This expert opinion provides detailed guidance on assessing obesity in secondary paediatric practice. This guidance builds on existing recommendations from National Institute of Health and Clinical Excellence in the UK, and is evidence based where possible. Guidance is provided on which obese children and young people are appropriate to be seen in secondary care and relevant history and investigations, and guidance on when further investigation of causes and obesity-related comorbidity is appropriate.
Statistics from Altmetric.com
Obese children and adolescents now form an increasing burden on children's health services internationally. Paediatricians are increasingly called upon to assess and manage obesity in children and adolescents. Yet there is little authoritative guidance to help with this task.
The American Academy of Paediatrics (AAP) updated their expert guidance on the assessment and management of childhood obesity in 2007.1 However, these recommendations are appropriate for USA and cannot be generalised to other medical systems. In the UK, the National Institute of Health and Clinical Excellence (NICE) systematically reviewed the literature and published guidance on the management of obesity in children and young people in 2006.2 However, this was a necessarily high-level review and provided little guidance on practical issues of detail for secondary care. Expert opinion has a place where quality evidence is lacking. This current document builds on the AAP and NICE recommendations to provide detailed guidance on assessing obesity in secondary paediatric practice. Our aim is to provide paediatricians with an evidence-based algorithm to undertake the following tasks:
(A) identify which of the many overweight children referred require assessment;
(B) identify secondary or genetic causes of obesity where they are known;
(C) recognise significant comorbidities;
(D) establish which treatments are appropriate for each obese child or adolescent.
Note that the authors did not aim to address primary care assessment and management of childhood obesity, which in the UK should be informed by NICE guidance and the joint Royal College of Paediatrics and Child Health (RCPCH) and National Obesity Forum guidance for the management of obesity in primary care.3
This guidance was authored by the Obesity Services for Children and Adolescents (OSCA) network, a network of paediatricians in the UK and Ireland with special interest in the management of childhood obesity. OSCA was formed in 2005, consists of general and community paediatricians, paediatric endocrinologists and gastroenterologists, and is linked to the UK RCPCH and to the Association for the Study of Obesity. The methods used to generate the guidance were those of expert review. The authors first discuss which children are appropriate for referral from primary to secondary care, then provide a schema for examination and investigation in secondary care, and then discuss issues of diagnosis.
Definition of obesity
Despite limitations, body mass index (BMI) definitions of obesity remain the only practical ones for clinical care. In the UK, NICE2 recommended that the most appropriate measure on which to define obesity is BMI≥98th BMI centile (2 SDs above the mean) on the UK 1990 growth reference.4 Use of the 95th BMI centile, such as in the US AAP guidelines,1 may result in excessive numbers being referred to secondary care. Use of other definitions, such as the International Obesity Taskforce thresholds,5 may be too conservative. We concur with NICE that the 98th centile is an appropriate definition on which to base management strategies.
There are no currently agreed definitions for extreme obesity in childhood. The authors suggest that any child with BMI >3.5 SD above mean (please refer flowchart for thresholds at different ages) should be regarded as having extreme obesity, as this is equivalent at age 18 years to the adult definition of class III (previously known as morbid) obesity (BMI ≥40 kg/m2).
Which obese children require referral to secondary care?
Given the high prevalence of obesity, the majority of obese children must be managed in primary care, whether by generalists (as in the UK) or by primary care paediatricians. Clear guidelines are needed to prevent unnecessary referrals to secondary care. Referral should be guided first by the degree of obesity and second by presence of comorbidities, likelihood of comorbidities (eg, family history) or where secondary obesity is suspected. Figure 1 outlines which children require assessment in secondary care.
(A) Extreme obesity (BMI greater than 3.5 SDs above mean). Those extremely obese should be referred regardless of additional risk factors.
(B) Obesity ≥98th centile.
Not all children with BMI centile >98th centile need referral to specialty services. The authors recommend that secondary care referral is appropriate for the following:
Secondary or genetic causes of obesity.
Short stature for parental growth potential is an important marker of a potential endocrine or genetic syndrome, as obese children are almost always tall for age. The presence of any significant dysmorphisms or associated learning difficulties should precipitate a referral to secondary care (refer table 1).
Obesity with significant comorbidities or high-risk of comorbidities.
