Malnutrition in a child (obesity, rickets) Flashcards
Define rickets.
Rickets refers to changes caused by deficient mineralisation at the growth plate of long bones, commonly due to nutritional deficiency of vitamin D.
What is the difference between osteomalacia and rickets? (When does each occur? Who is affected?)
Rickets and osteomalacia usually occur together while the growth plates are open in children but rickets only occurs in growing children before fusion of the epiphyses
Osteomalacia can occur after the growth plates have fused.
Other than nutritional vitamin D deficiency, what are the causes of rickets?
1. Calcium-deficient rickets with secondarily elevated PTH:
Lack of vitamin D due to:
- Decreased sun exposure
- Dietary lack
- Malabsorption
- Liver disease
- Anticonvulsant drugs
- Renal osteodystrophy
- defect in 1-alpha-hydroxylase –> no conversion of 25-hydroxyvitamin D into the active form (type I or pseudovitamin D-deficient rickets)
End-organ resistance
- Rare autosomal recessive disorder can cause mutations in the vitamin D receptor –> end-organ resistance to calcitriol (type II vitamin D-dependent rickets).
Dietary calcium deficiency.
2. Phosphate-deficient rickets (PTH not elevated) may be caused by:
- Renal phosphate wasting
- Phosphate deficiency from poor intake or malabsorption.
How do anticonvulsant drugs cause rickets?
Phenytoin may cause target organ resistance to calcitriol
How can liver disease cause rickets?
Affects conversion of colecalciferol to calcidiol
What are the causes of renal phosphate wasting?
Causes can be genetic or oncogenic.
- Genetic hypophosphataemic rickets e.g. X-linked/autosomal dominant or recessive/hereditary hypophosphataemic rickets, McCune-Albright syndrome, Fanconi syndrome, renal tubular acidosis (type 2/proximal)
- Oncogenic hypophosphataemia
What are the mechanims of vitamin D formation in the body?
Dependant on sunlight and enzymatic conversion in the liver and kidneys:
- 7-dehydrocholesterol –(UV)–> colecalciferol (vitD3)
OR
- dietary colecalciferol(D3)/ergocalciferol (D2) –(vitD 25-hydroxylase)–> calcidiol (25-hydroxyvitamin D)
- clacidiol –(1-alpha-hydroxylase)–> calcitriol (1,25-dihydroxyvitamin D)
Where is Vit D 25-hydroxylase found? Where is 1-alpha-hydroxylase found?
- vitamin D 25 hydroxylase - liver
- 1-alpha-hydroxylase - kidneys
What is the epidemiology of rickets?
Peak incidence at 6-23 months and 12-15 years
US incidence in those <3 years was 24 per 100,000 in 2000s
Genetic causes are very rare (<1 in 20,000 affected)
Why is increased skin pigmentation associated with rickets?
Increased skin pigmentation leads to reduced capacity to synthesise colecalciferol
What are the risk factors for rickets?
- Inadequate exposure to sunlight
- Age 6-23 months
- Breastfeeding
- Inadequate calcium and phosphate intake
- Family history
- Darker skin complexionn- requires increased sunlight exposure
What are the symptoms of rickets?
Bone pain
Muscle weakness
Paraesthesias /tetany /numbness /seizures (hypocalcaemia)
What are the signs of rickets on examination?
- Growth retardation
- Delayed achievement of motor milestones
- Bony deformities e.g. bowlegs, rachitic rosary of the chest
- Fractures
- Hypocalcaemia - Chvostek’s, Trousseau’s, carpopedal spasm
What investigations would you do for rickets?
Bloods and urine:
- Calcidiol levels (N:>25nm/L)
- Calcium (N:2.3-2.7mmol/L)
- Serum PTH (N:1-6picomoles/L; elevated)
- ALP(high = high bone turnover) and LFTs
- Creatinine and urea (for kidney disease)
- Urinary calcium and phopshate (low and high)
Imaging: X ray of long bones
What would an X ray of long bones show in rickets?
- Widening of the epiphyseal plate e.g. at wrist
- Loss of definition of zone of provisional calcification at epiphyseal/metaphyseal interface
- Cupping /splaying/fraying of metaphysis
- Looser’s zone (pseudofractures)
What is shown?
rosary beading of the chest in rickets
What is shown?
