Abstract
Eating disorders may result in medical complications that affect every body system with both acute and chronic consequences. Although some medical complications may require acute medical hospitalization to manage, other complications, such as low bone mineral density, may not present until malnutrition has become chronic. It is critical for team members to be aware of the early clinical signs of malnutrition and disordered eating behaviors, as well as longer-term complications that may affect their patients. When identifying eating disorder concerns, appropriate colleagues from the medical, nutrition, and psychiatric fields can be engaged in order to collaborate on stabilizing and improving the health of patients.
Keywords: Feeding and Eating Disorders, Anorexia Nervosa, Bulimia Nervosa, Medical Complications
Medical complications of eating disorders involve every organ system and can affect individuals both acutely and chronically (1–4). These clinical manifestations can result from starvation and malnutrition (at all weights), purging behaviors, or binge eating. Malnutrition can result from both intentional restriction of caloric intake, as seen in restrictive-type anorexia nervosa (AN), or in a relative insufficient caloric intake that can occur when an individual does not consume enough energy to compensate for their energy expenditures, as seen in relative energy deficiency in sport or the athlete triad (5). If a large amount of weight has been lost (weight suppression), regardless of an individual’s specific weight, as seen in atypical AN, they are at increased risk of medical complications (6, 7). The longer it takes to restore and stabilize an individual’s weight, the greater the risk of more chronic medical manifestations.
Contrary to many historical depictions, patients with eating disorders may be of any racial-ethnic background and may present at any age (8–12). Males, as well as sexual and gender minority individuals, are being recognized as at risk for eating disorders and are a focus of more recent research efforts (13–17). Although disordered eating behaviors in marginalized populations may have unique underpinnings, the resultant medical sequelae of malnutrition and extreme weight loss behaviors are predictable and important to recognize.
Given that individuals with eating disorders may present initially to a psychiatric provider or already be in treatment for a comorbid mood disorder, psychiatric providers play an important role in the identification and management of eating disorders. Being aware of the potential medical complications may enable a provider to better advocate for their patient’s health. Engagement with a multidisciplinary team can be critical to successful treatment of individuals with eating disorders.
Medical Complication of Eating Disorders
Electrolyte Abnormalities
There are no specific laboratory tests that accurately indicate the presence or severity of disordered eating behaviors. The body often does an impressive job maintaining normal electrolyte values, even in severe starvation (18). Thus, patients with restricting-type AN or avoidant/restrictive food intake disorder (ARFID) typically have normal electrolyte values (19, 20). Patients who engage in purging behaviors, however, are more likely to have electrolyte abnormalities (20, 21). Electrolyte abnormalities without another explanation may warrant screening a patient for a concealed eating disorder (22).
Hyponatremia (low sodium) can result from dehydration, such as in purging disorders (due to fluid loss from vomiting, use of laxatives, and diuretic effects) (21). Low sodium levels can also be caused by water loading and excessive water intake, or restriction of water and sodium intake, as can be seen in restricting-type AN (21, 23). Hypokalemia (low potassium) in patients with eating disorders is usually caused by purging behaviors (from renal and/or gastrointestinal losses) (24, 25). Dietary deficiencies of potassium are rare. Hypokalemia, hypochloremia, or a metabolic alkalosis present in a patient who reports (only) restriction, may warrant probing further about purging behaviors (21).
Refeeding syndrome describes the metabolic changes and the shifts in fluid and electrolytes that take place during the first stage of nutritional rehabilitation of a patient who is malnourished (26). It is caused by an increased glucose load that leads to a surge in insulin, which stimulates protein synthesis and the intracellular movement of potassium, magnesium, and phosphate. The clinical signs of refeeding syndrome include muscle weakness, edema, gastrointestinal complications, delirium, cardiac and/or respiratory failure, and, in rare cases, death (1, 27). Laboratory findings include hypophosphatemia, hypoglycemia, hypomagnesemia, hypokalemia, and hyponatremia (28). Refeeding syndrome risk corresponds directly with the degree of weight loss and malnutrition; see the guidelines for hospitalization and/or inpatient management in the following text (26, 29).
