Although eating disorders are on the psychiatric spectrum, they can have serious associated medical complications. Patients with eating disorders may present with complaints common to the emergency department such as abdominal pain, chest pain, syncope, or palpitations, but management of these conditions in eating disordered patients can pose a challenge. This issue provides a systems-based approach to the history, physical examination, evaluation, and treatment of acute complications of eating disorders, with a specific focus on the pathophysiology and management differences between an otherwise healthy patient and a patient with an eating disorder.
A 14-year-old girl with no known medical problems presents to the ED with worsening epigastric pain for 3 days. The girl says the pain worsens after eating. The patient denies associated symptoms including vomiting, diarrhea, constipation, dysuria, and fever. The patient also denies alcohol consumption, drug use, and sexual activity. Her vital signs are: heart rate, 55 beats/min; blood pressure, 90/50 mm Hg; respiratory rate, 18 breaths/min; and oxygen saturation, 100% on room air. On physical examination, you notice the patient has dry mucous membranes, discolored teeth, and a few scarred callouses on the dorsum of her right hand; the examination is otherwise normal. You are concerned about the patient’s vital signs, perplexed as to why she is not tachycardic despite her low blood pressure, and somewhat surprised that she is denying emesis or diarrhea, given her low blood pressure. You tell the patient’s parents that you will order fluids and some basic laboratory tests and then reassess. About 30 minutes later, the nurse calls you into the room because the patient's oxygen saturation has decreased to 85%, and she is in respiratory distress after completion of the fluid bolus. On auscultation, you hear diffuse crackles bilaterally. You place the patient on bilevel positive airway pressure and perform a bedside ultrasound that shows B-lines in bilateral lungs suggestive of pulmonary edema. A portable chest x-ray also shows evidence of pulmonary edema. Why did this patient rapidly develop pulmonary edema? Did the bolus worsen her condition? What diagnoses should be considered? Are there questions that you should ask the patient privately?
A previously healthy 17-year-old boy presents via ambulance after an episode of syncope during track practice. Per EMS, the patient was getting ready to start practice when he fell to the ground. His coach told them that the boy blacked out for a few seconds, but still had a pulse and did not stop breathing. The boy’s vital signs on arrival to the ED are: heart rate, 60 beats/min, but irregular; blood pressure, 90/50 mm Hg; respiratory rate, 18 breaths/min; temperature, 37°C (98.6°F); and oxygen saturation, 100% on room air. The review of systems is otherwise unremarkable. You are told that the boy’s parents are on their way to the hospital. The patient denies a prior history of syncopal episodes and reports that he remembered his heart was pounding, and the next thing he knew he was on the ground and his coach was standing over him. The boy reports intermittent episodes of palpitations recently, but he denies drug use. He admits he has been stressed about winning an upcoming track meet to secure a scholarship to college and believes the palpitations are secondary to stress. He also reports strict dieting and an increased workout regimen over the past few months. You are concerned about a possible underlying eating disorder, so you use the SCOFF questions as a screening tool. The patient answers “yes" to 2 of the 5 questions on the SCOFF questionnaire. How should the results of the questionnaire guide your diagnosis and the management of this patient? What studies should you order?
The lifetime prevalence of eating disorders in adolescents is 2.7%.1 Anorexia nervosa and bulimia nervosa, specifically, have a lifetime prevalence of 0.5% to 1% and 1% to 3%, respectively. Between 10% and 50% of female teenagers report occasional binge eating and purging behaviors.2 Eating disorders are more common among females than males; anorexia nervosa and bulimia nervosa occur at a 10:1 female-to-male ratio.3,4 Although eating disorders are not as common as other mental illnesses, they are associated with the highest mortality rates, when compared with other psychiatric disorders.5 In a 2009 study in the American Journal of Psychiatry, in which a longitudinal assessment of mortality was conducted, 2.8% of subjects with an eating disorder died of medical causes, followed by suicide (0.7%), substance use-related causes (0.5%), and traumatic causes (0.5%).6
Patients with undiagnosed eating disorders can present with complaints that are common to the emergency department (ED), such as abdominal pain, chest pain, syncope, and/or palpitations. This can make it difficult for the emergency clinician to recognize that these complaints arise from an underlying eating disorder. Likewise, many of the characteristic physical examination findings in patients with eating disorders are easily missed unless the clinician has a high index of suspicion. Failure to recognize an underlying eating disorder can lead to mismanagement and increased mortality if the cause of the complication is not determined and treated.
