
Contents
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
Introduction Introduction
-
Prevalence of childhood obesity Prevalence of childhood obesity
-
Clinical history, examination, and investigation Clinical history, examination, and investigation
-
Investigation Investigation
-
Genetic obesity syndromes Genetic obesity syndromes
-
Approach to treatment Approach to treatment
-
References References
-
-
-
-
-
-
-
-
-
-
-
-
-
12.1.3 Assessment and management of severe obesity in childhood and adolescence
-
Published:July 2011
Cite
Abstract
The true prevalence of obesity in childhood is difficult to determine as there is no internationally accepted definition of pathological adiposity in the paediatric age group. Body weight is reasonably well correlated with body fat but is also highly correlated with height, and children of the same weight but different heights can have differing amounts of adiposity. In children the relationship between body mass index (BMI) and body fat varies considerably with age and with pubertal maturation. BMI centile charts using national BMI reference data have now been published in several countries and aid the graphical plotting of serial BMI measurements in individual patients. However, such charts are often based on arbitrary statistical measures and not on biological data related to the risk of later morbidity. Cole et al. developed age- and gender-specific cut-off lines from BMI data derived from six countries, which extrapolate risk from the adult experience to children (1). The International Obesity Task Force (IOTF) has recommended the use of these age- and gender-specific BMI cut-offs (overweight as approximately 91st percentile or greater and obesity as approximately 99th percentile or greater) for the comparison of obesity prevalence in different populations (2). Although there is no accepted definition for severe obesity in childhood, a BMI SD >2.5 (weight off the chart) is often used in specialist centres and the crossing of weight percentile lines upwards is an early indication of the risk of severe obesity.
Introduction
The true prevalence of obesity in childhood is difficult to determine as there is no internationally accepted definition of pathological adiposity in the paediatric age group. Body weight is reasonably well correlated with body fat but is also highly correlated with height, and children of the same weight but different heights can have differing amounts of adiposity. In children the relationship between body mass index (BMI) and body fat varies considerably with age and with pubertal maturation. BMI centile charts using national BMI reference data have now been published in several countries and aid the graphical plotting of serial BMI measurements in individual patients. However, such charts are often based on arbitrary statistical measures and not on biological data related to the risk of later morbidity. Cole et al. developed age- and gender-specific cut-off lines from BMI data derived from six countries, which extrapolate risk from the adult experience to children (1). The International Obesity Task Force (IOTF) has recommended the use of these age- and gender-specific BMI cut-offs (overweight as approximately 91st percentile or greater and obesity as approximately 99th percentile or greater) for the comparison of obesity prevalence in different populations (2). Although there is no accepted definition for severe obesity in childhood, a BMI SD >2.5 (weight off the chart) is often used in specialist centres and the crossing of weight percentile lines upwards is an early indication of the risk of severe obesity.
Prevalence of childhood obesity
Depending on the criteria used, prevalence figures for childhood obesity range from 4% to 11% in most developed countries. In the 10 years between the National Health and Nutrition Examination Survey (NHANES) II (1976–80) and NHANES III (1988–91) the prevalence of overweight in the USA, based on body mass index corrected for age and sex, increased by approximately 40% (to 11% in the 6–11-year age group). The highest figures for overweight and obesity are found in the WHO Americas Region, the Eastern Mediterranean Region and the European Region, with the lowest rates in the Africa Region. Thus, childhood obesity is emerging as a global problem. Its immediate adverse effects include orthopaedic complications, sleep apnoea, and psychosocial disorders. As obese children are more likely to become obese adults, we may expect to see public health consequences as a result of the emergence in later life of associated comorbidities, such as type 2 diabetes mellitus and hypertension (3, 4).