Cardiovascular Complications
Bradycardia and hypotension are common findings in patients with restrictive eating disorders (30). Patients who are malnourished have low resting heart rates, but typically become tachycardic with minimal exertion (in contrast with conditioned athletes, in which heart rate remains low) (31, 32). Orthostatic hypotension can cause syncope. There may be increased prevalence of positional orthostatic tachycardia syndrome, although most orthostatic heart rate changes and autonomic dysregulation will eventually improve with weight restoration and resolution of malnutrition (32, 33). QTc prolongation can be found in patients with eating disorders related to factors such as hypokalemia or medication effects and may increase risk of torsades de pointes and sudden death (important to consider when prescribing other psychotropic medications that can prolong QTc) (34). Significant weight loss can cause cardiac structural changes—including left ventricular atrophy, mitral valve prolapse, and myocardial fibrosis (30). Pericardial effusion occurs in 22%–25% of patients with AN, although most patients remain asymptomatic (35, 36).
Gastrointestinal Complications
A wide range of gastrointestinal complaints are prevalent in patients with eating disorders—attributable to restriction or specific purging behaviors (37, 38). In patients with ARFID, the fear of gastrointestinal symptoms can contribute to disordered eating (39). Weight loss can cause gastroparesis (delayed emptying of the stomach), which can lead to bloating and early satiety and sometimes nausea, reflux, and vomiting (38). Symptoms of gastroparesis typically resolve with weight restoration (40). Weight restoration and regular eating patterns will also help to relieve constipation. Patients may experience gastroesophageal reflux, either from the effects of self-induced vomiting or from gastroparesis (41). AN often causes elevated liver transaminase levels, both prior to and during refeeding, and may correspond to illness severity (42). In bulimia nervosa, use of stimulant laxatives may cause bowel dependency, and discontinuing their use can lead to constipation and fluid retention (38). In some cases, other causes of gastrointestinal symptoms should be considered; studies have shown an association between AN and celiac disease, as well as between AN and inflammatory bowel disease (43, 44).
Endocrine Complications
Individuals with eating disorders experience many endocrine abnormalities (45). Malnutrition causes reduction of hepatic glycogen stores and disturbance of hepatic gluconeogenesis, which results in hypoglycemia (46, 47). Severe hypoglycemia in restrictive eating disorders has been associated with sudden death and indicates a need for nutritional rehabilitation in an inpatient setting (46, 48). Thyroid abnormalities in AN are usually consistent with euthyroid sick syndrome (low total thyroxine [T4] and triiodothyronine [T3], but normal thyroid-stimulating hormone [TSH]) (46–48).
With nutritional restriction, hypothalamic dysfunction, from interruption in pulsatile gonadotropin-releasing hormone signaling, leads to decreased gonadotropins (luteinizing hormone/follicle-stimulating hormone) and gonadal hormones (estrogen, progesterone, and testosterone) and hypothalamic amenorrhea (48). Irregular menstrual cycles are also common in bulimia nervosa and binge eating (49, 50). Recent studies have shown that individuals with AN also experience elevated serum cortisol levels (due to decreased clearance) (46, 48). These hormonal changes lead to increased bone resorption and decreased bone formation. Low bone density (osteopenia and osteoporosis) is a frequent and serious complication of eating disorders, which leads to increased fracture risk in both adolescents and adults (51–54).
A unique consideration of the child and adolescent population is the effect of malnutrition on growth and development. As puberty represents a time of significant growth, insufficient caloric intake can disrupt linear growth, as well as delay or halt normal pubertal progression. Although many of these issues can improve with normalized nutrition, it is unclear as to whether an individual will meet growth and bone potential (55, 56).
Neuropsychiatric Complications
Comorbid psychiatric diagnoses (including depression, anxiety, obsessive-compulsive disorder, and substance use disorder) are common among patients with eating disorders (57, 58). In addition, many of the psychological changes seen in patients with eating disorders can be attributed directly to the effects of starvation. The Minnesota Starvation Study by Keys et al. (1950) found that prolonged semistarvation produced increases in depression, preoccupation with food, and social isolation (59). Brain volume losses of both white and gray matter occur due to malnutrition and weight loss (60, 61). Although weight gain results in the restoration of white matter to premorbid levels, studies have shown that gray matter volume loss can remain in some cases—and potentially contribute to deficits in long-term cognitive function (62, 63).