NICE guidance recommends that professionals ‘consider referral to a specialist if the child has significant comorbidity or complex needs …’ The authors recommend that children with BMI ≥ 98th centile are assessed in secondary care if the child or family are seeking help and the child has one or more risk factors for either possible underlying pathology or future morbidity as listed in figure 1. Note that there should be a higher index of suspicion to investigate and refer children and young people from black or South Asian ethnicities, because of increased metabolic risk.
Children and adolescents with significant psychological comorbidities related to obesity may need to be managed in secondary care jointly between paediatrics and child mental health services. These include young people where there is significant family/individual distress related to obesity, for example, depression, self-harm and suicidal ideation, where there are concerns regarding an eating disorder, and where there are any child safeguarding concerns.
Medical history and examination in secondary care
An appropriate medical history and examination should be undertaken, with special reference to the following issues.
Accurate height and weight and calculation of BMI.
Plot BMI on UK 1990 BMI growth chart or calculate z-score (number of SDs above mean BMI for age and sex).
Pattern of obesity.
Note whether there is generalised obesity, or whether adiposity is primarily central or upper body. Those with marked central adiposity may be at particular risk of adverse cardiovascular outcomes. Upper body fat, for example, buffalo hump and neck, may be suggestive of Cushing syndrome.
Hypertension is defined as ≥95th centile on recent UK reference data.6 Blood pressure must be measured using an appropriate sized cuff. In general, an appropriate cuff size is a cuff with an inflatable bladder width that is at least 40% of the arm circumference at a point midway between the olecranon and the acromion. For such a cuff to be optimal for an arm, the cuff bladder length should cover 80–100% of the circumference of the arm.7 For obese patients, this can be difficult to assess. A more accurate method is to measure the subject's mid-arm circumference, and use this to determine the appropriate cuff size, using appropriate published data.7
Pubertal assessment and menstrual history.
The thickened velvety darkened skin of acanthosis nigricans (figure 2) is indicative of insulin resistance, but many with significant insulin resistance do not have it.8 It is usually seen first around the neck and in the axillae, but in severe cases may occur in all flexures.
Signs of endocrinopathy.
Endocrine causes of obesity are extremely unlikely in children and adolescents with long-term obesity and normal stature. Hypothyroidism as a primary cause of obesity is rare, especially when stature is normal. Signs include the following:
■ Short stature or reduced growth velocity.
■ Thickened yellow skin, dry coarse hair and brittle nails.
■ Psychomotor slowing, hung-up ankle jerks.
Steroid excess (eg, Cushing syndrome) is an extremely rare cause of obesity. Signs include striae, hypertension, short stature, hirsutism and telangiectasia. Note that striae are almost universal in obesity and by themselves are not a sign of Cushing (and Cushing is highly unlikely to present with striae as the only physical sign); striae caused by Cushing are more likely to be violacious/purple in colour, reflecting very rapid growth and thinning of the skin.
Signs of genetic obesity syndromes.
Dysmorphisms suggestive of genetic obesity syndromes are outlined in table 1. Particularly note early onset obesity, learning difficulties, deafness, epilepsy, retinitis, dysmorphic features, neuroendocrine abnormalities including hypogonadism and red hair outside the context of family history.
Concomitant drug use.
Drugs such as glucocorticoids (oral or moderate-high dose inhaled) and atypical antipsychotic medications are strongly associated with obesity and insulin resistance.
Obstructive sleep apnoea.
Typical symptoms of obstructive sleep apnoea (OSA) include snoring, morning headaches and fatigue. Three useful screening questions include the presence of the following:
Difficulty in breathing during sleep.
Morning headaches or fatigue.
If none of these are present, OSA is very unlikely. If one or more is present, formal sleep studies may be useful. For a more detailed assessment of sleep abnormalities, screening tools such as the Chervin Pediatric Sleep Questionnaire can be useful.9
It is unclear whether waist circumference is helpful in the clinical situation. A waist circumference at assessment may be useful for assessing risk of comorbidity associated with central adiposity by comparison with published UK centiles.10 However, the clinical utility of change in waist over time is unclear due to very poor reproducibility in clinical settings.8 At the current time, the authors do not recommend waist circumference be used as a clinical marker of adiposity change in obese children.
Investigations in secondary care
The investigation of obese children is a controversial area with little data available to guide practice. Investigations should not be regarded as routine, but are likely to be appropriate for assessment of either cause or consequences of obesity.