Managing a patient with a known diagnosis of an eating disorder can also be difficult for emergency clinicians. In a study that examined how comfortable residents from different specialties (including emergency medicine and pediatrics) felt when managing patients with a known eating disorder, participants reported comfort with assessment of these patients but not with management.7
This issue of Pediatric Emergency Medicine Practice outlines the diagnostic criteria for eating disorders, reviews the common—and sometimes subtle—physical examination findings associated with eating disorders, highlights physiologic differences between patients with eating disorders and healthy patients, and discusses the ED management of acute medical complications of eating disorders in pediatric patients.
A literature search was conducted using PubMed; the search terms included emergency care of eating disorders in pediatric patients, emergency care of anorexia and pediatric patients, emergency care of bulimia and pediatric patients, management of eating disorders in the emergency department of pediatric patients, medical complications of eating disorders in pediatric patients, and acute complications of eating disorders in pediatric patients. Abstracts and articles cited within the publications were also reviewed.
Literature on the management of eating disorders in the ED is lacking, especially in the pediatric population. A total of 38 articles were reviewed: 16 review articles, 9 case reports, 5 case-control studies, 1 retrospective study, 1 cross-sectional study, 3 survey studies, 1 comparative study, 1 meta-analysis, and 1 longitudinal study. The greatest limitation of this literature is that the majority of evidence on the management of emergent complications of eating disorders is from case reports and expert clinical opinion.
The etiology of eating disorders involves the interaction of genetics and the environment.8 There is an increased risk of developing an eating disorder among people who are first-degree relatives of someone with an eating disorder. Studies have also shown that rates of anorexia nervosa in monozygotic twins are significantly higher than in dizygotic twins.3 The exact mechanism as to how the genetic component contributes to the risk of developing an eating disorder remains unclear.9,10
Given the increased prevalence of obesity in the United States, there has been an increased focus on diet and exercise for obese children and adolescents, and strict dieting has been cited as a strong risk factor for the development of an eating disorder.11 Athletes, models, and dancers are especially susceptible to developing an eating disorder, given the rewards for a lean body habitus.11 Other environmental factors (eg, childhood sexual or physical abuse) are also cited as risk factors for the development of an eating disorder, especially in association with bulimia nervosa.12
When managing a patient with an eating disorder, maintain a broad differential that includes common diagnoses as well as more serious diagnoses. The differential diagnosis for managing a patient with acute complications of an eating disorder can be found in Table 1; many of the diagnoses listed on the differential are based on the chief complaints. The cause of a complaint of chest pain in a patient with an eating disorder can range from a benign complication to pneumomediastinum, esophageal rupture, pneumothorax, or pulmonary edema. Gastrointestinal complaints can stem from bingeing-purging behaviors or can arise from a common illness such as gastroenteritis.
As with all emergencies, the priority of EMS is to address the patient's airway, breathing, and circulation, and the patient should be transported to the hospital without delay. Currently, there are no established guidelines for the prehospital care of acute complications of eating disorders. Table 2, provides suggestions for the prehospital care of a patient with an eating disorder.
In a study that investigated ED visits among patients with an eating disorder compared to adolescents and young adults without an eating disorder, patients with an eating disorder were 1.6 times as likely to visit the ED at least once a year.13 This highlights the importance of emergency clinicians being prepared to screen for eating disorders, given that the likelihood of successful treatment of an eating disorder and prevention of its complications are directly related to early detection.
Important aspects of the history can be ascertained using the SCOFF questionnaire, which was designed to detect eating disorders.14 (See Table 3.) Implementing a tool such as the SCOFF questionnaire can help identify patients with an eating disorder to aid in appropriate management of acute complications in the ED and to ensure that these patients receive specialized inpatient or outpatient treatment earlier in the course of their disease. Two or more positive responses indicate a possible underlying eating disorder.
