Note: This chapter is written to benefit both professional and nonprofessional readers and is geared specifically to anorexia nervosa and bulimia nervosa. The reader is referred to other sources for information on binge eating disorder. An overview of the general medical concerns of these eating disorders is provided, as well as guidelines for a thorough medical assessment, including laboratory tests that must be performed. An in-depth discussion of the problems related to amenorrhea and bone density has also been added to this most recent edition.
Of the entire gamut of psychological disorders treated by clinicians, anorexia nervosa and bulimia nervosa are the ones most frequently punctuated by accompanying medical complications. Although many of these are more annoying than serious, a distinct number of them are indeed potentially life threatening. The mortality rate for these disorders exceeds that found in any other psychiatric illness and approaches 20 percent in the advanced stages of anorexia nervosa. Thus, a clinician cannot simply assume that the physical symptoms associated with these eating disorders are just functional in origin. Physical complaints must be judiciously investigated and organic disease systematically excluded by appropriate tests. Conversely, it is important, from a treatment vantage point, to avoid subjecting the patient to expensive, unnecessary, and potentially invasive tests.
Competent and comprehensive care of eating disorders must involve understanding the medical aspects of these illnesses, not just for physicians but for any clinician treating them, regardless of discipline or orientation. A therapist must know what to look for, what certain symptoms might mean, and when to send a patient for an initial medical evaluation as well as for follow-up. A dietitian will likely be the team member who performs the nutrition evaluation, instead of the physician, and must have adequate knowledge of all medical/nutritional aspects of eating disorders. A psychiatrist may prescribe medication for an underlying mood or thought disorder and must coordinate this with the rest of the treatment.
The eating disorder medical complications that arise vary with each individual. Two persons with the same behaviors may develop completely different physical symptoms or the same symptoms within different time frames. Some patients who self-induce vomiting have low electrolytes and a bleeding esophagus; others can vomit for years without ever developing these symptoms. People have died from ingesting ipecac or excessive pressure on their diaphragms from a binge, while others have performed these same behaviors with no evidence of medical complications. It is critical to keep this in mind. A bulimic woman who binges and vomits eighteen times a day or a 79-pound anorexic can both have normal lab results. It is necessary to have a well-trained and experienced physician as part of the treatment of an eating disordered patient. Not only do these physicians have to treat symptoms that they find, but they have to anticipate what is to come, and discuss what is not revealed by medical lab data.
A physician treating a patient with an eating disorder needs to know what to look for and what laboratory or other tests to perform. The physician must have some empathy and understanding of the overall picture involved in an eating disorder to avoid minimizing symptoms, misunderstanding, or giving conflicting advice. Unfortunately, physicians with special training and/or experience in diagnosing and treating eating disorders are not very common, and furthermore, patients who seek psychotherapy for an eating disorder often have their own family doctors they may prefer to use rather than one the therapist refers them to. Physicians not trained in eating disorders may overlook or disregard certain findings to the detriment of the patient. In fact, eating disorders often go undetected for long periods of time even when the individual has been to a physician. Weight loss of unknown origin, failure to grow at a normal rate, unexplained amenorrhea, hypothyroid or high cholesterol can all be signs of undiagnosed anorexia nervosa that physicians too often fail to act on or attribute to other causes. Patients have been known to have loss of dental enamel, parotid gland enlargement, damaged esophagi, high serum amylase levels, and scars on the back of the hand from self-induced vomiting, and yet still be undiagnosed with bulimia nervosa!
Although there is clearly a continuum in the spectrum of physical illnesses encountered in anorexia and bulimia, with much clinical overlap, the discussions of anorexia and bulimia and their unique medical complications are also useful.
Most medical complications in anorexia are a direct result of weight loss. There are a number of easily observable skin abnormalities that are seen including brittle nails, thinning hair, yellow-tinged skin, and a fine downy growth of hair on the face, back, and arms, which is referred to as lanugo hair. All of these changes revert to normal with weight restoration. There are other, more serious complications involving a variety of systems in the body.
Most anorexics can be treated as outpatients. Inpatient hospitalization is recommended for patients whose weight loss is rapidly progressive or whose weight loss is greater than 30 percent of ideal body weight, as well as for those with cardiac arrhythmias or symptoms of inadequate blood flow to the brain.