- Widening of the epiphyseal plate
- Loss of definition of zone of provisional calcification at epiphyseal/metaphyseal interface
- Cupping /splaying/fraying of metaphysis
How many units of vitamin D are in 5 micrograms or colecalciferol/ergocalciferol?
200 units
What is the management of rickets in children?
Loading dose regimens used for 8-12 weeks
What is the loading dose regimen for infants 1-5 months old?
3000 IU daily for 8-12 weeks
What is the loading dose regimen for children 8 years old?
6 months to 11 years: 6000 IU daily for 8-12 weeks
What is the loading dose regimen for teenagers?
12-18 year olds: 10,000 IU daily for 8-12 weeks (a single or divided dose orally of 300,000 IU can be considered if there is concern about compliance with treatment)
How do you manage vitamin D deficiency in a patient who is non compliant with daily medication?
Equivalent weekly or fornightly doses can be given instead and are as effective.
What is the vitamin D preparation of choice for rickets?
Colecalciferol (vitamin D3)
What if someone cannot take vitamin D3 for religious, cultural or dieary reasons?
Vitamin D2 can be given instead (ergocalciferol)
*NB: VitD3 is an animal source, or gelatine may be used in some preparations
What is Stoss therapy?
A high dose of oral vitamin D2 given as a single dose
Is wrist enlargement reversible?
May be reversible with calcium supplementation within 6 months but knee deformity may not resolve spontaneously
What is hungry bone syndrome?
Whereby vitamin D therapy in hypocalcaemic rickets leads to worsening hypocalcaemia. Consider supprementing breastfed infants with calcium during first few days of therapy to prevent seizures.
How is obesity defined in children?
In children, BMI (weight in kg/height in m2) is expressed as BMI centile in relation to age and sex matched population
What is the definition of overweight and obesity in children?
Overweight = BMI over 91st centile
Obese = BMI over 98th centile
What are the complications of obesity?
- Orthopaedic – slipped upper femoral epiphysis, tibia vara (bow legs), abnormal foot structure and function
- Idiopathic intracranial hypertension (headaches, blurred optic disc margins)
- Hypoventilation syndrome (daytime somnolence, sleep apnoea, snoring, hypercapnia, heart failure)
- Non-alcoholic fatty liver disease
- Gall bladder disease/gallstones
- Polycystic ovarian syndrome
- Type 2 diabetes mellitus
- Hypertension
- Abnormal blood lipids
- Other medical sequelae, e.g. asthma, changes in left ventricular mass, increased risk of certain malignancies (endometrial, breast, and colon cancer)
- Psychological sequelae – low self-esteem, teasing, depression
What screening programme is available for obesity?
In the UK, the National Child Measurement Programme measures height and weight to assess overweight and obesity in children in:
- reception class at school (aged 4–5 years)
- in year 6 (aged 10–11 years)
What is the aetiology of obesity?
- No conclusive evidence that obese children eat more
- But children’s energy expenditure has decreased - less walking, more sedentary activities
- Low socioeconomic homes are more likely to be obese
At what age group has obesity most increased between 1994 to 2014?
All age groups but mostly 11-15 year olds
More in boys than girls
In terms of height for age, how do obese children fare?
Should be above the 50th centile for height (tall and obese)
If a child is obese and short, an endogenous cause, i.e. hypothyroidism and Cushing syndrome, should be considered.
What is the management of obesity in childhood?
SUSTAINED lifestyle changes:
- Healthy eating
- Pyshical activity
- Limiting TV and small screen activities
Drug treatment and surgery - only applicable in those aged >12 years with extreme obesity (BMI >40kg/m2) or BMI >35kg/m2 and complucations of obesity.
- Orlistat - lipase inhibitor reducing fat absorption
- Bariatric surgery - not appropriate unless achieved maturity or very severe complications of obesity are found
These should be used in conjunction with diet and exercise behavioural weight management programmes and be restricted to specialist centres with multidisciplinary expertise in managing severe obesity
More integration of services for obesity is needed overall.
What is the prognosis with obesity managements?
Lifestyle changes are difficult to achieve and even harder to maintain.
A cultural change from an obesogenic environment is needed, e.g. reduction or removal of unhealthy food and drinks and a more integrated approach involving health, local government and other key partners.
