Obesity Challenge Center

The patient's history, symptomatology, and assessments suggest a diagnosis of nonalcoholic fatty liver disease (NAFLD). The primary care physician recommends referral to a hepatologist for evaluation and possible liver biopsy. 

NAFLD involves an accumulation of triglycerides and other fats in the liver (unrelated to alcohol consumption and other liver disease), with the presence of hepatic steatosis in more than 5% of hepatocytes. NAFLD affects 25% to 35% of the general population, making it the most common cause of chronic liver disease. The rate increases among patients with obesity, 80% of whom are affected by NAFLD. 

NAFLD should be considered in patients with unexplained elevations in serum aminotransferases (without positive viral markers or autoantibodies and no history of alcohol use) and a high risk for steatohepatitis, including obesity. The standard NAFLD assessment for biopsy specimens is the Brunt system, and disease stage is determined using the NAFLD activity score and the amount of fibrosis present.

A study of the natural history of NAFLD in patients who were followed for 3 years showed that without pharmacologic intervention, one third experienced disease progression, one third remained stable, and one third improved. An independent risk factor for progression of nonalcoholic steatohepatitis was abnormal glucose tolerance testing. In another natural history study, a 10% higher rate of mortality over 10 years was demonstrated among those with NAFLD vs controls, with the top three causes of death being cancer, heart disease, and liver-related disease. Prevalence of chronic liver disease and cirrhosis has been shown to be elevated in Latino and Japanese American populations.

Patients with NAFLD should be seen regularly to assess for disease progression and receive guidance on weight management interventions and exercise. A weight loss of more than 5% has been shown to reduce liver fat and provide cardiometabolic benefits; a weight reduction of more than 10% can help reverse steatohepatitis or liver fibrosis. In addition to weight loss management strategies, physicians should discuss the importance of controlling hyperlipidemia, insulin resistance, and T2D with their patients and share the importance of avoiding alcohol and other hepatotoxic substances.

According to the American Association of Clinical Endocrinology Clinical Practice Guideline: "There are no U.S. Food and Drug Administration-approved medications for the treatment of NAFLD; however, some diabetes and anti-obesity medications can be beneficial. Bariatric surgery is also effective for weight loss and reducing liver fat in persons with severe obesity."

Courtney Whittle, MD, MSW, Diplomate of ABOM, Pediatric Lead, Obesity Champion, TSPMG, Weight A Minute Clinic, Atlanta, Georgia.

Courtney Whittle, MD, MSW, Diplomate of ABOM, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The patient's history, symptomatology, and assessments suggest a diagnosis of nonalcoholic fatty liver disease (NAFLD). The primary care physician recommends referral to a hepatologist for evaluation and possible liver biopsy. 

NAFLD involves an accumulation of triglycerides and other fats in the liver (unrelated to alcohol consumption and other liver disease), with the presence of hepatic steatosis in more than 5% of hepatocytes. NAFLD affects 25% to 35% of the general population, making it the most common cause of chronic liver disease. The rate increases among patients with obesity, 80% of whom are affected by NAFLD. 

NAFLD should be considered in patients with unexplained elevations in serum aminotransferases (without positive viral markers or autoantibodies and no history of alcohol use) and a high risk for steatohepatitis, including obesity. The standard NAFLD assessment for biopsy specimens is the Brunt system, and disease stage is determined using the NAFLD activity score and the amount of fibrosis present.

A study of the natural history of NAFLD in patients who were followed for 3 years showed that without pharmacologic intervention, one third experienced disease progression, one third remained stable, and one third improved. An independent risk factor for progression of nonalcoholic steatohepatitis was abnormal glucose tolerance testing. In another natural history study, a 10% higher rate of mortality over 10 years was demonstrated among those with NAFLD vs controls, with the top three causes of death being cancer, heart disease, and liver-related disease. Prevalence of chronic liver disease and cirrhosis has been shown to be elevated in Latino and Japanese American populations.