Thorough history-taking regarding specific behaviors can help guide a clinician to early diagnosis of an eating disorder. Table 4 outlines the American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) diagnostic criteria for anorexia nervosa and bulimia nervosa.12,15
Growth charts that show growth stunting or failure to make expected gains in weight or height may indicate an underlying eating disorder. Decreases in height or weight percentiles can begin without obvious weight loss.11 Growth stunting can occur if eating disorder behaviors occur prior to the closure of the epiphyses. Additionally, not all patients with an eating disorder are thin. Overweight or obese pediatric patients, especially boys, are at risk for delayed diagnosis and complications.16
Sialadenosis (salivary gland enlargement that begins 3 to 4 days after cessation of excessive self-induced vomiting) may be evident on physical examination.17 The physiology is thought to be due to stimulation of lingual receptors by pancreatic proteolytic enzymes that enter the mouth by vomiting, regurgitation of acidic contents, or the result of bingeing on carbohydrate-dense foods.18 Parotid gland enlargement is seen more often than enlargement of other salivary glands and is usually bilateral.17,18 (See Figure 1.) For information regarding the treatment of sialadenosis, see the "Other Considerations" section.
Dental abnormalities are more commonly found in patients who engage often in self-induced vomiting. The frequent exposure of dentin to stomach acid causes erosive dental lesions, especially on the buccal and lingual surfaces.17 Physical examination may reveal tooth discoloration, dental erosion, or enamel loss. (See Figure 2.)
Patients with an eating disorder who engage in self-induced vomiting may also complain of sore throat or hoarseness. Recurrent episodes of self-induced vomiting allow regurgitated acidic stomach contents to damage structures in the laryngopharynx, including the vocal cords.18
Lanugo (fine, soft hair) is often seen in patients with an eating disorder. The most commonly affected areas are the back, abdomen, and forearms. Lanugo is not to be confused with virilization, as lanugo due to an eating disorder does not usually have a male pattern distribution.19
Perhaps the most characteristic physical examination finding in patients with a purging-type eating disorder is the Russell sign, which are calluses found on the dorsal side of the hand, usually on the patient’s dominant hand. (See Figure 3.) Calluses are formed secondary to trauma from repeated grazing by the teeth as the hand is inserted into the mouth to initiate the gag reflex.19
Due to decreased cardiac muscle mass from malnutrition, patients with an eating disorder have decreased contractility and cardiac output.20 The body compensates for the weakened heart with a lower systolic and diastolic blood pressure, often < 90/60 mm Hg. Therefore, rapid administration of a fluid bolus should be avoided, as it may precipitate heart failure. If fluid administration cannot be avoided, in order to prevent pulmonary edema, the patient’s weight must be considered when determining the appropriate amount for a fluid bolus.
In a study that investigated the cardiac effects of starvation in a group of adolescents with anorexia nervosa, sinus bradycardia was the most common arrhythmia.21 Bradycardia, often in the range of 50 to 60 beats/min, is a consequence of increased vagal tone in patients with an eating disorder; this is the body’s effort to preserve energy in the presence of decreased caloric intake.22 Therefore, emergency clinicians may not need to treat bradycardia in a patient with an eating disorder. Of note, in patients with a known eating disorder, a heart rate of 70 beats/min or higher should be considered tachycardia.15
Patients with an eating disorder often complain of chest pain, which is thought to be related to an underlying mitral valve prolapse. Although cardiac muscle mass decreases, the size of the mitral valve remains the same, leading to prolapse. Mitral valve prolapse is seen in 30% to 50% of patients with moderate to severe anorexia nervosa (weight < 70% of ideal body weight).20 Other serious complications to consider in a patient with an eating disorder who presents with chest pain are Boerhaave syndrome and pneumomediastinum (see the “Gastrointestinal Findings” section, the “Pulmonary Findings” section and the “Surgical Emergencies” section).