If blood is being taken, the authors recommend consideration of the following investigations:
A. For aetiology/secondary obesity.
If there are no abnormalities on examination or history suggestive of secondary obesity, these should be limited to thyroid function (thyroid stimulating hormone (TSH), free T4). Note that many obese children have a TSH at the top of or just above the upper limit of the normal range.
B. For comorbidities.
Figure 1 shows the key investigations required. Note that fasting venepuncture should be undertaken after an 8-h fast. Interpretation of findings is discussed below.
Glucose and insulin homeostasis
The American Diabetes Association definitions of impaired fasting glucose (6.1–6.9 mmol/l) and diabetes (≥7 mmol/l) should be used.
This should be measured to assess insulin resistance, either as a direct measure of insulin resistance or by calculating the Homeostatic model assessment (HOMA)-IR index. Temporary insulin insensitivity is a normal feature of puberty with peak insulin resistance at Tanner stages 3 and 4.11 Normative values from large samples are only available from the USA: in 1802, non-diabetic adolescents across the range of BMI, mean insulin was 12 mU/l at age 12 years, 13 at 13 years, 15 at 14 years, falling back to 12–13 mU/l by 16–19 years.12 See table 3 for recommended thresholds for hyperinsulinaemia in obesity by pubertal stage. Note that these are conservative by comparison to the US reference data above. Note that insulin may be expressed as mU/l or as picomoles. For conversion, 1 mU/l=6.95 pmol/l.
HOMA is a calculated estimate of insulin resistance where the gold standard (hyperinsulinaemic euglycaemic clamp)13 is not practical for use. There are some data to support the use of the HOMA estimate of insulin resistance (HOMA-IR) in children and adolescents, although not to support the β-cell function estimates. There is little evidence that HOMA-IR is more useful than simple fasting insulin levels as a measure of insulin resistance.11
Population reference data have been published for adolescents in the US: the 98th centile for 12–19 year olds is 4.4.12 The authors therefore recommend HOMA-IR ≥4.5 as the most practical definition of insulin resistance in children and adolescence in the current state of knowledge.
Definitions of hyperinsulinaemia, prediabetes and diabetes are shown in Section ‘Additional investigations that may be appropriate in some children and adolescents’.
It is important to measure HDL-cholesterol (HDL-C) and triglycerides as well as total cholesterol after an 8-h fast. Quality reference data for lipids in paediatric populations are only available from the USA. Detailed growth curves for lipoproteins throughout adolescence that provide reference ranges linked to the US National Cholesterol Education Program (NCEP) adult thresholds (in a manner to derivation of the International Obesity Task Force growth curves) have been published.14 However, the authors recommend use of the NCEP Report of the Expert Panel on Blood Cholesterol Levels in Children and Adolescents15 and the American Heart Association16 recommendations for abnormal lipids in children and adolescents (shown in table 2).
The ratio of total cholesterol to HDL-C is used in adult medicine as an integrative marker of lipid risk, with ratios of 2.5 being normal and >4.0 being associated with risk of adverse cardiovascular events. Published normative data for this ratio are not available in children and adolescents. However, data from the ALSPAC (Avon Longitudinal Study of Parents and Children) study in 8-year-olds supports the use of the adult ratios with children and adolescents (50th centile for ratio was 2.54, with the 95th centile being 3.6 and the 99th centile being 4.3; personal communication, Ken Ong, Cambridge).
Raised ALT (≥twice normal range for measuring laboratory, approx 70 U/l) is the best indicator of probable non-alcoholic fatty liver disease, which is the hepatic manifestation of insulin resistance. The authors suggest the following algorithm for managing raised ALT (alanine aminotransferase).
■ ALT ≥twice upper limit of normal range – repeat in 3 months and if persistently raised, suggest liver ultrasound and screening for other causes of hepatitis (eg, Wilsons, autoimmune, infectious and α 1 antitrypsin deficiency).
■ ALT ≥120 U/l – repeat immediately and if persistently raised, suggest consultation with gastroenterology or hepatology service for further investigations and possible liver biopsy.
Additional investigations that may be appropriate in some children and adolescents
A. Further investigations for aetiology.
Genetic studies including chromosome analysis should be routine in those with extreme obesity. Genetic studies should also be organised in those with lesser levels of obesity who have significant dysmorphisms and learning difficulties. Within the UK, families can be offered participation in the Genetics of Obesity study, which investigates monogenic causes of early onset obesity. If there are significant concerns or signs of obesity-related syndromes, referral to a geneticist is appropriate.
