Assessment and Staging: Identification and Evaluation of the High-Risk Patient

W. Timothy Garvey

CASE STUDY

A 55-year-old woman makes an appointment after being told that her fasting glucose was elevated on a worksite screening test. She has also recently noted increased shortness of breath on exertion, daytime lethargy, and low back pain. Past medical history is significant for hypertension, hypercholesterolemia, depression, and obesity. Medications include enal-april 20 mg/day, atenolol 100 mg/day, atorvastatin 40 mg/day, and paroxetine 40 mg/day.

She is single, lives alone, and likes her work as a paralegal but is guarded in social settings because of her weight. In high school, she weighed 105 lb. She lost her fiancé to an auto accident when she was 26 years of age, quit exercising, started overeating, and began showing signs of depression. She gained weight progressively until she sought help in the Weight Watchers program at the age of 50 years and lost 10 lb. However, she regained the weight due to an inability to change her lifestyle. She feels that paroxetine helps her depression, but she still lacks confidence in her ability to lose weight by changing her lifestyle. In particular, she gets hungry at night and engages in excessive snacking while watching television. She relies on fast food for lunch and often picks something up for dinner on her way home from work. She does not engage in regular exercise but she does enjoy walking her dog.

On examination, her weight = 228 lb, height = 64 inches, body mass index (BMI) = 39.1 kg/m², waist circumference = 38 inches, blood pressure (BP) = 144/91, heart rate (HR) = 88. The remainder of the examination is unremarkable. Laboratory tests show a fasting glucose = 118 mg/dL, HbA1c = 6.2%; lipids (mg/dL): total cholesterol = 189, low-density lipoprotein cholesterol (LDL-c) = 105, high-density lipoprotein cholesterol (HDL-c) = 42, triglycerides 194; alanine transaminase (ALT) = 95 U/L, aspartate transaminase (AST) = 34 U/L; complete blood count (CBC), creatinine, and electrocardiogram (ECG) are normal. Polysomnography done to evaluate daytime lethargy shows an apnea-hypopnea index (AHI) of 25.

CLINICAL SIGNIFICANCE

Optimal obesity care requires individualized assessment and treatment plans involving medical evaluation, a multidisciplinary team, resources for lifestyle therapy, access to medications and surgical procedures, and long-term management. However, the impact of excess adiposity on health varies widely and not all patients require intensive interventions. Like other chronic diseases, the complications of obesity are responsible for impairing health and quality of life. The presence and severity of complications vary widely among patients, and this necessitates an evaluation of complications as a guide to developing care plans and treatment goals.¹,² Risk assessment and disease staging allow the clinician to match the aggressiveness of interventions to disease severity. More aggressive treatments can then be employed in those at high risk in a manner that optimizes effectiveness, safety, health benefits, and cost effectiveness.

An additional aspect underscores the need to individualize the treatment plan rather an employing a “one size fits all” approach. Optimal therapy entails behavior change regarding caloric intake and physical
activity. A personalized treatment plan must, therefore, take into account each patient’s capability for adherence to a lifestyle intervention based on personal and cultural preferences and psychological, social, and environmental factors. Interventions that do not take these factors into account are likely to lead to a poorer outcome. Accordingly, the diagnostic evaluation of obesity must provide clinical data that address psychosocial, behavioral, and environmental factors in addition to the presence of complications and their impact on quality of life. The diagnosis of overweight and obesity as well as risk stratification and determination of which treatment approaches are appropriate has historically been based on the American Heart Association (AHA) and World Health Organization (WHO) guidelines which exclusively use BMI and waist circumference. The use of new clinical staging systems that take into account other characteristics besides simply BMI provides the opportunity for healthcare providers (HCPs) to match and prioritize treatments to individuals with obesity depending upon the severity and complications of their disease.

KEY COMPONENTS OF THE PATIENT EVALUATION AND OVERALL VIEW

Figure 3.1 illustrates the clinical findings and considerations required for identifying high-risk patients with obesity. These assessments evaluate the impact of the disease on health and identify factors that place patients at risk of poor clinical outcomes. Of critical importance are findings pertaining to the risk, presence, and severity of obesity-related complications, since these complications confer morbidity and mortality and indicate that obesity is having an adverse impact on health.