Patients with NAFLD should be seen regularly to assess for disease progression and receive guidance on weight management interventions and exercise. A weight loss of more than 5% has been shown to reduce liver fat and provide cardiometabolic benefits; a weight reduction of more than 10% can help reverse steatohepatitis or liver fibrosis. In addition to weight loss management strategies, physicians should discuss the importance of controlling hyperlipidemia, insulin resistance, and T2D with their patients and share the importance of avoiding alcohol and other hepatotoxic substances.

According to the American Association of Clinical Endocrinology Clinical Practice Guideline: "There are no U.S. Food and Drug Administration-approved medications for the treatment of NAFLD; however, some diabetes and anti-obesity medications can be beneficial. Bariatric surgery is also effective for weight loss and reducing liver fat in persons with severe obesity."

Courtney Whittle, MD, MSW, Diplomate of ABOM, Pediatric Lead, Obesity Champion, TSPMG, Weight A Minute Clinic, Atlanta, Georgia.

Courtney Whittle, MD, MSW, Diplomate of ABOM, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The patient's history, symptomatology, and assessments suggest a diagnosis of nonalcoholic fatty liver disease (NAFLD). The primary care physician recommends referral to a hepatologist for evaluation and possible liver biopsy. 

NAFLD involves an accumulation of triglycerides and other fats in the liver (unrelated to alcohol consumption and other liver disease), with the presence of hepatic steatosis in more than 5% of hepatocytes. NAFLD affects 25% to 35% of the general population, making it the most common cause of chronic liver disease. The rate increases among patients with obesity, 80% of whom are affected by NAFLD. 

NAFLD should be considered in patients with unexplained elevations in serum aminotransferases (without positive viral markers or autoantibodies and no history of alcohol use) and a high risk for steatohepatitis, including obesity. The standard NAFLD assessment for biopsy specimens is the Brunt system, and disease stage is determined using the NAFLD activity score and the amount of fibrosis present.

A study of the natural history of NAFLD in patients who were followed for 3 years showed that without pharmacologic intervention, one third experienced disease progression, one third remained stable, and one third improved. An independent risk factor for progression of nonalcoholic steatohepatitis was abnormal glucose tolerance testing. In another natural history study, a 10% higher rate of mortality over 10 years was demonstrated among those with NAFLD vs controls, with the top three causes of death being cancer, heart disease, and liver-related disease. Prevalence of chronic liver disease and cirrhosis has been shown to be elevated in Latino and Japanese American populations.

Patients with NAFLD should be seen regularly to assess for disease progression and receive guidance on weight management interventions and exercise. A weight loss of more than 5% has been shown to reduce liver fat and provide cardiometabolic benefits; a weight reduction of more than 10% can help reverse steatohepatitis or liver fibrosis. In addition to weight loss management strategies, physicians should discuss the importance of controlling hyperlipidemia, insulin resistance, and T2D with their patients and share the importance of avoiding alcohol and other hepatotoxic substances.

According to the American Association of Clinical Endocrinology Clinical Practice Guideline: "There are no U.S. Food and Drug Administration-approved medications for the treatment of NAFLD; however, some diabetes and anti-obesity medications can be beneficial. Bariatric surgery is also effective for weight loss and reducing liver fat in persons with severe obesity."

Courtney Whittle, MD, MSW, Diplomate of ABOM, Pediatric Lead, Obesity Champion, TSPMG, Weight A Minute Clinic, Atlanta, Georgia.

Courtney Whittle, MD, MSW, Diplomate of ABOM, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

This patient's clinical presentation and laboratory findings are consistent with a diagnosis of Cushing syndrome (CS).

CS is a rare endocrine disease caused by prolonged exposure to high circulating cortisol levels. Exogenous hypercortisolism is the most common cause of CS. It is largely iatrogenic and results from the prolonged use of glucocorticoids. Less frequently, endogenous CS may occur as the result of excessive production of cortisol by adrenal glands. Endogenous CS can be ACTH-dependent or ACTH-independent. ACTH-dependent CS results from ACTH-secreting pituitary adenomas (Cushing disease) and ectopic ACTH secretion by neoplasms, whereas adrenal hyperplasia, adenoma, and carcinoma are the primary causes of ACTH-independent CS.