The gastrointestinal tract is affected by the weight loss inherent to anorexia nervosa. There are two main issues in this regard.
Complaints of early satiety and abdominal pain. It has been shown by well-performed studies that the transit time of food out of the stomach and through the digestive tract is significantly slowed in individuals with anorexia nervosa. This, in turn, can produce complaints of early satiety (fullness) and abdominal pain. Although it is clearly logical to surmise that such a complaint in this population may be part of the illness and represent an attempt to avoid the psychological pain of beginning to once again eat normally, there may clearly be an organic basis to this concern. A quality, thorough physical examination and evaluation will be able to define the correct source of these complaints. If the complaints are truly organic and no metabolic cause is found to explain them, treatment with an agent that speeds emptying of the stomach should afford the patient relief; reducing the caloric load and rate of refeeding (beginning to eat normally after self-induced starvation) will also be therapeutic. These problems resolve with weight gain.
Complaints of constipation. Many anorexics are troubled by constipation, particularly early on in the refeeding process. This is in part attributable to the slowed gastrointestinal transit time described above. In addition, there is a poor reflex functioning of the colon secondary to a history of inadequate food intake. It is important to keep in mind that complaints of constipation are frequently due to a patient's false perception of what causes constipation. It is important to forewarn these patients from the outset that it normally may take three to six days for food to pass through the digestive system. Thus, it may be impractical to expect a bowel movement the first day after beginning to increase daily caloric intake. In addition to forewarning, it is important to educate patients about intake of adequate liquids and fiber as well as a judicious amount of walking, because the bowel becomes sluggish when an individual is sedentary. An extensive medical workup for constipation is generally unnecessary unless a series of abdominal examinations confirms obstruction and progressive distention (bloating).
Just as the other body systems are affected by weight loss, the cardiovascular system is also not spared. Severe weight loss causes thinning of the heart muscle fibers and a resultant diminished cardiac volume. As a result of this process, there is a reduction in maximal work capacity and aerobic capacity. A slowed heart rate (40 to 60 beats/minute) and low blood pressure (systolics of 70 to 90 mm Hg) are commonly found in these patients. These changes are not dangerous unless there is coexisting evidence of heart failure or an arrhythmia (irregular heartbeat). There is also an increased prevalence of a heart valve abnormality known as mitral valve prolapse. While generally benign and reversible with weight gain, it can produce palpitations, chest pain, and even arrhythmias.
One other cardiac concern is known as the refeeding syndrome. All malnourished patients are at risk for the refeeding syndrome when nutritional repletion is initiated. This syndrome was first des-cribed in survivors of concentration camps after World War II. There are multiple causes for this syndrome. The potential for starvation-induced low blood levels of phosphorus following intake of foods high in calories or glucose is one of the main causes of this sobering syndrome. Phosphorous depletion produces widespread abnormalities in the cardiorespiratory system, which can be fatal. In addition to phosphorous, the refeeding syndrome also evolves due to changes in potassium and magnesium levels. Further, abrupt blood volume expansion and inappropriately aggressive nutritional intake may place excessive strain on the shrunken heart and cause the inability of the heart to maintain adequate circulation.
The crucial issue when refeeding anorexic patients is to identify beforehand which patients may be at risk. Generally speaking, it is the severely emaciated, malnourished patient with prolonged starvation who is at risk for refeeding syndrome. However, in some cases, patients who have been deprived of nutrition for seven to ten days are potentially in this category. There are general guidelines to follow to avoid these problems. The overall general rule in adding calories is "Start low, go slow." It is of extreme importance to monitor electrolytes during the refeeding period and to ensure that they are normal prior to the beginning of refeeding. In severe cases, particularly patients requiring hospitalization or tube feeding, checking electrolytes every two to three days for the first two weeks and then, if stable, decreasing the frequency seems wise. A supplement may be indicated to help avoid phosphorous depletion. From a clinical standpoint, following the pulse and respiratory rates for unexpected increases from the baseline as well as checking for fluid retention are a crucial part of the treatment plan in avoiding refeeding syndrome.
EKG abnormalities are also common in anorexia, such as sinus brachycardia (slow heart rate), which is usually not dangerous. However, some cardiac irregularities can be dangerous, for example, prolonged QT intervals (measurement of electrical impulses) and ventricular dysrhythmia (abnormal heart rhythms). Some have opined that a baseline EKG is therefore indicated to screen for these findings.