Obesity is a chronic disease with opportunities for primary, secondary, and tertiary prevention. Primary prevention prevents the development of obesity in the first place and can involve health education and changing the built environment. With the development of excess adiposity but prior to emergence of complications, clinicians are in a secondary prevention mode of treatment with the goal of preventing further weight gain and the emergence of complications. Once obesity complications are present, this signifies that the degree of adiposity regardless of the BMI level is sufficient to impair the health of the patient. The HCP is then in a tertiary prevention mode when weight loss therapy must be sufficient to prevent further disease deterioration and treat the complications. For this reason, there is an emphasis on complications that can be prevented or ameliorated with weight loss. Since the purpose of treatment is to improve the health and quality of life of the patient, the goal of weight loss therapy is to achieve sufficient weight loss to result in clinically meaningful improvements in complications and/or a reduction in the risk of complications. There are several straightforward and useful approaches to stage the severity of obesity based on the presence and severity of complications discussed below.¹,³ For the most part, these approaches use objective clinical criteria for the diagnosis of complications and assessment of the severity of complications.

FIGURE 3.1 Identification of the high-risk patient with overweight or obesity.

In addition to the objective clinical assessment of obesity complications, it is important to assess the degree of symptom formation and functional impairment regarding complications, and the extent to which these symptoms worsen quality of life. Patients with degenerative osteoarthritis who have similar changes on knee x-ray could exhibit marked differences in the severity of symptoms as a consequence of this complication. Therefore, it is also important to assess the subjective severity of symptoms and the degree to which these symptoms adversely impact function and quality of life. These considerations are analogous to patient-reported outcomes and indicate complication severity according to the patient’s experience.

Finally, the HCP must assess aggravating factors that place the patient at risk for poor outcomes. These can include medications prescribed for various purposes that promote weight gain, as well as “psychological overlay” including stigmatization, poor self-esteem, depression, or binge eating disorder, which can predominate as causes of decreased quality of life. In many patients, these factors must be incorporated into a personalized treatment approach or addressed specifically if the weight loss intervention is to be successful. Social and environmental determinants of obesity can also present obstacles to effective treatment and must be addressed in an individualized care plan. It is important to gauge
factors such as personal and cultural preferences for food and physical activity, the built environment with access to unprocessed food or exercise facilities, support systems, and health literacy in developing effective lifestyle prescriptions.

These aspects of the patient evaluation will be described in more detail; however, two points are salient at this juncture. First, while these evaluations are required to identify high-risk patients, it is important to understand that this is part of the clinical assessment for all patients in treating obesity as a disease. All patients should be examined for disease complications, the impact of these complications on quality of life, and aggravating factors in devising personalized and effective treatment plans. Second, it will become clear that this does not entail an extraordinary effort on the part of the HCP outside of a standard intake evaluation consisting of an obesity-focused history, review of systems (ROS), physical examination, and appropriate laboratory tests. Like diabetes, obesity is a metabolic disease that can systemically affect multiple organ systems and involves lifestyle and behavioral change as components of therapy. The evaluation should be considered as a standard of care for medical management of obesity. The evaluation is required for the staging of all patients across the full spectrum of disease risk and severity and provides the basis for rational selection of treatment modality and intensity and for establishing goals and desired treatment outcomes.

THE DIAGNOSTIC EVALUATION OF OBESITY

Anthropometric and Clinical Components of the Diagnosis

The initial evaluation of patients with obesity was discussed in Chapter 2. Key components of the assessment are reviewed here with a focus on staging the severity of obesity and providing individualized care.

FIGURE 3.2 The diagnostic evaluation of patients with obesity has both anthropometric and clinical components. BMI, body mass index.

The Anthropometric Component

The identification of the high-risk patient with obesity begins with the diagnostic evaluation, which has both anthropometric and clinical components,⁴ as shown in Figure 3.2. The anthropometric component is largely satisfied by BMI as outlined in the AHA guidelines. The anthropometric component of the diagnosis of “obesity” is applied to adults with BMI of ≥30 kg/m² and “overweight” with BMI 25 to 29.9 kg/m², while epidemiological data justify the lower cutoffs of BMI 23 to 24.9 kg/m² as overweight and BMI of ≥25 kg/m² as the definition of obesity in many Southeast Asian populations.⁵ Waist circumference measurements provide additional information regarding fat distribution and cardiometabolic disease risk, as well as a simple measure to monitor weight loss progress that can be shared with patients.

