with resultant depletion of serum ferritin (the body’s stored form of iron). IDA is defined as a decrease in hemoglobin greater than 2SD below the mean for age and gender or hemoglobin less than 11 mg/dL in children less than 5 years.4,5 ID and IDA may adversely affect the long-term neurodevelopmental and behavioral outcomes of affected children, but causal effect between ID/IDA and poorer neurodevelopmental outcomes has yet to be established.4,5

Practitioners need to understand the importance of routine surveillance for risks of ID and IDA at all well checks and follow the American Academy of Pediatrics guidelines for universal screening by obtaining a hemoglobin level at 12 months of age and whenever there is an assessed risk. Risk factors for ID and IDA in infants and toddlers include:

  • Prematurity: Premature infants are born with lower body iron stores (the deficit in body iron store increases with decreasing gestation age) coupled with increased postnatal iron demands required to meet the rapid catch-up growth. These high demands may not be sufficiently met by the iron provided through breast milk or formula.
  • Exclusive breastfeeding (after 6 months of age): Breast milk is the best form of feeding for all infants, but it contains a low amount of iron with high bioavailability. Breast milk iron is sufficient to support growth needs for term infants from birth to age 4 to 6 months, after which supplementation with foods rich in iron (meats, iron-fortified cereal, and green, leafy vegetables) must be initiated.
  • Conditions that decrease gastrointestinal iron absorption, while increasing iron loss through bleeding: These include milk-protein allergies and proctocolitis, celiac disease, and inflammatory bowel disease. These require prompt identification and appropriate treatment.
  • The use of non-iron-fortified formula or cow’s milk (before 12 months of age) ID is also common in patients who consume more than 24 oz/day of cow’s milk after the age of 12 months.

Assessment for risks and prevention of ID and IDA are an integral part of well-child checks that all practitioners must implement. Prevention of ID and IDA and the associated poor neurodevelopmental outcomes can be achieved by:

  • Initiating iron supplementation for all premature infants starting at age 1 month through 12 months or until catch-up growth is completed
  • Introduction of iron-rich foods like red meat, iron-fortified cereal, and green, leafy vegetables for all infants aged 4 to 6 months
  • Provision of vitamin C-rich foods like fruits, which improve enteral absorption of iron
  • Avoidance of non-iron-fortified formula and cow’s milk before age 12 months
  • Limiting cow’s milk intake to less than 24 oz/day after age 12 months
  • Universal screening for IDA at age 12 months by obtaining a hemoglobin level and targeted screening for high-risk children
  • Further investigation for those with low hemoglobin (less than 11 mg/dL) by looking for indicators for ID/IDA like low hemoglobin mean corpuscular volume (MCV), low ferritin level, low reticulocyte count, and a high total iron-binding capacity (TIBC)
  • Patients with ID/IDA should receive 3 mg/kg/day of elemental iron until normal hemoglobin is achieved and continue the treatment for 1 to 2 months thereafter.

Interaction of IDA and Lead Poisoning
Practitioners must be reminded that IDA is associated with serum increased lead concentration in patients with lead poisoning. Pre-existing IDA decreases the efficiency of lead-chelation therapy, which can be corrected by iron supplementation.2 In contrast, iron supplementation in a child with IDA who also has lead poisoning without chelation therapy seems to increase blood lead levels and decreases basal lead excretion.4 Primary prevention of ID and IDA greatly contributes toward the prevention of lead poisoning, which in turn, prevents the associated poor neurodevelopmental outcomes.


  1. Harrington JW, Allen K. The clinician’s guide to autism. Pediatr Rev. 2014;35(2):62-78. doi:10.1542/pir.35-2-62
  2. Alqanatish JT, Alqahtani F, Alsewairi WM, Al-kenaizan S. Childhood scurvy: an unusual cause of refusal to walk in a child. Pediatr Rheumatol Online J. 2015;13:23. doi:10.1186/s12969-015-0020-1
  3. Improving food selectivity of children with autism. Association for Science in Autism Treatment. Accessed March 22, 2022.
  4. Baker Rd, Greer Fr; Committee on Nutritional American Academy of Pediatrics. Diagnosis and prevention of iron deficiency and iron deficiency amenia in infants and young children (0-3 years of age). Pediatrics. Nov;126(5):1040-50. doi:10.1542/peds.2010-2576
  5. Powers JM, Motil KJ, Drutz JE, Abrams SA, O’Brien S, Hoppin AG. Iron deficiency in infants and children <12 years: screening, prevention, clinical manifestations, and diagnosis. UpToDate. Accessed on March 22, 2022. Updated October 20, 2021.