Dysrhythmias may be observed in patients with moderate to severe anorexia nervosa. Patients with anorexia nervosa tend to have longer QT intervals, making them more susceptible to torsades de pointes.23 Causes of QT prolongation in this population (QTc > 450 msec in males, > 470 msec in females) include hypokalemia, hypomagnesemia, metoclopramide use, or congenital long QT syndrome.20
There are multiple studies evaluating prolonged QT intervals in patients with an eating disorder and the association with sudden death.23,24 However, more recent studies show that QT dispersion and decreased heart rate variability contribute more to sudden cardiac death than prolonged QT interval alone.20 QT dispersion, the variation between the shortest and longest QT intervals, reflects disorganized ventricular depolarization, which leads to ventricular dysrhythmias. Decreased heart rate variability has also been shown to lead to sudden cardiac death.20
Ipecac syrup may be used by patients with purging-type eating disorders to induce emesis. This medication has been shown to induce potentially reversible cardiomyopathy. Emetine, found in ipecac syrup, is a known cardiotoxic substance. Its use can also cause ventricular dysrhythmias, heart failure, and death. Management includes discontinuing use of ipecac syrup and providing supportive measures.25
Pseudo-Bartter syndrome can be seen in patients with an eating disorder. The renin-angiotensin system is activated in patients who become dehydrated after engaging in purging behaviors, such as with self-induced vomiting, diuretic use, or laxative use. Aldosterone is secreted, sodium and bicarbonate are renally absorbed, and potassium is secreted in the urine. This leads to a hypokalemic metabolic alkalosis. Table 5 lists the electrolyte changes seen in the different types of purging.
Endocrine abnormalities are often seen in patients with anorexia nervosa. These patients tend to have low gonadotropin and sex hormone levels, which can lead to delayed puberty, delayed linear growth, and menstrual dysfunction. They may also have low T4 and T3 levels and, if severely malnourished, patients with an eating disorder may present with sick euthyroid syndrome (normal thyroid function with low thyroid hormone levels),16 which resolves with reversal of the malnourished state.
Patients with an eating disorder may experience reflux-like symptoms such as heartburn, chronic cough, dysphagia, or odynophagia. These symptoms are thought to be secondary to damage caused by repeated exposure of the esophagus to gastric contents in patients who induce vomiting. The gastric contents cause injury to the epithelium of the esophagus, and repetitive vomiting may lead to Barrett esophagus, esophagitis, erosions, ulcers, or bleeding. Barrett esophagus (the changed mucosal lining of the esophagus due to repeated exposure of acidic contents) is a risk factor for esophageal cancer.18
Perhaps the most imminently dangerous consequence of repeated self-induced vomiting is rupture of the esophagus, also known as Boerhaave syndrome. Boerhaave syndrome is a surgical emergency and should be considered in any patient with a purging-type eating disorder who presents with chest pain (especially when yawning), shortness of breath, tachypnea, tachycardia, and severe distress.18
Other gastrointestinal complaints common to patients with an eating disorder include bloating, constipation, nausea, and a sensation of fullness.26 Pathogenesis is a combination of psychopathological distress and dysfunction in gastric motility due to severe malnutrition.27
Another serious consequence of self-induced vomiting, although rare, is pneumomediastinum (alveolar wall rupture). Pneumomediastinum can be seen on chest x-ray or computed tomography (CT) imaging. The risk is thought to be increased in patients with severe malnutrition, causing weakness of the alveolar wall and thinning of the connective tissue. Pneumomediastinum can occur from retching, or even rarer, spontaneously. Patients typically complain of chest pain. Management includes oxygen therapy, surgical consultation, and admission.28,29
Spontaneous or low-impact fractures can occur in patients with an eating disorder. Patients with severe anorexia nervosa commonly suffer from osteoporosis. Therefore, for patients with an eating disorder who complain of back or hip pain, management should include imaging studies.20
Rhabdomyolysis, although uncommon, can also occur in patients with an eating disorder. Patients may complain of muscle pain and weakness.30 Causes of rhabdomyolysis in patients with an eating disorder include hypokalemia due to excessive exercise, malnutrition, or purging with self-induced vomiting, laxatives, or diuretics.
Patients with eating disorders have high rates of mood disorders and substance abuse. In a cross-sectional survey that examined the relationship between eating disorders and mood disorders or substance use in patients aged 14 to 20 years, patients with an eating disorder were 3 times as likely to screen positive for a mood disorder and 2 times as likely to screen positive for substance abuse when compared to controls.31 Understanding of this high prevalence of comorbidities may facilitate early identification of an underlying eating disorder in patients who have not yet been diagnosed.