The limitations of BMI as a measure of body fat are described in Chapter 2. Other technologies that can be used to practically measure adipose tissue mass and % body fat include bioelectric impedance plethysmography, air displacement plethysmography, and dual-energy X-ray absorptiometry (DEXA), although they are not in general use in primary care settings. Body fat percentage cut points for obesity have been proposed as 25% and 35% for men and women, respectively.⁶ In most patients, an elevated BMI with clinical confirmation of excess adiposity will suffice.

The Clinical Component

While the use of BMI categories to stage patients with overweight and obesity has been useful, a major shortcoming of focusing exclusively on BMI and waist circumference is that these measures do not provide specific information about the impact of excess adiposity on the health of the patient. As with any chronic disease, complications confer morbidity and mortality and adversely affect health. For this reason, the diagnostic evaluation of obesity extends beyond the anthropometric measure
of BMI to include a clinical component. The clinical component of the diagnosis involves a full medical history and examination that assess the risk, presence, and severity of complications and establishes the degree to which an increase in adipose mass affects the patient’s health. The development of weight-related complications varies markedly among patients at any given BMI level.¹ While the likelihood of weight-related complications generally increases as a function of progressive obesity, there can be a poor correlation between BMI and the emergence of complications. Patients with obesity need not have weight-related complications and can be free of increased risk for certain disease-related morbidity and mortality. On the other hand, patients with comparable degrees of excess adipose tissue can develop multiple cardiometabolic and biomechanical complications in a manner that is independent of the increased BMI. Thus, the clinical evaluation can provide the basis for the identification of the high-risk patient and disease staging. Since weight loss will ameliorate or prevent many weight-related complications, the clinical component of the diagnosis also helps guide the intensity and modality of treatment and helps inform the end points of therapy.

Adiposity-Based Chronic Disease

The diagnosis of obesity based only on BMI has led to confusion among the lay public and healthcare professionals regarding significance of obesity and the appreciation of obesity as a chronic disease.⁴ This is primarily because BMI conveys little information about complications associated with excess adiposity that adversely affect health. Furthermore, the term obesity carries with it stigma that can generate negative perceptions about the personal character of patients, generating guilt, depression, and shame. The bias and uncertainty regarding health implications help perpetuate factors that limit access of patients to effective therapy. Adiposity-based chronic disease (ABCD) has been proposed as a diagnostic term that conceptualizes obesity as a chronic disease associated with complications, considers the pathophysiological basis of the disease, and avoids the stigmata, ambiguity, differential use, and multiple meanings of the term obesity.⁷,⁸ This term alludes to what we are treating and why we are treating it. As illustrated in Figure 3.3, the phrase “adiposity-based” is used because the disease is primarily due to abnormalities in the mass, distribution, and/or function of adipose tissue. The phrase “chronic disease” is apropos because the disease is lifelong, associated with complications that confer morbidity and mortality, and has a natural history that offers opportunities for primary, secondary, and tertiary prevention. Abnormalities in adipose tissue mass predispose to biomechanical complications, and defects in the function and distribution of adipose tissue lead to cardiometabolic disease complications as well as other health problems. The new diagnostic term provides a conceptual basis that can help inform and structure the evaluation and diagnosis of patients with obesity, as well as identifying high-risk patients suffering from disease complications. The term ABCD underscores the principle that the diagnostic evaluation of obesity as a disease will require both anthropometric and clinical components. Finally, ABCD is a new disease coding and classification system that has been proposed as an alternative to the current International Classification of Diseases (ICD) paradigm, which provides rational implications for diagnosis, disease staging, treatment, and billing for medical services.⁹

FIGURE 3.3 Adiposity-based chronic disease (ABCD). ABCD as a diagnostic term for obesity signifies: (1) “what we are treating” which relates to abnormalities in the mass, distribution, or function of adipose tissue, and (2) “why we are treating it” as a chronic disease which is to prevent or ameliorate obesity complications that confer morbidity and mortality and impair the quality of life.

History, Physical Examination, and Clinical Laboratory

Consistent with general standards of clinical care, patients with the disease of obesity require an initial medical evaluation with history, ROS, physical examination, and laboratory testing. In addition to a generalized clinical assessment, these components are adapted in specific ways to evaluate the impact of excess adiposity on health and to obtain information needed to develop a personalized care plan. Details of the comprehensive evaluation process are discussed in Chapter 2.