In addition to the low white cell count, anorexic patients typically have low body temperature. Thus, the two traditional markers of infection, namely fever and a high white cell count, are often lacking in these patients. Therefore, there has to be heightened vigilance toward the possibility of an infectious process when these patients report some unusual symptom.
The hematological system is thus similar to other body systems that can be ravaged by anorexia nervosa. However, nutritional rehabilitation, if done in a timely and well-planned fashion, in concert with competent medical supervision, promotes a return to normal in all these systems.
Anorexia nervosa can have profound negative effects on the endocrine system. Two major effects are the cessation of menstrual periods and osteoporosis, both of which are physiologically interrelated. While the exact cause of amenorrhea (lack of menstruation) is not known, low levels of the hormones involved in menstruation and ovulation are present in the setting of an inadequate body fat content or insufficient weight. Clearly, there is also an important contribution from the tenuous emotional state of these patients. Reversion to the age-appropriate secretion of these hormones requires both weight gain and remission of the disorder.
Due to the increased risk of osteoporosis seen in eating disordered patients who have amenorhea and to the fact that some studies suggest that the lost bone density may be irreversible, hormone replacement therapy (HRT) has often been suggested for these individuals. In the past, the traditional line of thinking has been that if the amenorrhea persists for longer than six months, HRT should be used empirically if there are no contraindications for such treatment. However, the results of recent research are unclear as to whether (and, if so, when) HRT should take place; consequently there has been much controversy over this issue. For further discussion of this important topic, see "Bone Density" below.
Since the first edition of this book was published, there has been continued research in the area of bone mineral density (bone density) and hormone replacement therapy for eating disordered individuals with amenorrhea. Results have been conflicting. Bone loss or insufficient bone density is an important and possibly irreversible medical consequence of anorexia nervosa and, although less often, of bulimia nervosa as well. Therefore a thorough discussion of the current information is warranted.
There is increasing evidence that peak bone density is reached fairly early in life, at about age fifteen. After this, bone density increases very slightly until about the mid-thirties, when it begins to decline. This means that a teenager who suffers anorexia nervosa for as little as six months may develop a long-lasting bone deficiency. Bone density tests have shown that many twenty- to twenty-five-year-olds with anorexia nervosa have the bone densities of seventy- to eighty-year-old women. Whether bone density deficiency is permanent or whether it can be restored remains unknown.
Postmenopausal versus anorexia-caused bone deficiency. "Results of recent studies from London, Harvard, and other teaching centers are showing that the bone deficiency caused by anorexia is not identical to that of postmenopausal women. The major deficiency in postmenopausal osteoporosis is of estrogen and, to some extent, calcium. In contrast, in anorexia nervosa, chronic low weight and malnutrition often make estrogen ineffective, even when it is present through oral contraceptives" (Anderson and Holman 1997). Other factors that likely contribute to bone density problems in anorexia include inadequate dietary calcium; diminished body fat, which is necessary for the metabolism of estrogen; low body weight; and elevated serum cortisol levels from weight loss and comorbid depression.
Treatment options. Numerous therapeutic interventions are possible, even though there is not yet enough evidence to prove that bone mineral density deficiency resulting from anorexia nervosa can be reversed.
One easy intervention is for patients to take 1,500 mg of calcium per day for restoration. (The current RDA is 1,200 mg per day.)
Weight-bearing exercise is helpful but avoid high-impact cardio exercise, which burns too many calories (interfering with weight gain) and may lead to fractures.
The administration of oral contraceptives or HRT is controversial, as many professionals prefer to wait until the individual gains enough weight for menses to return naturally, particularly for young teens with amenorrhea.
According to researchers at Massachusetts General Hospital in Boston, weight was highly correlated with bone density while estrogen supplementation was not. Dr. David Herzog and his colleagues used bone density screening by dual-energy X-ray aborptiometry (DEXA) and correlates of low bone density among ninety-four women with anorexia nervosa ("Weight, Not Estrogen Use, Correlates with Bone Density" 1999). Bone density was no different in patients who had used estrogen than in those who hadn't been prescribed estrogen. In contrast, a highly significant correlation was established between bone density and body mass index (BMI). Thus, weight, a measure of overall nutritional status, was highly correlated with bone density. This study is indicative of the important and independent effect of malnutrition on bone loss among these patients. It was also noted in this study that more than half of all women with anorexia nervosa have bone loss greater than two standard deviations below normal.