Evaluation
The initial evaluation of a patient with a suspected eating disorder should include assessment of medical and psychiatric stability. Potential complications can be discovered by obtaining a detailed history and physical examination and suggested laboratory and diagnostic studies (1–4, 64). These findings will inform as to whether a patient may require urgent hospitalization or is stable enough to pursue outpatient treatment.
History
During an eating disorder evaluation, queries should assess weight history (including highest, lowest, and goal weight), body image concerns, diet and exercise history, and purging behaviors (1–4). Purging behaviors include vomiting, diet pill use, excessive caffeine or laxative use, or excessive exercise engagement. Individuals may be less likely to disclose these behaviors, so it is prudent to ask about them specifically. A targeted review of systems is helpful for assessing possible medical complications that might be the result of disordered eating practices. Disclosures of dizziness, fatigue, difficulty in concentrating, heart palpitations, constipation, and abdominal pain are not unusual among patients with malnutrition and may warrant more immediate medical attention. With functional hypogonadism, individuals may report irregular or missed menses, lower libido, or decrease in either erections and/or nocturnal emissions. Although issues of functional hypogonadism are not medical emergencies, they are often a significant concern for the older adolescent and adult population. Mood dysregulation, increased anxiety, and increased irritability are commonly reported concerns that may be secondary to or increased by malnutrition.
Physical Examination
Weight, height, and vital signs are key components of the physical examination that will be used to determine medical stability. For children and adolescents, growth curves are critical for assessing the current degree of malnutrition, as well as the degree of weight and growth suppression. Because children have increasing body mass index (BMI) goals as they age and progress through puberty, an unchanged weight, without weight loss, may be indicative of restrictive eating and malnutrition. Due to the importance of reviewing BMI relative to expected growth for a patient’s age, “percentage of median BMI” or “BMI Z-score” is the preferred nomenclature when discussing growth in children and adolescents (4, 65). Percentage of median BMI is calculated as current BMI divided by the 50th percentile BMI for age (based on the growth chart standard), multiplied by 100 (4). In addition to percentage of median BMI, the degree of malnutrition may also be classified according to the amount of weight loss in both magnitude and rapidity (4). For example, a patient may be at the 50th percentile for their current BMI, but still be considered severely malnourished if they have lost greater than 5% of their body weight in the past month (4).
Vital sign measurements include temperature, pulse, and blood pressure readings (1–4). Ideally, pulse and blood pressure are measured in two positions, supine and standing, so that orthostatic changes can be calculated. Supine measurements should be taken after a patient has been lying down for 5 minutes. Upon completion of the supine measurement, the patient should stand for 2 minutes and have vital signs repeated.
A comprehensive physical examination is recommended as part of the initial evaluation; however, it may be limited within the context of a psychiatry visit. Despite potential limitations, several important examination findings can be assessed by visual inspection. These include thin body habitus or appearance of weight loss; unsteadiness with standing or walking; thinning or loss of hair or appearance of fine hair on the arms or torso (lanugo); pallor or yellow discoloration to the skin that is particularly noticeable on the palms (hypercarotenemia); facial fullness resulting from parotid hypertrophy; and finger abrasions, known as Russell’s sign, from scraping of the teeth during induced vomiting.
Laboratory and Diagnostic Studies
Depending on the clinical scenario, laboratory evaluation is recommended to assess for primary etiologies that may be underlying malnutrition, as well as medical sequelae resulting from malnutrition (see Table 1 [1–4]). Since other medical diagnoses can present with symptoms similar to eating disorders (such as brain tumors, inflammatory bowel disease, thyroid disease), working closely with a medical clinician to ensure a thorough, but targeted, evaluation is essential for an accurate diagnosis. Restrictive consumption of calories and nutrients can result in vitamin and mineral deficiencies, such as low vitamin D or ferritin, that require specific supplementation upon identification. Vomiting or use of laxatives and diuretics may result in electrolyte imbalances such as severe hypokalemia, which may warrant immediate medical attention.
TABLE 1.