Clinical history, examination, and investigation
The assessment of severely obese children and adolescents should include screening for potentially treatable endocrine and neurological conditions and identifying genetic conditions so that appropriate genetic counselling and in some cases treatment can be instituted. Much of the information needed can be obtained from a careful medical history and physical examination (Box 12.1.3.1), which should also address the potential hidden complications of severe obesity, such as sleep apnoea (Box 12.1.3.2). In addition to a general medical history, a specific weight history should be taken carefully establishing the age of onset (clinical photographs are helpful here), as it is useful to distinguish obesity which began in early childhood (stronger genetic component), from that occurring in relation to specific physiological ‘critical periods’ such as puberty, illness, or concomitant medications. A history of previous treatment for obesity, diet, and levels of physical activity should be noted. A careful familial history of obesity and of the presence of conditions such as type 2 diabetes, dyslipidaemia and hypertension as well as exposure to gestational diabetes in utero should be documented, as such parameters may help identify a child at increased risk for early development of obesity-related complications. Height should be measured accurately using a stadiometer and weight measured by accurate scales calibrated against known weights. Anthropometric measures should be evaluated in the context of ethnic background (as some ethnicities are prone to develop obesity-related comorbidities at lower BMI thresholds) and of family history of disease. In addition to height, weight, and calculation of the BMI, waist circumference, a surrogate of intra-abdominal fat, should be measured. Waist circumference has been shown to correlate more closely than BMI with cardiovascular risk factors typically observed in obese children and adolescents. A significant proportion of severely obese children and adolescents have a spectrum of psychiatric disorders, such as eating disorders or depression. Addressing such psychological problems is a key to the success of any intervention, thus a screening psychological evaluation is highly recommended. The history and examination can then guide the appropriate use of diagnostic tests which may affect the management of the patient.
Age of onset—use of growth charts and family photographs. Early onset (<3 years of age) may suggest a genetic cause. Patterns of ‘catch up growth’ should be detected.
Duration of obesity—short history suggests endocrine or central cause.
A history of damage to the central nervous system (CNS) (e.g., infection, trauma, haemorrhage, radiation therapy, seizures) suggests hypothalamic obesity with or without pituitary growth hormone deficiency or pituitary hypothyroidism.
A history of dry skin, constipation, intolerance to cold, or fatigue suggests hypothyroidism. Mood disturbance and central obesity suggests Cushing’s syndrome. Frequent infections and fatigue may suggest adrenocorticotropic hormone (ACTH) deficiency due to POMC mutations.
Hyperphagia—specific questions, such as waking at night to eat, demanding food very soon after a meal suggest hyperphagia. If severe, especially in children, suggests a genetic cause for obesity.
Developmental delay—milestones, educational history, behavioural disorders. Consider craniopharyngioma or structural causes (often relatively short history) and genetic causes.
Visual impairment and deafness can suggest genetic causes.
Onset and tempo of pubertal development—onset can be early or delayed in children and adolescents.
Family history—consanguineous relationships, other children affected, family photographs useful. Severity may differ due to environmental effects.
Treatment with certain drugs or medications—glucocorticoids, psychotropic medications such as risperidone, clozapine.
Document weight and height compared with normal centiles. Calculate body mass index. In children, obtain parental heights and weights where possible.
Short stature or a reduced rate of linear growth in a child with obesity suggests the possibility of growth hormone deficiency, hypothyroidism, cortisol excess, pseudohypoparathyroidism, or a genetic syndrome such as Prader–Willi syndrome.
Body fat distribution—central distribution with purple striae suggests Cushing’s syndrome.
Dysmorphic features or skeletal dysplasia.
Pubertal development/secondary sexual characteristics. Most obese adolescents grow at a normal or excessive rate and enter puberty at the appropriate age; many mature more quickly than children with normal weight, and bone age commonly is advanced. In contrast, growth rate and pubertal development are diminished or delayed in growth hormone deficiency, hypothyroidism, cortisol excess, and a variety of genetic syndromes. Conversely, growth rate and pubertal development are accelerated in precocious puberty and in some girls with polycystic ovarian syndrome.
Acanthosis nigricans.
Valgus deformities in severe childhood obesity.
Sleep apnoea
Asthma
Pickwickian syndrome
Idiopathic intracranial hypertension (e.g. pseudotumour cerebri)
Insulin resistance/impaired glucose tolerance
Type 2 diabetes
Menstrual abnormalities
Polycystic ovary syndrome
Slipped capital epiphyses
Blount’s disease (tibia vara)
Tibial torsion
Flat feet
Ankle sprains
Increased risk of fractures
Cholelithiasis
Liver steatosis/nonalcoholic fatty liver
Gastro-oesophageal reflux
Hypertension
Dyslipidaemia
Investigation
Some useful tests to consider are fasting plasma glucose or 2-h postprandial glucose levels and serum lipid levels. Thyroid-stimulating hormone may be helpful in excluding hypothyroidism yet this rarely explains severe obesity. Urinary free cortisol can be obtained if hypercortisolism is suspected clinically. Genetic testing is needed to confirm the diagnosis in patients with rare genetic disorders. The measurement of serum leptin is not recommended as a routine examination, but in cases of severe early-onset obesity this should be undertaken, since, although it is rare, congenital leptin deficiency is a potentially treatable disorder. Serum insulin, for assessment of indices of insulin resistance, such as HOMA-IR, is not recommended because of lack of appropriate references and the variety of different assays used, which make its interpretation problematic.