In the January/February 1997 issue of Eating Disorders Review, British researcher Dr. Janet Treasure and her colleagues reported that "anorexia nervosa seems to be associated with a high level of bone resorption that is dissociated from bone formation" (Treasure et al. 1997). Weight gain seemed to reverse this pattern, resulting in increased bone formation and decreased bone resorption. The results also suggested that sufficient intake of calcium and vitamin D (vitamin D stimulates osteoblast activity) may be a component of treatment for osteoporosis caused by anorexia nervosa. See Table 15.1 for steps in managing osteoporosis in patients with chronic anorexia nervosa.
Table 15.1 makes it clear that these researchers do not recommend HRT unless the individual has suffered from anorexia nervosa for more than ten years.
A study on the resumption of menses in teens with anorexia nervosa showed that "(1) return of menses (ROM) does not depend on a patient's percent body fat, and (2) measuring serum estradiol levels may help predict ROM. . . . Neville H. Golden, M.D., and his colleagues at Albert Einstein College of Medicine studied factors associated with ROM. In contrast to the theory that ROM depends on a fixed critical weight, these researchers hypothesized that ROM depends upon restoration of hypothalamic-pituitary-ovarian function. The latter would require nutritional rehabilitation and weight gain, but could occur independently of percent of body weight as fat" (Lyon 1998).
In this study, subjects who regained menses and those who remained amenorrheic also gained weight and increased their BMI. However, "when the authors compared those with ROM and those without, the estradiol levels of the ROM group increased from baseline to follow-up and were significantly related to ROM. The estradiol levels of the subjects who remained amenorrheic did not change. Estradiol levels at or above 110 mmol/1 correctly identified 90 percent of the individuals with ROM and 81 percent of those who remained amenorrheic. The authors point out that these results support the use of serum estradiol levels to assess ROM in adolescents with anorexia" (Lyon 1998). The results of this study suggest that ROM requires restoration of hypothalamic-pituitary-ovarian function and is not dependent on achieving a specific level of body fat. The researchers concluded that the low estradiol levels in anorexia nervosa were due to decreased ovarian production secondary to hypothalamic-pituitary suppression, not to reduced body fat.
Although this research strongly suggests that HRT is not the treatment of choice, one cannot ignore studies like the one published in the November/December 1998 issue of Eating Disorders Review entitled "Dual Hormone Therapy Prevents Bone Loss." According to Baylor researchers, after one year, women who were amenorrheic due to disordered eating or excessive exercising (a condition called hypothalamic amenorrhea) and who received an estrogen-progestin combination had significantly more mineral in their total skeletons and lower spines than the other groups. It is speculated that the estrogen-progestin combination may mimic the hormonal pattern of a normal menstrual cycle and may be warranted until medical care can improve well-being and until normal menstruation returns.
Physicians should also consider prescribing alendronate (Fosa-max®), a recently approved form of bisphosphonate. Differing from estrogen, alendronate has been shown to positively affect postmenopausal osteoporosis by inhibiting bone resorption. Alendronate can be used either in addition to estrogen or in cases where estrogen treatment is not clinically appropriate. However, alendronate often causes gastrointestinal side effects that can be quite distressing to patients with eating disorders.
Clearly, the treatment protocol for eating disordered patients with amenorrhea has not been established. It would be wise at this point to vigorously treat patients whose deficiencies have been long-lasting or severe (i.e., two standard deviations below age-matched norms) using a variety of methods, including HRT and alendronate. Those with less severe deficiencies may be treated by more moderate methods, such as calcium and vitamin D supplements, possibly with the addition of an estrogen-progestin combination if necessary.
Unlike anorexia nervosa, most of the medical complications of bulimia nervosa directly result from the different modes of purging utilized by these patients. It is functionally more understandable if the complications inherent to a particular mode of purging are reviewed separately.