The annual incidence and prevalence of CS are unknown; the reported incidence of newly diagnosed cases has ranged from 1.2 to 2.4 per million people per year. Women are affected more often than are men, with a peak of incidence in the third to fourth decade of life. CS is associated with various metabolic, psychiatric, musculoskeletal, and cardiovascular comorbidities. Untreated, it is associated with increased mortality, typically as the result of cardiovascular and infectious complications; however, even in appropriately treated patients, mortality is elevated.

The chronic elevations of glucocorticoid concentrations in CS result in its characteristic phenotype, which includes weight gain, moon-shaped face, buffalo hump, muscle weakness, increased bruising, skin atrophy, red abdominal striae, menstrual irregularities, hirsutism, and acne. It is also associated with numerous comorbidities including diabetes, hypertension, hypercholesterolemia, and osteoporosis. Patients often experience mental health complications, such as depression, emotional lability, and cognitive dysfunction.

Given the rarity of CS and the fact that these symptoms overlap with other conditions, delayed diagnosis is common. The current obesity epidemic also poses diagnostic challenges because true CS can be difficult to differentiate from metabolic syndrome. The duration of hypercortisolism appears to be the most significant factor associated with the degree of morbidity and preterm mortality in CS; thus, an accurate diagnosis as early as possible is important.

Screening and diagnostic tests for CS evaluate cortisol secretion. Available options include late-night salivary cortisol (LNSC), impaired glucocorticoid feedback with overnight 1-mg DST or low-dose 2-day dexamethasone test (LDDT) and increased bioavailable cortisol with 24-hour UFC.

A 2021 consensus statement by Fleseriu and colleagues provides recommendations for the diagnosis of CS. If CS is suspected: begin with UFC, LNSC, or both; DST is an option if LNSC not feasible. If CS because of adrenal tumor is suspected: begin with DST because LNSC has lower specificity in these patients. To confirm CS, any of these tests can be used.

An individualized approach is recommended for the treatment of CS. The optimal approach for iatrogenic CS is to slowly taper exogenous steroids. Chronic exposure to steroids can suppress adrenal functioning; as such, recovery may take several months. Surgical resection is the first-line option for hypercortisolism because of Cushing disease, adrenal tumor, or ectopic tumor. Patients should be closely monitored after surgery to evaluate for possible recurrence. Radiotherapy may be recommended after failed transsphenoidal surgery or in Cushing disease with mass effect or invasion of surrounding structures. Medical therapy, such as pasireotide, cabergoline, and mifepristone, are also sometimes used. In addition, the treatment of comorbidities, such as obesity and type 2 diabetes, hypertension, osteoporosis, psychiatric issues, and electrolyte disorders, is critical.

Courtney Whittle, MD, MSW, Diplomate of ABOM, Pediatric Lead, Obesity Champion, TSPMG, Weight A Minute Clinic, Atlanta, Georgia.

Courtney Whittle, MD, MSW, Diplomate of ABOM, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

This patient's clinical presentation and laboratory findings are consistent with a diagnosis of Cushing syndrome (CS).

CS is a rare endocrine disease caused by prolonged exposure to high circulating cortisol levels. Exogenous hypercortisolism is the most common cause of CS. It is largely iatrogenic and results from the prolonged use of glucocorticoids. Less frequently, endogenous CS may occur as the result of excessive production of cortisol by adrenal glands. Endogenous CS can be ACTH-dependent or ACTH-independent. ACTH-dependent CS results from ACTH-secreting pituitary adenomas (Cushing disease) and ectopic ACTH secretion by neoplasms, whereas adrenal hyperplasia, adenoma, and carcinoma are the primary causes of ACTH-independent CS.