Table 6 includes suggestions for diagnostic studies to facilitate the management of pediatric patients with acute complications of eating disorders in the ED. All of the tests do not need to be performed on every patient with acute complications of an eating disorder; the clinical picture should guide the choice of diagnostic studies. For example, if a patient with an eating disorder does not complain of abdominal pain, measurement of a serum lipase level would not be needed. Typically, a complete blood cell (CBC) count, comprehensive metabolic panel, and magnesium and phosphorus levels should be considered for patients with an eating disorder who present to the ED. Patients who present with chest pain should be evaluated with an electrocardiogram, chest x-ray, and telemonitoring.
Laboratory abnormalities that may be seen in patients with an eating disorder include elevated transaminases, including elevation in total bilirubin. In rare cases, severe hepatic failure may ensue due to hypoperfusion from severe dehydration. De Caprio et al described a case report of an 18-year-old woman with a history of anorexia nervosa who was found to have severe hepatic failure. In that study, they hypothesized that the acute liver failure was due to hypoperfusion from dehydration, bradycardia, hypotension, and hypothermia.32
Table 7 provides general guidelines for acute management of complications of eating disorders in the ED. Though robust evidence is lacking, general guidance from the literature is based on case reports and expert clinical opinion.
Admission is often required for patients with symptomatic bradycardia or hypotension that may present as presyncope, syncope, dizziness, lightheadedness, fatigue, or exercise intolerance. These patients should be admitted for telemonitoring, especially if their vital signs demonstrate severe bradycardia (< 50 beats/min during the day and < 45 beats/min at night).20
Rapid administration of a fluid bolus should be avoided, as this may precipitate an acute heart failure exacerbation. Hypotension or syncope may be due to an underlying cardiomyopathy rather than dehydration. If fluid administration cannot be avoided, in order to prevent pulmonary edema, the patient’s weight must be taken into consideration when determining the appropriate amount for fluid boluses. The recommended intravenous (IV) bolus is 20 mL/kg normal saline, administered slowly. A heart rate of 80 to 100 beats/min in a previously bradycardic patient may indicate some cardiac stress and impending pulmonary edema, and may warrant cessation of the fluid bolus or decreasing the rate of fluid administration. For flash pulmonary edema, treatment for patients with an eating disorder is similar to that for patients without an eating disorder, and includes the use of diuretics, nitroglycerin, and bilevel positive airway pressure in the appropriate clinical context.
Patients with an eating disorder should be placed on telemetry monitoring, especially patients with severe bradycardia, presyncope, syncope, exercise intolerance, dizziness, or lightheadedness. Atropine is not recommended for bradycardia. Dysrhythmias should be managed with the evaluation and repletion of electrolytes as needed. Specifically, torsades de pointes should be managed in patients with an eating disorder the same way it is managed in patients without an eating disorder (magnesium sulfate 2 g IV bolus). Other important management recommendations include avoidance of QT-prolonging medications, including some antiemetics, and admission with telemonitoring.
One of the main goals of hospital management of patients with an eating disorder is weight gain, specifically in patients with severely low body mass indexes. However, the most dangerous electrolyte complication associated with eating disorders is refeeding syndrome, which occurs upon reintroduction of carbohydrates. Patients who are severely malnourished are constantly in a catabolic state. Introduction of carbohydrates shifts metabolism to an anabolic state, leading to the rapid uptake of phosphorus, potassium, magnesium, glucose, and thiamine. If supplementation of these vitamins and minerals does not occur alongside reintroduction of carbohydrates, severe hypophosphatemia, hypokalemia, hypomagnesemia, and decreased thiamine levels will occur, known as refeeding syndrome. (See Figure 4.)
Associated complications of refeeding syndrome include depressed myocardial sarcomere contractility secondary to depleted adenosine triphosphate levels, ventricular arrhythmias, cardiac arrest, muscle weakness, seizures, respiratory insufficiency, cranial nerve palsy, paralysis, and decreased delivery of oxygen to tissues due to red blood cell dysfunction.33-35
Refeeding should be reserved for inpatient management, and food should therefore be restricted initially. Food restriction may be counterintuitive, but it is recommended while the patient is in the ED unless a nutrition consultation can be made and recommendations followed while the patient is in the ED.