An early complication resulting from self-induced vomiting is parotid gland enlargement. This condition, referred to as sialadenosis, causes a round swelling near the area between the jawbone and the neck and in severe cases gives rise to the chipmunk-type faces seen in chronic vomiters. The reason for parotid swelling in bulimia has not been definitively ascertained. Clinically, in bulimic patients, it develops three to six days after a binge-purge episode has stopped. Generally, abstinence from vomiting is associated with the ultimate reversal of the parotid swelling. Standard treatment modalities include heat applications to the swollen glands, salivary substitutes, and the use of agents that promote salivation, most commonly tart candies. In the majority of cases, these are effective interventions. For stubborn cases, an agent such as pilocarpine, may promote shrinking of the size of the glands. Rarely, parotidectomies (removal of the glands) have to be performed to alleviate this problem.
Another oral complication of self-induced vomiting is perimyolysis. This refers to erosion of the enamel on the surface of the teeth near the tongue, which is presumably due to the presence of the acid in vomit that passes through the mouth. Patients who induce vomiting at a minimum frequency of three times per week for a year will show erosion of tooth enamel. Vomiting may also cause an increased incidence of dental cavities, inflammation of the gums, and other periodontal diseases. At the same time, a frequently voiced complaint of extreme sensitivity to cold or hot food is a result of exposed teeth dentin.
The proper dental hygiene for these patients is somewhat unclear. However, it is obvious that they need to be cautioned against immediately brushing their teeth after vomiting because it will hasten the erosion of the weakened enamel. Rather, rinsing with a neutralizing agent, such as baking soda, has been recommended. Patients should also be encouraged to seek regular dental treatment.
A potentially more serious complication of self-induced vomiting is the damage it causes to the esophagus. These patients complain of heartburn due to the stomach acid's irritant effect on the esophageal lining, which causes a condition known as esophagitis. Similarly, repeated exposure of the esophageal lining to the acidic stomach contents can result in the development of a precancerous lesion referred to as Barrett's esophagus. Another esophageal complication of vomiting presents as a history of vomiting bright-red blood. This condition is known as a Mallory-Weiss tear, which is due to a tear in the mucosal lining.
Aside from encouraging the cessation of vomiting, the approach to complaints that involve dyspepsia (heartburn/sour taste in the mouth) or dysplagia (difficulty swallowing) is comparable to that utilized in the general population with these complaints. Initially, together with the recommendation to cease vomiting, the simple suggestion of antacids is offered. The second level of intervention involves drugs known as histamine antagonists, such as cimetidine, plus an agent that induces gastric contractions such as cisapride, to strengthen the gate between the stomach and the esophagus, which in turn prevents acidic contents from refluxing back and irritating the esophagus. Proton-pump-inhibitors that inhibit acid secretion in the stomach, such as omeprazole, are the third line and most potent therapy for resistant cases. Generally, this will suffice for most patients and resolve their symptoms. The important point to be aware of is the potential harmful implications of severe and stubborn dyspepsia. Since resistant cases may be harbingers of a more serious process, referral to a gastroenterologist should be recommended so that an endoscopy can be performed and a definitive diagnosis made.
One other important condition with regard to the esophagus is Boerhaave's syndrome, which refers to a traumatic rupture of the esophagus due to forceful vomiting. It is a true medical emergency. Patients with this condition complain of the acute onset of severe chest pain that is worsened by yawning, breathing, and swallowing. If this condition is suspected, prompt referral to an emergency room is indicated.
Lastly, vomiting causes two main electrolyte disorders: hypo-kalemia (low potassium) and alkalosis (high blood alkaline level). Either of these, if severe enough, can result in serious cardiac arrhythmia, seizures, and muscle spasms. It does not suffice to place these patients on supplemental potassium, because the body cannot absorb the potassium. The beneficial effects of supplemental potassium are nullified unless there is restoration of the volume status either with intravenous saline or oral rehydration solutions such as Pedialite or Gatorade. One final point about self-induced vomiting: some bulimics use ipecac to induce vomiting. This is dangerous because it is toxic to the heart. Because of ipecac's long elimination time, repeated ingestion can result in potentially fatal cumulative doses. Heart failure and arrhythmia can result.
If the mode of purging is through laxative abuse, there are also potential problems with potassium and acid-base aberrations. It is worth telling patients that laxatives are a very ineffective method to induce weight loss because caloric absorption occurs in the small bowel and laxatives affect the large bowel by promoting the loss of large volumes of watery diarrhea and electrolyte depletion.