The annual incidence and prevalence of CS are unknown; the reported incidence of newly diagnosed cases has ranged from 1.2 to 2.4 per million people per year. Women are affected more often than are men, with a peak of incidence in the third to fourth decade of life. CS is associated with various metabolic, psychiatric, musculoskeletal, and cardiovascular comorbidities. Untreated, it is associated with increased mortality, typically as the result of cardiovascular and infectious complications; however, even in appropriately treated patients, mortality is elevated.

The chronic elevations of glucocorticoid concentrations in CS result in its characteristic phenotype, which includes weight gain, moon-shaped face, buffalo hump, muscle weakness, increased bruising, skin atrophy, red abdominal striae, menstrual irregularities, hirsutism, and acne. It is also associated with numerous comorbidities including diabetes, hypertension, hypercholesterolemia, and osteoporosis. Patients often experience mental health complications, such as depression, emotional lability, and cognitive dysfunction.

Given the rarity of CS and the fact that these symptoms overlap with other conditions, delayed diagnosis is common. The current obesity epidemic also poses diagnostic challenges because true CS can be difficult to differentiate from metabolic syndrome. The duration of hypercortisolism appears to be the most significant factor associated with the degree of morbidity and preterm mortality in CS; thus, an accurate diagnosis as early as possible is important.

Screening and diagnostic tests for CS evaluate cortisol secretion. Available options include late-night salivary cortisol (LNSC), impaired glucocorticoid feedback with overnight 1-mg DST or low-dose 2-day dexamethasone test (LDDT) and increased bioavailable cortisol with 24-hour UFC.

A 2021 consensus statement by Fleseriu and colleagues provides recommendations for the diagnosis of CS. If CS is suspected: begin with UFC, LNSC, or both; DST is an option if LNSC not feasible. If CS because of adrenal tumor is suspected: begin with DST because LNSC has lower specificity in these patients. To confirm CS, any of these tests can be used.

An individualized approach is recommended for the treatment of CS. The optimal approach for iatrogenic CS is to slowly taper exogenous steroids. Chronic exposure to steroids can suppress adrenal functioning; as such, recovery may take several months. Surgical resection is the first-line option for hypercortisolism because of Cushing disease, adrenal tumor, or ectopic tumor. Patients should be closely monitored after surgery to evaluate for possible recurrence. Radiotherapy may be recommended after failed transsphenoidal surgery or in Cushing disease with mass effect or invasion of surrounding structures. Medical therapy, such as pasireotide, cabergoline, and mifepristone, are also sometimes used. In addition, the treatment of comorbidities, such as obesity and type 2 diabetes, hypertension, osteoporosis, psychiatric issues, and electrolyte disorders, is critical.

Courtney Whittle, MD, MSW, Diplomate of ABOM, Pediatric Lead, Obesity Champion, TSPMG, Weight A Minute Clinic, Atlanta, Georgia.

Courtney Whittle, MD, MSW, Diplomate of ABOM, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

This patient's clinical presentation and laboratory findings are consistent with a diagnosis of Cushing syndrome (CS).

CS is a rare endocrine disease caused by prolonged exposure to high circulating cortisol levels. Exogenous hypercortisolism is the most common cause of CS. It is largely iatrogenic and results from the prolonged use of glucocorticoids. Less frequently, endogenous CS may occur as the result of excessive production of cortisol by adrenal glands. Endogenous CS can be ACTH-dependent or ACTH-independent. ACTH-dependent CS results from ACTH-secreting pituitary adenomas (Cushing disease) and ectopic ACTH secretion by neoplasms, whereas adrenal hyperplasia, adenoma, and carcinoma are the primary causes of ACTH-independent CS.

The annual incidence and prevalence of CS are unknown; the reported incidence of newly diagnosed cases has ranged from 1.2 to 2.4 per million people per year. Women are affected more often than are men, with a peak of incidence in the third to fourth decade of life. CS is associated with various metabolic, psychiatric, musculoskeletal, and cardiovascular comorbidities. Untreated, it is associated with increased mortality, typically as the result of cardiovascular and infectious complications; however, even in appropriately treated patients, mortality is elevated.