Patients may present to the ED with complications of refeeding if the reintroduction of carbohydrates was initiated at home after a prolonged period of starvation. If refeeding syndrome is evident upon laboratory evaluation of potassium, phosphorus, and magnesium levels, treatment involves supplementation with phosphorus, potassium, magnesium, and thiamine. There are currently no validated guidelines on recommended doses for supplementation or maintenance fluids for the treatment of refeeding syndrome. Recommendations based on expert opinion include IV administration instead of oral supplementation, and fluid administration at the minimal amount required to allow for normal renal function (usually 20-30 mL/kg/day).35 Patients presenting with refeeding syndrome should be admitted to the pediatric intensive care unit.
Diagnosis or suspicion of Boerhaave syndrome should prompt immediate surgical consultation; patients should be given nothing by mouth and admitted to the hospital. Antibiotics should be started to empirically treat mediastinitis. Management of pneumomediastinum includes oxygen supplementation, surgical consultation, and admission.
For a patient with sialadenosis, treatment includes nonsteroidal anti-inflammatory drugs for pain, sialogogues, warm packs, and cessation of self-induced vomiting.17 Hypothermic patients (< 35.6°C, < 96°F) should be treated with a warming blanket (eg, a forced-air warming blanket) with a goal of normothermia. Evaluation of patients who present with musculoskeletal pain should include analysis of creatine kinase level and imaging. Evaluation of patients with rhabdomyolysis should include an assessment of renal injury with evaluation of blood urea nitrogen and creatinine levels. Patients with rhabdomyolysis (creatine kinase > 1000 units/L) with or without renal injury should be admitted. All female patients of childbearing age should have a pregnancy test. All patients who present with a refusal to eat should be admitted due to the risk of continued medical compromise and malnutrition. Arrested growth and development is also an indication for admission. Arrested growth and development occurs when the patient has reached a plateau in weight gain and/or height, which is typically determined using a growth chart. The age of the patient should be considered when assessing for arrested growth and development, as height increase usually stops by age 18 years.
Early consultation with neuropsychiatry and psychiatry is vital, as early management helps improve long-term care and reduce relapse.
There are no established differences in the assessment, imaging, or treatment of the acute complications of eating disorders in pregnant patients. In fact, many women with eating disorders experience remission of symptoms during pregnancy. According to a qualitative study that examined the factors that contribute to remission of symptoms of eating disorders during pregnancy, subjects reported separating their eating disorder from their pregnancy and acceptance of expected weight gain during pregnancy.36,37 The only caution when managing pregnant patients with a history of an eating disorder is in performing imaging studies to assess back or hip pain in a pregnant patient when there is concern for an acute fracture. In this circumstance, magnetic resonance imaging may be the best option.
The decision to admit a patient with an eating disorder is based on comprehensive clinical assessment. If possible, the patient should be admitted to an eating disorder center, as these centers specialize in the treatment of patients with eating disorders. If it is not possible to admit the patient to an eating disorder center or one is not available, the patient can be admitted to the inpatient pediatric floor or pediatric intensive care unit, depending on the clinical condition of the patient. Table 8 lists criteria supporting inpatient hospitalization for patients with an eating disorder.38 Important aspects to consider are physiologic instability, degree of malnutrition based on body mass index, electrolyte disturbances, electrocardiogram abnormalities, and severe medical complications of malnutrition; these factors, if left untreated, can lead to increased morbidity and mortality.
Eating disorders can be difficult to recognize in undiagnosed patients, and they can be difficult to manage even in patients with a known eating disorder. Patients with an eating disorder have a high mortality rate, with the highest risk of death in patients with anorexia nervosa.39 Diagnosis of an eating disorder is based on the history and physical examination findings. The SCOFF questionnaire contains specific questions about the history to help to make the diagnosis. Characteristic physical examination findings can include the Russell sign, dental erosion, enamel loss, and growth stunting or failure to make expected gains in weight or height. Laboratory studies are used to guide management, not to make the diagnosis. Major differences in the management of patients with active eating disorders include: recognizing that a resting blood pressure < 90/60 mm Hg is common; using caution when administering fluid boluses (especially to treat hypotension); having a low threshold for obtaining laboratory studies and an electrocardiogram; liberally imaging patients with chest pain, back pain, or hip pain; and obtaining psychiatric and neuropsychiatry consultations early in management. Refeeding should be reserved for inpatient management. Based on a comprehensive assessment, a decision must be made to admit the patient to an eating disorder center, pediatric ward, pediatric intensive care unit, or to discharge with close outpatient psychiatric follow-up.