Suspicion of secondary obesity.
Repeatedly abnormal thyroid function tests should trigger measurement of free T3 and antithyroid antibodies and appropriate thyroid imaging. Measurement of calcium and phosphate is also appropriate to exclude pseudohypoparathyroidism.
The following signs should trigger further investigation of Cushing syndrome:
■ height deceleration;
■ obesity is of short duration or there has been rapid recent weight gain;
■ severe hypertension, acne or hirsuitism (although these are seen frequently in simple obesity).
Appropriate investigations to be undertaken by a paediatric endocrinologist include 24-h urinary free cortisol, repeated midnight and 8 am plasma cortisol and a dexamethasone suppression test.
B. Further investigation of comorbidities.
Oral glucose tolerance test.
While the Oral glucose tolerance test (OGTT) is undertaken to diagnose hyperinsulinaemia and pre-diabetes conditions more commonly than diabetes itself, the value of a formal OGTT remains unclear in obese children.11 Fasting samples will miss those with prediabetic conditions such as impaired glucose tolerance (IGT). Some children have normal fasting insulin but marked hyperinsulinism at 30–60 min after glucose challenge. While the population prevalence of IGT in British children is unknown, approximately 11% of a very obese British clinical sample were noted to have IGT.8
The authors suggest that the following patients should be considered for an OGTT (adapted from the American Diabetes Association Recommendations for children):
BMI ≥98th centile and has two or more of the following:
■ Family history of type 2 diabetes (1st or 2nd degree relatives).
■ Ethnicity associated with higher risk: (South Asian, Middle-Eastern, Hispanic, black Caribbean or black African).
■ Clinical signs of potential insulin resistance syndrome (acanthosis nigricans, hypertension).
■ Investigatory evidence of the insulin resistance syndrome (fasting hyperinsulinaemia, and/or dyslipidaemia).
■ Signs and symptoms of polycystic ovarian syndrome (PCOS). Investigations for PCOS – see below for more information.
All patients with extreme obesity (>3.5 SD above mean).
Clinical judgement should be used to test high-risk patients who do not meet these criteria.
The most useful OGTT protocol would measure glucose and insulin every 30 min. If this is not possible, the priority values are the 0 and 120 min glucose, and the 0 and 30–60 min insulin. There are few data on the utility of repeating the OGTT. The authors suggest repeating the test every 2 years unless there has been significant weight loss.
Investigations for PCOS
PCOS should be suspected in girls with signs of insulin resistance (acanthosis nigricans), androgen excess (acne and hirsuitism) and oligo-amenorrhoea. In pubertal girls with symptoms of PCOS, undertake the following:
■ Adrenal androgens (androstenedione, dehydroepiandrosterone sulphate and testosterone).
■ Follicle-stimulating hormone (FSH) and luteinising hormone (LH) (baseline only).
■ 17 hydroxy-progesterone.
■ Sex hormone binding globulin.
This should only be attempted in adolescents if a skilled operator is available. Note that interpretation of pelvic ultrasounds by those inexperienced with adolescents may overdiagnose polycystic changes.
See Section ‘Diagnostic issues’ for details on the diagnosis of PCOS.
Symptoms suggestive of OSA include significant snoring, paradoxical chest movements, excessive movement during sleep and frequent awakenings, daytime sleepiness and behavioural and cognitive problems. Examination is usually unremarkable.17 The most useful initial screening questions concern snoring and difficulty in breathing during sleep. If these are present, simple and convenient questionnaires such as the Chervin Pediatric Sleep Questionnaire or the Cleveland Adolescent Sleepiness Questionnaire can be useful to identify OSA and distinguish it from simple snoring.9 18 Significant symptoms plus a score of ≥8 on the Chervin questionnaire should prompt further investigation, such as overnight oximetry monitoring in the first instance. If positive, further dedicated respiratory sleep assessment should be undertaken.
It is useful to add some clarity to the diagnosis of obesity, as diagnosis should directly inform management. The current International Classification of Diseases 10 (ICD10) categories are outdated and confused and have little utility for paediatric practice. The E66 code is for all obesity, with E66.0 used for obesity ‘due to excess calories’, E66.1 for drug-induced obesity, E66.8 representing ‘morbid obesity’ and E66.9 representing obesity not otherwise specified. Diagnostic issues are changing as we better understand the genetic underpinning of obesity. The authors suggest that division into three categories as follows is useful:
Category 1: primary obesity.