Aggravating Factors

In the context of the high-risk patient, certain aspects of the evaluation deserve emphasis. A care plan that is not individualized places the patient at risk of poor outcomes due to nonadherence, and this requires that key pieces of information be obtained during the initial evaluation. This includes personal and cultural preferences for diet and physical activity in formulating lifestyle prescriptions. In addition, certain aggravating factors exacerbate obesity and should be accounted for in a personalized management plan, as shown in Table 3.1. These factors are unique to each patient in the natural history of their disease and are critically important in designing personalized approaches for effective treatment. There are three general categories of aggravating factors: medications that promote weight gain, psychological and psychiatric factors, and social and environmental determinants of health.⁹ In many patients, treatment will not be successful unless these issues are addressed and incorporated into a personalized therapeutic plan.

TABLE 3.1 Aggravating Factors and Social and Environmental Determinants

	FACTORS AFFECTING INDIVIDUALIZED CARE PLAN	POSSIBLE INTERVENTIONS
Medications	Examples: insulin, TZDs, sulfonylureas; β-adrenergic receptor blockers; antipsychotics; certain antidepressants; antiepileptics; glucocorticoids	Assess the need for offending medication Substitute with weight neutral alternative
Psychological/psychiatric factors	Depression Anxiety disorder Psychosis Binge eating disorder Night eating syndrome Stigmatization Stress	Psychological screening Counseling Referral Medications Antidepressants Anxiolytics Antiobesity medications to address cravings
Social and environmental determinants	Behaviors Cultural factors Time management Access to unprocessed foods Physical activity resources Work related Health literacy Access to clinics/hospitals Economic status Health insurance	Motivational interviewing Counseling (personal and family) Dietitian referral Education Social work referral Information regarding community resources
TZDs, thiazolidinediones.

Medications that can promote weight gain should be identified and consideration given to possibly discontinuing these or substituting them with a weight neutral alternative (see Chapter 8 on Pharmacotherapy). Psychological factors can also contribute to obesity and mitigate against successful treatment outcomes unless these issues are addressed directly as a component of the care plan. Depression, anxiety, stress, stigmatization, and binge eating should be assessed as contributors to obesity on an individual basis. Specific interventions including counseling, medications, or referrals that address psychological factors may be required to assure optimal effectiveness of lifestyle and medical therapy.

Social and environmental determinants of obesity can directly impact the feasibility and effectiveness of the care plan, and it is important to be aware of these factors and act to minimize their adverse impact on successful treatment. Poor health literacy, limited access to healthcare facilities, and absence of insurance impair
the empowerment of patients for self-care and the availability of evidence-based treatments. Lack of access to unprocessed and healthy foods or outlets for physical activity can reduce the effectiveness of prescriptions for lifestyle therapy. Behavioral attributes, cultural preferences, work patterns, and time management issues can also impede therapeutic success if not identified and addressed. Solutions to address these social and environmental determinants can involve culturally appropriate education and lifestyle modifications, individualized counseling, and referrals to social workers, registered dietitian nutritionist (RDN), and community resources.

Obesity Due to Overt Etiologic Influences and Genetic Abnormalities

Most patients with obesity have idiopathic or common type disease without an overt etiologic cause. Idiopathic obesity arises from the interaction of over 900 identified susceptibility genes,¹⁰ each conferring a small relative disease risk, which then interact with each other and with biological, environmental, and behavioral factors unique to each individual. However, HCPs should be aware that a minority of patients will have obesity that can be directly attributed to identifiable causal influences. While obesity due to overt causal influences is less common, these patients may require specific modalities of therapy and attention to specific patterns of complications. These include genetic mutations or chromosomal abnormalities producing forms of monogenic or syndromic obesity. Table 3.2 lists features of the medical history, family history, and physical findings that can provide a clue as to whether a genetic form of obesity may be present. Other patients with overt causal inferences may have obesity arising from or aggravated by endocrine disease or disability/immobility. The HCP should be alerted to hallmark findings in the history and physical examination that portend the presence of these disease processes, as shown in Table 3.2. This is critical in evaluating and identifying high-risk patients and has direct implications regarding the development of effective therapeutic interventions. Patients with overt causes of obesity may need to be referred to geneticists, endocrinologists, or rehabilitation medicine specialists for subspecialty care.