The main body system affected by laxatives is the colorectal area. This information refers strictly to stimulant laxatives that contain senna, cascara, or phenolphthalein and directly stimulate colonic activity. These types of laxatives, if used in excess, damage the colonic neurons that normally control gut motility and contractions. The result is an inert, noncontractile tube referred to as the "cathartic colon syndrome." This causes significant problems with fecal retention, constipation, and abdominal discomfort. Loss of colonic function can become so severe that a colectomy (surgery) is needed to treat intractable constipation.
It is crucial to identify laxative abusers early in the course of treatment, before permanent colonic damage has occurred, so that they can be encouraged to seek the assistance of a physician who is adept at withdrawing patients from stimulant laxatives. Laxative withdrawal can be an extremely difficult situation, which is made worse by fluid retention, bloating, and swelling. The mainstays of treatment involve educating patients that it may take weeks to accomplish restoration of normal bowel habits. Patients need to be advised about the importance of ample fluid intake, a high-fiber diet, and judicious amounts of exercise. If constipation persists, a glycerin suppository or a nonstimulating osmotic laxative (works by shifting fluids), such as lactulose, may be useful. Most patients are successfully detoxed with this type of program, but patience is necessary to endure the transient bloating that will resolve in one to two weeks with salt restriction and leg elevation. Progressive abdominal pain, constipation, or distention warrants an abdominal X ray and further evaluation.
Another mode of purging that can produce medical problems is the abuse of diuretics. This mode is infrequently utilized except by medical personnel who may have access to these medications, although they are also available in over-the-counter preparations containing pamabrom, caffeine, or ammonium chloride. The main complication associated with diuretic abuse is fluid and electrolyte imbalance. In fact, the electrolyte pattern is basically the same as that seen with self-induced vomiting, which is potentially dangerous due to heart problems caused by low potassium levels.
There is also a reflexive development of lower leg edema (swelling) with abrupt cessation of diuretic abuse. Generally the edema can be controlled and treated with salt restriction and leg elevation. It is worthwhile to give a brief educational talk to patients with edema explaining that the condition is self-limited and caused by a reaction from the body which diuretics promote, albeit transiently.
Another method used to avoid weight gain and/or promote weight loss is the use of diet pills. Diet pills are not actually considered a form of purging but are used as a compensatory reaction to binge eating in the category of bulimia nervosa known as "nonpurging type." Most diet pills stimulate the sympathetic nervous system and are amphetamine-type derivatives. The adverse effects of diet pills include hypertension (high blood pressure), palpitations, seizures, and anxiety attacks. There is no long-term dependence syndrome associated with the usage of diet pills, and abrupt cessation is medically safe.
Individuals suffering from anorexia nervosa or bulimia nervosa may be troubled with a myriad of medical complications. However, with proper identification and an effective and safe treatment plan, most of these are reversible. Medical management may thus be the building block for a successful psychiatric treatment program.
Aside from an emaciated look in anorexia nervosa, it may be difficult to detect health problems in individuals with eating disorders, especially in the early stages of the illness. Over time, however, individuals who are starving, purging, or taxing the body through excessive exercise take on a generally lackluster appearance.
On close inspection, one can notice things such as dry skin or blotchy red marks on the skin, dry hair, thinning of hair at the scalp, or a general loss of hair altogether. On the other hand, growth of downy hair (lanugo) on the arms or stomach can be detected in extremely thin patients as the body responds to protect itself from the cold when it lacks body fat as an isulator.
One should look for broken blood vessels in the eyes and for swelling of the parotid gland (in the neck below the ear and behind the cheek bone), which is caused by vomiting. Swollen parotid glands are often visible, but they can also be discovered by palpating the parotid glands to check for enlargement. Hypothermia, low body temperature, and bradycardia (irregular pulse) are also common and should be investigated and monitored closely.
All patients should be questioned about and examined for hair loss; cold intolerance; dizziness; fatigue; cracked lips; oligomenorrhea (irregular menstruation) or amenorrhea (lack of menstruation); sleep disturbance; constipation; diarrhea; abdominal bloating, pain, or distension; esophageal reflux; dental erosion; poor concentration; and headaches.