This is the commonest category, accounting for >95% of cases. This should be the diagnosis if examination or history does not lead to further investigations, or if further investigations are negative. It is unhelpful to call this ‘nutritional obesity’ or obesity due to excess calories (ICD10 code E66.0) as all obesity is due to an excess of calorie intake over requirement.
Category 2: monogenic causes of obesity.
Note this category may expand with advances in knowledge. See table 1 for genetic syndromes associated with obesity.
Category 3: secondary obesity.
Secondary to or associated with endocrinopathy, central nervous system abnormalities, drugs or other medical pathology.
Cut offs for the diagnosis of glucose-insulin, blood pressure, lipid and liver function abnormalities are given earlier in this paper and for lipids in table 2.
The ‘metabolic syndrome’
While glucose and insulin, blood pressure and lipid abnormalities clearly cluster together, often termed the metabolic or insulin resistance syndrome, it is unclear whether the diagnosis of this clustering in individuals is of clinical utility. There is currently an ongoing debate about the diagnosis and the utility of diagnosis of the insulin resistance syndrome or metabolic syndrome (MS) in children and adolescents. However, there is evidence that an MS-like syndrome in childhood is predictive of both the MS and actual cardiovascular disease in adult life; the Princeton Lipid Research Clinics study suggested that the MS in childhood increased risk of adult cardiovascular disease approximately 15-fold.19
Practically, the authors suggest that obese children and young people with two or more of the following cardiovascular risk factors are very likely to constitute a high-risk group:
(1) Impaired fasting glucose or impaired glucose tolerance.
(3) Abnormal lipids (see above and table 2).
(4) Hypertension (see above).
Population-based data from the USA suggest that 22% of children and adolescents with BMI ≥98th centile have ≥2 risk factors in addition to their obesity, rising to 33% of those ≥99th centile.20 Clinic-based data in UK children suggest that around 20–25% of obese children and adolescents have two or more of the above risk factors in addition to obesity.8
Polycystic ovarian syndrome
The internationally accepted Rotterdam 2003 consensus21 for diagnosing PCOS required two of the following three criteria to be present:
(1) Oligo- or anovulation.
(2) Clinical and/or biochemical signs of hyperandrogenism (male pattern hirsuitism, alopecia).
(3) Polycystic ovarian morphology.
Note that there is some difficulty in applying this to adolescents, as oligomenorrhoea (a strict definition is bleeding intervals >35 days) is developmentally normal for some years after menarche. Furthermore, it is unclear whether a diagnosis of PCOS can be strictly made before menarche.
Biochemical signs of hyperandrogenism are adrenal and/or ovarian androgens (DHEA-S, androstenedione and testosterone) above the normal adult female range. Clinicians frequently regard an LH:FSH ratio of >3:1 to be suggestive of PCOS, however this is not supported in the Rotterdam guidelines.
Obstructive sleep apnoea
Obesity increases the risk of OSA approximately fivefold. Diagnosis of OSA is based on clinical suspicion, history and physical findings, with confirmation made by polysomnography if needed.17
This guidance provides expert opinion for the assessment of obesity and its comorbidities in secondary care. Recommendations are based upon best available evidence, however, it must be noted that in many cases, quality evidence is lacking and recommendations are based on clinical experience.
The authors honour the contributions and memory of former OSCA member, Dr. Catherine Hall, former Consultant Paediatric Endocrinologist, Royal Manchester Children's Hospital, who died in 2010. The authors would like to thank the Royal College of Paediatrics and Child Health for supporting OSCA with funds for meetings and travel. The authors would also like to thank the Association for the Study of Obesity (ASO) for supporting us with an initial small grant for travel. Individuals who have contributed outside the OSCA group include Prof. Barry Taylor, Dunedin School of Medicine, New Zealand, who provided general advice on the guidance, and Dr Shahrad Taheri, Senior Lecturer in Medicine, Diabetes and Endocrinology, University of Birmingham, who provided advice on the investigation of obstructive sleep apnoea.
Collaborators This expert opinion is authored by the OSCA (Obesity Services for Children and Adolescents) Group.
Funding OSCA meetings were funded by the Royal College of Paediatrics and Child Health, and the Association for the Study of Obesity (UK).
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.