The chronic elevations of glucocorticoid concentrations in CS result in its characteristic phenotype, which includes weight gain, moon-shaped face, buffalo hump, muscle weakness, increased bruising, skin atrophy, red abdominal striae, menstrual irregularities, hirsutism, and acne. It is also associated with numerous comorbidities including diabetes, hypertension, hypercholesterolemia, and osteoporosis. Patients often experience mental health complications, such as depression, emotional lability, and cognitive dysfunction.

Given the rarity of CS and the fact that these symptoms overlap with other conditions, delayed diagnosis is common. The current obesity epidemic also poses diagnostic challenges because true CS can be difficult to differentiate from metabolic syndrome. The duration of hypercortisolism appears to be the most significant factor associated with the degree of morbidity and preterm mortality in CS; thus, an accurate diagnosis as early as possible is important.

Screening and diagnostic tests for CS evaluate cortisol secretion. Available options include late-night salivary cortisol (LNSC), impaired glucocorticoid feedback with overnight 1-mg DST or low-dose 2-day dexamethasone test (LDDT) and increased bioavailable cortisol with 24-hour UFC.

A 2021 consensus statement by Fleseriu and colleagues provides recommendations for the diagnosis of CS. If CS is suspected: begin with UFC, LNSC, or both; DST is an option if LNSC not feasible. If CS because of adrenal tumor is suspected: begin with DST because LNSC has lower specificity in these patients. To confirm CS, any of these tests can be used.

An individualized approach is recommended for the treatment of CS. The optimal approach for iatrogenic CS is to slowly taper exogenous steroids. Chronic exposure to steroids can suppress adrenal functioning; as such, recovery may take several months. Surgical resection is the first-line option for hypercortisolism because of Cushing disease, adrenal tumor, or ectopic tumor. Patients should be closely monitored after surgery to evaluate for possible recurrence. Radiotherapy may be recommended after failed transsphenoidal surgery or in Cushing disease with mass effect or invasion of surrounding structures. Medical therapy, such as pasireotide, cabergoline, and mifepristone, are also sometimes used. In addition, the treatment of comorbidities, such as obesity and type 2 diabetes, hypertension, osteoporosis, psychiatric issues, and electrolyte disorders, is critical.

Courtney Whittle, MD, MSW, Diplomate of ABOM, Pediatric Lead, Obesity Champion, TSPMG, Weight A Minute Clinic, Atlanta, Georgia.

Courtney Whittle, MD, MSW, Diplomate of ABOM, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The patient is sent for lymphoscintigraphy, which showed impaired lymphatic drainage of both lower extremities consistent with obesity-induced lymphedema. 

Lymphedema is a chronic condition caused by the abnormal development of the lymphatic system (primary lymphedema) or injury to lymphatic vasculature (secondary lymphedema). Chronic interstitial fluid accumulation may lead to fibrosis, persistent inflammation, and adipose deposition, which often results in massive hypertrophy. Obesity, which affects approximately 40% of the US population, is a rising cause of secondary lymphedema. Obesity-induced lymphedema (OIL) is a result of external compression of the lymphatic system by adipose tissue and increased production of lymph, which results in direct injury to the lymphatic endothelium. As BMI increases, lymphedema worsens and ambulation becomes more difficult, placing patients in an unfavorable cycle of weight gain and lymphatic injury. 

The diagnosis of OIL is made by history and physical and is confirmed with diagnostic imaging. The classic presentation of lymphedema is edema of the lower extremities and a positive Stemmer sign. The Stemmer sign is positive if the examiner is unable to grab the dorsal skin between the thumb and index finger. The gold standard for lymphatic imaging is radionuclide lymphoscintigraphy. It involves injecting a tracer protein into the distal extremity, which should be taken up by the lymphatic vasculature and visualized in patients with normal lymphatic function. Lymphoscintigraphy has a high sensitivity (96%) and specificity (100%) for the diagnosis of lymphedema. 