A thorough physical should include questions about the patient's general diet, as well as her preoccupation with food, food fears, carbohydrate craving, and nighttime eating. Asking about these things helps indicate to the patient that all of these issues may directly affect his health.
The physician should also inquire about symptoms related to anxiety (e.g., racing heartbeat, sweaty palms, and nail biting), depression (e.g., hypersomnia and frequent crying spells or thoughts of suicide),obsessive-compulsive disorder (e.g., constantly weighing oneself or food, having to have clothes or other things in a perfect order, obsessing about germs or cleanliness, and having to do things in a certain order or at certain times only). Knowing about these conditions is essential if the physician, as well as the treatment team, are to fully understand the clinical status of each individual and develop a thorough treatment plan.
It is important that a physician orders an "eating disorder laboratory panel" as part of the medical assessment. This panel of tests will include those not routinely performed in a physical exam but which should be done with an eating disordered patient.
Tests generally recommended include:
Which of these tests to run and when to run them are the subject of much debate and should be worked out with the physician. Please see "Bone Density" on page 233 for further information.
Other tests should be selectively performed. These include:
Other tests, such as twenty-four-hour urinary calcium measurements to study calcium intake and absorption, and an osteocalcin study to measure bone activity, may also be considered. It is important for the physician not only to check for any medical complications that must be attended to but also to establish a baseline for future comparisons. It must always be kept in mind that medical tests often fall short of revealing problems until the more advanced stages of the illness. Patients engaging in ultimately dangerous behaviors whose laboratory tests come back normal may get the wrong message. It must be explained to them that the body finds ways to compensate for starvation; for example, decreasing the metabolic rate to conserve energy. It usually takes a long time for the body to break down to the point of serious, life-threatening danger.
Most eating disorder complaints, like headaches, stomachaches, insomnia, fatigue, weakness, dizzy spells, and even fainting do not show up on lab results. Parents, therapists, and doctors too often make the mistake of expecting to scare patients into improving their behaviors by having them get a physical exam in order to discover whatever damage has been done. For one thing, patients are rarely motivated by medical consequences and often have the attitude that being thin is more important than being healthy, or nothing bad is really going to happen to them, or they don't care if it does. Furthermore, patients can appear to be healthy and receive normal lab results even though they have been starving, bingeing, or vomiting for months and, in some cases, years. The following journal entries from patients reveal how disturbing this can be.
When I first was dragged into the doctor's office by my mother when my weight had dropped from 135 to 90 pounds, all my lab tests came back fine! I felt vindicated. I just felt like, "See, I told you so, I'm fine, so leave me alone." My doctor told me then, "You may seem healthy now but these things will show up later. You are doing damage to your body that may not show itself for years." I didn't believe it and even if I did, I felt helpless to do anything about it.
When I went for an exam and lab work I was bingeing and vomiting up to twelve times daily and was also smoking marijuana and snorting cocaine regularly. I was very worried about my health! On the way to the doctor's office I snorted cocaine. When my lab test came back normal, I felt excited thinking, "I can get away with this." In some ways I wish the tests had been worse, I wish they would have scared me, maybe it would have helped me to stop. Now, I feel like since it hasn't done any damage, why stop. I know I am damaging myself, my voice is raspy and my salivary glands are swollen from the constant acid wash of the vomit. My skin is grayish and my hair is falling out, but . . . my lab tests were fine!
A NOTE ON BINGE EATING DISORDER
Managing binge eating disorder patients most likely involves the same medical considerations to be taken into account when treating obese individuals, such as heart or gallbladder disease, diabetes, high blood pressure, and so on. Most symptoms of binge eating will be a result of the accompanying weight gain associated with this disorder. Occasionally people have binged to the point of becoming breathless when their distended stomachs press up on their diaphragms. In very rare cases a medical emergency may occur if the stomach wall becomes so stretched that it is damaged or even tears. The reader is referred to other sources on obesity and binge eating disorder for further information on this topic.
One last aspect of medical management involves the use of medication to treat the coexisting psychological conditions that cause or contribute to eating disorders. Prescribing and managing this type of medication are sometimes undertaken by the family physician or internist but is more often relegated to a psychiatrist who has special training in psychopharmacology. The information regarding mind- altering medication for use with eating disorders is extensive and is covered in chapter 14.