Time- and cost-effective strategies in the management of acute complications of eating disorders in pediatric patients include the use of the SCOFF questionnaire to help make the diagnosis, early consultation with neuropsychiatry and psychiatry, food and visitor restriction, telemonitoring, obtaining a baseline electrocardiogram, and early disposition with admission based on criteria listed in Table 8.
1. “I thought he was dehydrated, so I gave him a fluid bolus, and he decompensated.”
Patients with eating disorders may present with hypotension and/or syncope due to an underlying cardiomyopathy rather than dehydration. A large fluid bolus, though indicated if the problem is dehydration, may cause the patient to develop flash pulmonary edema from decompensated heart failure.
2. “She was underweight, so we ordered food.”
Refeeding syndrome can be one of the most dangerous complications of eating disorders. A sudden infusion of carbohydrates in a patient in a catabolic state from chronic starvation can cause sudden electrolyte shifts that can result in arrhythmias or other fatal complications.
3. “He said his palpitations were from anxiety, so I didn’t investigate further.”
Though eating disorders are on the psychiatric spectrum, they do have medical complications. Various arrhythmias, including long QT syndrome, are associated with eating disorders and can worsen with electrolyte shifts or certain medications.
4. “She has presented with chest pain before and previously had a normal chest x-ray.”
Patients with eating disorders often have cardiopulmonary complications, including cardiomyopathies, pneumomediastinum, or Boerhaave syndrome. These findings can be acute and dynamic and may be missed if a chest x-ray is not ordered.
5. “He has been admitted previously for his eating disorder. Now he’s back with more episodes of syncope.”
Eating disorders are chronic psychiatric and medical illnesses. Psychiatry and neuropsychiatry should be involved early in management to improve long-term care and aid in reducing relapses and further ED utilization.
6. “She denied having an eating disorder. How was I expected to diagnose it?”
Examination findings for anorexia nervosa and bulimia nervosa can be subtle and require a high level of suspicion and detailed examination. The mouth and hands should be examined carefully for signs of purging. Lanugo and dry skin can be an indicator of fasting.
7. “He presented with syncope on a hot day. I didn’t even consider an eating disorder.”
Patients with eating disorders often present with complaints common in the ED (eg, abdominal pain, chest pain, and syncope). The diagnosis of an eating disorder cannot be made if it is not added to the differential.
8. “She was obese, so she couldn’t have an eating disorder.”
A minority of patients with eating disorders actually present weighing < 75% of their ideal body weight. Often, these individuals are normal weight for height, or even obese. Trends in growth charts or use of other physical examination findings can help lead to the diagnosis.
9. “He can’t have anorexia, that’s a female problem.”
Though eating disorders are much more common among females, male patients can still present with anorexia nervosa and/or bulimia nervosa. Ignoring the signs or not including eating disorders on the differential for a male patient will only delay diagnosis and could result in greater complications for the patient.
10. “I know what a patient with an eating disorder looks like.”
Research in numerous fields has shown that clinicians have internal biases, causing them to miss diagnoses. Questionnaires such as the SCOFF questionnaire can help illuminate subtle presentations of eating disorders that may have otherwise been missed.
You asked the 14-year-old girl's parents to step out of the room so that you could ask her some questions in private. Once her parents had left, you asked her the SCOFF questions, and she answered “yes” to 3 of the 5 questions (lost > 14 lbs in a 3-month period, felt fat even though she was thin, had thoughts and fears about food and weight dominating her life). The patient also reported self-induced vomiting. You ordered a CBC, BMP, magnesium and phosphorus levels, chest x-ray, and echocardiogram and restricted food and visitors. Further fluid boluses were held. Psychiatry and neuropsychiatry were consulted. The patient was admitted to the PICU on bilevel positive airway pressure.