The risk for lymphatic dysfunction increases with elevated BMI. A BMI threshold appears to exist between 53 and 59, at which point lower-extremity lymphatic dysfunction begins to occur and is almost universal when BMI exceeds 60. Sixty percent of patients with OIL will develop massive localized lymphedema; the higher the BMI, the greater the risk for massive localized lymphedema. Typical areas of localized lymphedema include the lower extremities, genitals, and abdominal wall. In addition, patients with OIL are at increased risk for infections, such as cellulitis. Other complications of OIL include functional disabilities, psychosocial morbidity, and malignant transformation. 

Patients at risk for OIL should be counseled and educated about weight management interventions, such as intensive treatment programs, lifestyle changes, and medications before their BMI reaches 50, a threshold where irreversible lower-extremity lymphedema may occur. Although weight loss may reduce symptoms of OIL, irreversible lymphatic dysfunction also may occur. Individuals at risk for OIL are often referred to a bariatric surgical weight management center. 

Lymphedema management consists of compression regimens, physiotherapy, and manual lymphatic drainage. Adipose deposition in the late stages of lymphedema may decrease the response to such manual treatments. Operative procedures are typically used when these treatment options have been inadequate. Patients with chronic advanced lymphedema, in whom lymphatic impairment is accompanied by deposition of fibroadipose tissue, may also require debulking surgery. 

Courtney Whittle, MD, MSW, Diplomate of ABOM, Pediatric Lead, Obesity Champion, TSPMG, Weight A Minute Clinic, Atlanta, Georgia.

Courtney Whittle, MD, MSW, Diplomate of ABOM, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The patient is sent for lymphoscintigraphy, which showed impaired lymphatic drainage of both lower extremities consistent with obesity-induced lymphedema. 

Lymphedema is a chronic condition caused by the abnormal development of the lymphatic system (primary lymphedema) or injury to lymphatic vasculature (secondary lymphedema). Chronic interstitial fluid accumulation may lead to fibrosis, persistent inflammation, and adipose deposition, which often results in massive hypertrophy. Obesity, which affects approximately 40% of the US population, is a rising cause of secondary lymphedema. Obesity-induced lymphedema (OIL) is a result of external compression of the lymphatic system by adipose tissue and increased production of lymph, which results in direct injury to the lymphatic endothelium. As BMI increases, lymphedema worsens and ambulation becomes more difficult, placing patients in an unfavorable cycle of weight gain and lymphatic injury. 

The diagnosis of OIL is made by history and physical and is confirmed with diagnostic imaging. The classic presentation of lymphedema is edema of the lower extremities and a positive Stemmer sign. The Stemmer sign is positive if the examiner is unable to grab the dorsal skin between the thumb and index finger. The gold standard for lymphatic imaging is radionuclide lymphoscintigraphy. It involves injecting a tracer protein into the distal extremity, which should be taken up by the lymphatic vasculature and visualized in patients with normal lymphatic function. Lymphoscintigraphy has a high sensitivity (96%) and specificity (100%) for the diagnosis of lymphedema. 

The risk for lymphatic dysfunction increases with elevated BMI. A BMI threshold appears to exist between 53 and 59, at which point lower-extremity lymphatic dysfunction begins to occur and is almost universal when BMI exceeds 60. Sixty percent of patients with OIL will develop massive localized lymphedema; the higher the BMI, the greater the risk for massive localized lymphedema. Typical areas of localized lymphedema include the lower extremities, genitals, and abdominal wall. In addition, patients with OIL are at increased risk for infections, such as cellulitis. Other complications of OIL include functional disabilities, psychosocial morbidity, and malignant transformation. 