Genetic obesity syndromes
Classically, patients affected by genetic obesity syndromes have been identified as a result of their association with developmental delay, dysmorphic features, and/or other developmental abnormalities. More recently, several single-gene disorders resulting from disruption of the hypothalamic leptin–melanocortin signalling pathway have been identified. In these disorders, obesity itself is the predominant presenting feature, although frequently accompanied by characteristic patterns of neuroendocrine dysfunction, which only become apparent on investigation (see Chapter 12.1.2).
Approach to treatment
Once an underlying genetic or other organic disorder that can explain the development of obesity has been ruled out, as is the case in the majority of obese children and adolescents, the physician is faced with the difficult task of providing an appropriate protocol to the child. The goals of treating overweight children are to half further weight gain, in some cases decrease body weight, optimize body composition, improve wellbeing and lifestyle, and to prevent or reverse insulin resistance, metabolic syndrome, diabetes, and other related comorbidities. Such interventions must be comprehensive, focusing on optimizing nutrition, weight loss, increasing physical activity, and inducing behaviour change for the child and family. As such interventions are aimed at changing behavioural patterns and part of the home environment, parental participation is crucial in order to provide a positive role model and to initiate dietary and behavioural changes. Studies have shown that participants in a child and parent weight management programme have significantly greater decreases in per cent overweight 5 and 10 years post intervention (–11.2% and –7.5%, respectively) than a child-only group, or a group with variable family participation. It is important to define realistic expectations to the patient and the parents and to emphasize that immediate results should neither be desired nor be expected.
While lifestyle interventions are safe and effective, pharmacotherapy must be viewed as an adjunct to participation in such programmes in cases of severe obesity or in obese children with apparent comorbidities. The use of medications to treat obesity, insulin resistance, or the metabolic syndrome must be done with caution for several reasons: only two drugs are currently approved by the US Food and Drug Administration (FDA) for use in children; and there are few well-controlled scientific studies of short-term safety and efficacy of pharmacological intervention in children, with no data to show their long-term efficacy. The risk for significant adverse events must be weighed against the long-term potential for reduction in obesity-related morbidity and mortality as the use of many drugs for the treatment of obesity in adults has resulted in unforeseen complications. Lifestyle modifications have been proven to be more efficacious than pharmacotherapy for diabetes prevention (in adults) yet no comparative data has been shown for children and adolescents.
A third option that is recently gaining popularity in some countries is the performance of bariatric surgical procedures in severely obese adolescents. Such procedures have been shown to have a sustained long-term effect on weight reduction in adults, yet there are no long-term paediatric data. Such procedures should be reserved only for adolescents who have completed the majority of their growth (bone age >15 years for boys and >13 years for girls) and have a significant obesity related comorbidity, such as type 2 diabetes, significant sleep apnoea, or biopsy-proven steatohepatitis. In addition, the surgical option should be reserved only for exceptional cases, who: have failed losing weight during participation in an organized family-oriented weight reduction programme; have shown commitment to adhere to nutritional guidelines appropriate for the pre- and postsurgical period; and have undergone a comprehensive personal and familial psychological evaluation aimed to rule out emotional/psychiatric problems that may affect the success of the procedure and show that a supportive familial environment exists. The bariatric procedure of choice in the adolescent patient has not been determined and depends on the comorbidities present as well as on the experience of the surgeon. Bariatric surgery in adolescents should be performed only in medical centres that can provide all the subspecialists needed to evaluate the obese patient before the procedure and to provide long-term follow-up. Such teams should include, in addition to the bariatric surgeon, at least a paediatric obesity specialist, a nutritionist with expertise in bariatric surgery patients and in children, and a psychologist.
References
1.
2.
3.
4.
Month: | Total Views: |
---|---|
October 2022 | 5 |
November 2022 | 1 |
December 2022 | 2 |
January 2023 | 2 |
February 2023 | 4 |
March 2023 | 4 |
April 2023 | 1 |
May 2023 | 1 |
June 2023 | 2 |
July 2023 | 2 |
August 2023 | 2 |
September 2023 | 2 |
October 2023 | 2 |
November 2023 | 2 |
December 2023 | 2 |
January 2024 | 1 |
February 2024 | 1 |
March 2024 | 2 |
April 2024 | 1 |
May 2024 | 1 |
June 2024 | 2 |
July 2024 | 1 |
August 2024 | 2 |