The 17-year-old boy reported bingeing-purging, with self-induced vomiting. The laboratory studies were notable for mild hypochloremic metabolic alkalosis and hypokalemia, consistent with bingeing-purging behavior. The patient was placed on telemetry. An electrocardiogram showed sinus bradycardia but was otherwise unremarkable. Food was restricted, fluid administration and refeeding were deferred to inpatient management, and psychiatry and neuropsychiatry were consulted.
Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report.
To help the reader judge the strength of each reference, pertinent information about the study is included in bold type following the reference, where available. In addition, the most informative references cited in this paper, as determined by the author, are highlighted.
Rhonda L. Philopena, MD; Erin M. Hanley, MD; Kayla Dueland-Kuhn, MD
Jeffrey R. Avner, MD, FAAP; Nicole Gerber, MD
January 2, 2020
February 1, 2023
4 AMA PRA Category 1 Credits™, 4 ACEP Category I Credits, 4 AAP Prescribed Credits, 4 AOA Category 2-A or 2-B Credits. Specialty CME Credits: Included as part of the 4 credits, this CME activity is eligible for 4 Infectious Disease CME and 0.5 Pharmacology CME credits.
Date of Original Release: January 1, 2019. Date of most recent review: December 15, 2019. Termination date: January 1, 2023.
Accreditation: EB Medicine is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. This activity has been planned and implemented in accordance with the accreditation requirements and policies of the ACCME.
Credit Designation: EB Medicine designates this enduring material for a maximum of 4 AMA PRA Category 1 CreditsTM. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Specialty CME: Included as part of the 4 credits, this CME activity is eligible for 4 Infectious Disease CME and 0.5 Pharmacology CME credits, subject to your state and institutional approval.
ACEP Accreditation: Pediatric Emergency Medicine Practice is also approved by the American College of Emergency Physicians for 48 hours of ACEP Category I credit per annual subscription.
AAP Accreditation: This continuing medical education activity has been reviewed by the American Academy of Pediatrics and is acceptable for a maximum of 48 AAP credits per year. These credits can be applied toward the AAP CME/CPD Award available to Fellows and Candidate Fellows of the American Academy of Pediatrics.
AOA Accreditation: Pediatric Emergency Medicine Practice is eligible for up to 48 American Osteopathic Association Category 2-A or 2-B credit hours per year.
Needs Assessment: The need for this educational activity was determined by a survey of medical staff, including the editorial board of this publication; review of morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; and evaluation of prior activities for emergency physicians.
Target Audience: This enduring material is designed for emergency medicine physicians, physician assistants, nurse practitioners, and residents.
Goals: Upon completion of this activity, you should be able to: (1) demonstrate medical decision-making based on the strongest clinical evidence; (2) cost-effectively diagnose and treat the most critical ED presentations; and (3) describe the most common medicolegal pitfalls for each topic covered.
Discussion of Investigational Information: As part of the journal, faculty may be presenting investigational information about pharmaceutical products that is outside Food and Drug Administration approved labeling. Information presented as part of this activity is intended solely as continuing medical education and is not intended to promote off-label use of any pharmaceutical product.
Faculty Disclosures: It is the policy of EB Medicine to ensure objectivity, balance, independence, transparency, and scientific rigor in all CME-sponsored educational activities. All faculty participating in the planning or implementation of a sponsored activity are expected to disclose to the audience any relevant financial relationships and to assist in resolving any conflict of interest that may arise from the relationship. Presenters must also make a meaningful disclosure to the audience of their discussions of unlabeled or unapproved drugs or devices. In compliance with all ACCME Essentials, Standards, and Guidelines, all faculty for this CME activity were asked to complete a full disclosure statement. The information received is as follows: Dr. Philopena, Dr. Hanley, Dr. Dueland-Kuhn, Dr. Avner, Dr. Gerber, Dr. Mishler, Dr. Claudius, Dr. Horeczko, and their related parties report no significant financial interest or other relationship with the manufacturer(s) of any commercial product(s) discussed in this educational presentation.
Commercial Support: This issue of Pediatric Emergency Medicine Practice did not receive any commercial support.
Earning Credit: Two Convenient Methods: (1) Go online to www.ebmedicine.net/CME and click on the title of this article. (2) Mail or fax the CME Answer And Evaluation Form with your June and December issues to Pediatric Emergency Medicine Practice.
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