Patients at risk for OIL should be counseled and educated about weight management interventions, such as intensive treatment programs, lifestyle changes, and medications before their BMI reaches 50, a threshold where irreversible lower-extremity lymphedema may occur. Although weight loss may reduce symptoms of OIL, irreversible lymphatic dysfunction also may occur. Individuals at risk for OIL are often referred to a bariatric surgical weight management center. 

Lymphedema management consists of compression regimens, physiotherapy, and manual lymphatic drainage. Adipose deposition in the late stages of lymphedema may decrease the response to such manual treatments. Operative procedures are typically used when these treatment options have been inadequate. Patients with chronic advanced lymphedema, in whom lymphatic impairment is accompanied by deposition of fibroadipose tissue, may also require debulking surgery. 

Courtney Whittle, MD, MSW, Diplomate of ABOM, Pediatric Lead, Obesity Champion, TSPMG, Weight A Minute Clinic, Atlanta, Georgia.

Courtney Whittle, MD, MSW, Diplomate of ABOM, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The patient is sent for lymphoscintigraphy, which showed impaired lymphatic drainage of both lower extremities consistent with obesity-induced lymphedema. 

Lymphedema is a chronic condition caused by the abnormal development of the lymphatic system (primary lymphedema) or injury to lymphatic vasculature (secondary lymphedema). Chronic interstitial fluid accumulation may lead to fibrosis, persistent inflammation, and adipose deposition, which often results in massive hypertrophy. Obesity, which affects approximately 40% of the US population, is a rising cause of secondary lymphedema. Obesity-induced lymphedema (OIL) is a result of external compression of the lymphatic system by adipose tissue and increased production of lymph, which results in direct injury to the lymphatic endothelium. As BMI increases, lymphedema worsens and ambulation becomes more difficult, placing patients in an unfavorable cycle of weight gain and lymphatic injury. 

The diagnosis of OIL is made by history and physical and is confirmed with diagnostic imaging. The classic presentation of lymphedema is edema of the lower extremities and a positive Stemmer sign. The Stemmer sign is positive if the examiner is unable to grab the dorsal skin between the thumb and index finger. The gold standard for lymphatic imaging is radionuclide lymphoscintigraphy. It involves injecting a tracer protein into the distal extremity, which should be taken up by the lymphatic vasculature and visualized in patients with normal lymphatic function. Lymphoscintigraphy has a high sensitivity (96%) and specificity (100%) for the diagnosis of lymphedema. 

The risk for lymphatic dysfunction increases with elevated BMI. A BMI threshold appears to exist between 53 and 59, at which point lower-extremity lymphatic dysfunction begins to occur and is almost universal when BMI exceeds 60. Sixty percent of patients with OIL will develop massive localized lymphedema; the higher the BMI, the greater the risk for massive localized lymphedema. Typical areas of localized lymphedema include the lower extremities, genitals, and abdominal wall. In addition, patients with OIL are at increased risk for infections, such as cellulitis. Other complications of OIL include functional disabilities, psychosocial morbidity, and malignant transformation. 

Patients at risk for OIL should be counseled and educated about weight management interventions, such as intensive treatment programs, lifestyle changes, and medications before their BMI reaches 50, a threshold where irreversible lower-extremity lymphedema may occur. Although weight loss may reduce symptoms of OIL, irreversible lymphatic dysfunction also may occur. Individuals at risk for OIL are often referred to a bariatric surgical weight management center. 

Lymphedema management consists of compression regimens, physiotherapy, and manual lymphatic drainage. Adipose deposition in the late stages of lymphedema may decrease the response to such manual treatments. Operative procedures are typically used when these treatment options have been inadequate. Patients with chronic advanced lymphedema, in whom lymphatic impairment is accompanied by deposition of fibroadipose tissue, may also require debulking surgery. 

Courtney Whittle, MD, MSW, Diplomate of ABOM, Pediatric Lead, Obesity Champion, TSPMG, Weight A Minute Clinic, Atlanta, Georgia.

Courtney Whittle, MD, MSW, Diplomate of ABOM, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.