IDENTIFICATION AND STAGING OF THE HIGH-RISK PATIENT WITH OBESITY

Complications of Obesity/ABCD

The presence and severity of obesity complications constitute the basis for the identification of the high-risk patient. Many complications of obesity can be ameliorated or reversed by weight loss.¹ The treatable complications comprise three pathophysiological categories, namely, biomechanical, cardiometabolic, and abnormalities involving sex steroids. Since these complications confer morbidity and impair health, the goal of therapy is to achieve sufficient weight loss to treat and reverse these complications in the management of obesity as a disease. Other complications are not responsive to weight loss therapy. An example is gall stones which can be exacerbated by weight loss. Another example is depression that occurs with increased frequency in patients with obesity. While depression may improve during therapy, the beneficial effects are largely not related to the degree of weight loss and might be explained as a function of increased contact and care by healthcare professionals.¹ For this reason, depression, binge eating, stigmatization, poor self-esteem, and other psychological disorders are considered as aggravating factors that can drive weight gain and need to be addressed in developing effective individualized care plans, sometimes requiring specific treatment (Table 3.1).

Within the context of the ABCD staging system,⁷ biomechanical complications arise due to an increase in adipose tissue mass and produce impairment in mechanical function including obstructive sleep apnea, obesity-hypoventilation syndrome, osteoarthritis of knee or hip, urinary stress incontinence, gastroesophageal reflux disease, pain syndromes, and immobility/disability. Cardiometabolic complications arise due to abnormalities in the distribution and function of adipose tissue and a pathophysiological process that produces both end-stage metabolic and vascular sequela.¹¹ The progression of cardiometabolic complications begins with insulin resistance, progresses to the high-risk states of metabolic syndrome (MetS) and prediabetes, and then culminates in type 2 diabetes (T2D), nonalcoholic steatohepatitis (NASH), cardiovascular disease (CVD), or all three in single individuals. Dyslipidemia is characterized by increased triglycerides, decreased HDL-c, and increased concentration of atherogenic small dense LDL particles without necessarily an overall increase in LDL-c. Obesity exacerbates insulin resistance and can propel cardiometabolic disease progression toward T2D and CVD.¹¹ Thus, beyond simple increases in adipose tissue mass causing biomechanical complications, abnormalities in adipose tissue function and distribution are causally involved in the pathogenesis of cardiometabolic complications in obesity.⁷ An additional category of complications involves sex steroids leading to abnormal gonadal function and infertility in patients with polycystic ovary syndrome, female infertility, and male hypogonadism.

Table 3.3 lists obesity complications by organ system that HCPs should evaluate in the management of high-risk patients with obesity. The table delineates symptoms, physical examination findings, and clinical laboratory relevant to each complication. In some
instances, further testing beyond the intake evaluation may be necessary for the diagnosis and assessing the severity of individual complications.

TABLE 3.2 Underlying Causes of or Aggravating Factors Causing Obesity

CAUSE OF OBESITY	SPECIFIC DISORDER	SIGNS AND SYMPTOMS
Monogenic or syndromic	Prader-Willi syndrome	Onset in childhood Strong family history Infertility/hypogonadism Delayed or absent puberty Short stature or macrosomia Intellectual disability Behavior problems Unexplained organ system defects (e.g., heart, kidney) Visual or olfactory impairment Dysmorphic features (e.g., face, digits)
	MC4R deficiency
	Leptin deficiency
	Leptin receptor deficiency
	POMC deficiency
	Alström syndrome
	Bardet-Biedl syndrome
	Beckwith-Wiedemann syndrome
	WAGR-O syndrome (BDNF deficiency)
	Wilson-Turner syndrome
Aggravating endocrine disorders	Hypothyroidism	Cold intolerance, lethargy, weakness Constipation Delayed reflexes Bradycardia
	Hypercortisolism	Weakness, poor concentration Bruising and purple striae Acne, moon facies Thin skin and central fat redistribution
	Hypothalamic/CNS injury	Lethargy Decreased libido Polyuria
Aggravated by disability	Immobilization	Muscle weakness Gait abnormality Disability evident on presentation
	Neuromuscular disease or injury
	Movement disorder
Idiopathic/common type		Most common Diagnosis of exclusion No identifiable causal influence
BDNF, brain-derived neurotrophic factor; CNS, central nervous system POMC, pro-opiomelanocortin, WAGR-O, Wilms tumor, aniridia, genitourinary anomalies, and mental retardation and obesity.