Recommended laboratory studies to consider when evaluating for an eating disordera
| Laboratory test | Specific testing suggestions | Potential findings |
|---|---|---|
| Complete blood count (CBC) | | Anemia, leukopenia, thrombocytopenia may be present due to malnutrition. |
| Electrolytes | Complete metabolic panel | With purging, may have low potassium, elevated CO2. With water-loading, may have low sodium. With refeeding syndrome, may have low potassium, magnesium, and/or phosphorus. |
| Liver function tests | AST, ALT | With malnutrition or refeeding syndrome, may have elevated AST and ALT. |
| Thyroid tests | TSH, free T4, total T3 | May have low total T3 due to malnutrition. Abnormal TSH and free T4 can be seen with euthyroid sick syndrome. |
| Erythrocyte sedimentation rate (ESR) | | If elevated, should consider other etiologies to weight loss. |
| Sex hormone assessment | FSH, LH, estradiol, testosterone | May be low due to malnutrition. |
| 25-OH vitamin D | | May be low due to malnutrition. |
| Iron levels | Total iron, ferritin | May be low due to malnutrition. |
| Vitamin B12 | | May be low due to malnutrition. |
| Zinc | | May be low due to malnutrition. |
25-OH, 25-hydroxy vitamin D; CO2, carbon dioxide; AST, aspartate transaminase; ALT, alanine aminotransferase; TSH, thyroid-stimulating hormone; T4, thyroxine; T3, triiodothyronine; FSH, follicle-stimulating hormone; LH, luteinizing hormone.
Initial diagnostic studies will vary on the basis of clinical concerns for each patient. At a minimum, an electrocardiogram should be obtained to assess for any conduction abnormalities such as bradycardia or prolonged QTc interval (1–4). A bone dual-energy X-ray absorptiometry (DXA) may be obtained if there are concerns regarding potential low bone mineral density following prolonged amenorrhea, typically defined as more than 6 months of no menses (66). DXA recommendations for males are not as clear and still require additional evidence-based recommendations (51). In children with growth suppression, a bone age may be obtained to better interpret their current growth status and to assess their future growth potential.
Management
One of the first steps in medical management is determining whether a patient is suitable for outpatient care or requires an inpatient admission. When determining medical stability, multiple societies have recommendations for vital signs, BMI, and laboratory findings that could indicate the need for an inpatient medical admission (1–4). Vital sign and laboratory or diagnostic instabilities that may warrant an inpatient medical admission include bradycardia (heart rate of less than 50 beat per minute during the day); hypotension (blood pressure of less than 90/45 mmHg in adolescents, less than 90/60 mmHg in adults); orthostasis by pulse (change in pulse of more than 40 beats per minute in adolescents, more than 30 beats per minute in adults, when moving from a supine to standing position); orthostasis by blood pressure (drop in systolic blood pressure of more than 20 mmHg in both adolescents and adults when moving from a supine to a standing position); BMI (less than 75% median BMI in children and adolescents, BMI less than 15 kg/m2 in adults); electrocardiogram abnormalities (such as prolonged QTc); and electrolyte disturbances.
Generally, most patients with eating disorders can be safely managed in the outpatient setting. However, if an individual is bradycardic, hypotensive, orthostatic, or has laboratory or electrocardiogram abnormalities, it is important to either review the clinical concern with an appropriate inpatient provider or refer the patient to their primary care clinician, urgent care clinic, or emergency department for evaluation.
Comprehensive management from a multidisciplinary team is recommended for individuals with eating disorders (1–4). In addition to stabilizing the medical status, goals of management include normalizing eating behaviors as well as building a more positive body image and relationship with food. The outpatient team may be comprised of a medical provider, dietician, psychotherapist, and psychiatrist, as needed. Other essential team members, depending on the social situation of the individual, may include parents and partners, as well as key support individuals such as coaches. Typically, with nutrition stabilization and weight restoration, most medical complications secondary to malnutrition will resolve. However, ongoing medical surveillance and management may be warranted for specific issues, such as bone health, given its longer-term effects.
Conclusions
Early identification and targeted intervention for individuals with eating disorders is key to successful treatment. Psychiatrists and psychotherapists may be the first point of contact with the health care system for patients, so it is critical to recognize concerning symptoms and understand when to engage additional medical support.
Footnotes
Dr. Lemly reports being Supervising Physician with Equip Health. Dr. Carlson reports no financial relationships with commercial interests.
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