Coronary bypass surgery

This article is requested by Mr. Ayoub Motaeri Nejad.

Definition
Coronary bypass surgery is a procedure to allow blood to flow to your heart muscle despite blocked arteries. Coronary bypass surgery uses a healthy blood vessel taken from your leg, arm, chest or abdomen and connects it to the other arteries in your heart so that blood is bypassed around the diseased or blocked area. After a coronary bypass surgery, normal blood flow is restored. Coronary bypass surgery is just one option to treat heart disease.

Just like all the other organs in your body, your heart needs blood and oxygen to do its job. Coronary arteries snake across the surface of your heart, delivering a constant supply of blood and oxygen to the heart muscle. When one or more of these arteries become narrowed or blocked, blood and oxygen are reduced and heart muscle is damaged. Coronary bypass surgery can minimize this damage.

Why it's done
If lifestyle changes and medication haven't relieved your heart disease symptoms of angina, or if you have life-threatening blockages, you and your doctor will need to consider whether coronary bypass surgery or another artery-opening procedure such as angioplasty or stenting is right for you.
Coronary bypass surgery is an option if:
You have severe chest pain caused by narrowing of several of the arteries that supply your heart muscle, leaving the muscle short of blood during even light exercise or at rest. Sometimes angioplasty and stenting will bring relief in this situation, but for some types of blockages, coronary bypass surgery may be the best option.
You have more than one diseased coronary artery and the heart's main pump — the left ventricle — is not functioning well.
Your left main coronary artery is severely narrowed or blocked. This artery supplies most of the blood to the left ventricle.
You have an artery blockage for which angioplasty isn't appropriate, you've had a previous angioplasty or stent placement that hasn't been successful, or you've had stent placement but the artery has narrowed again (restenosis), then your doctor may recommend coronary artery bypass surgery.
Coronary bypass surgery doesn't cure the underlying heart disease that caused blockages in the first place. This disease is referred to as atherosclerosis or coronary artery disease. Even if you have coronary bypass surgery, lifestyle changes are still a necessary part of treatment after surgery. Medications are routine after coronary bypass surgery to lower your blood cholesterol, reduce the risk of developing a blood clot and help your heart function as well as possible.

Risks
Although they rarely occur, the most common complications of coronary bypass surgery are:
1. Bleeding
2. Heart rhythm irregularities (arrhythmias)
3. Kidney failure
4. Infections of the chest wound
5. Memory loss or troubles with thinking clearly, which often go away within six to 12 months
6. Stroke
Your risk of developing these complications depends on your health before the surgery. Talk to your doctor to get a better idea of the likelihood of experiencing these risks.
If you're having a scheduled coronary bypass surgery, your risk of death is usually low, but still depends on your overall health. The risk is higher if the operation is done as an emergency or if you have other significant medical conditions such as emphysema, kidney disease, diabetes or peripheral vascular disease.

How you prepare
To prepare for coronary bypass surgery, your doctor will give you specific instructions about any activity restrictions and changes in your diet or medications you should follow before surgery. You'll need several presurgical tests, often including chest X-rays, blood tests, an electrocardiogram and a coronary angiogram, which is a special type of X-ray procedure that uses dye to visualize the arteries that feed your heart. Most people are admitted to the hospital the morning of the day of surgery.
Be sure to make arrangements for the weeks following your surgery. It will take about four to six weeks for you to recover to the point when you can resume driving, going to work and performing daily chores.

What you can expect
During the procedureCoronary bypass surgery generally takes between three and six hours and requires general anesthesia. On average, surgeons repair two to four coronary arteries. The number of bypasses required depends on the location and severity of blockages in your heart.
Most coronary bypass surgeries are done through a large incision in the chest while blood flow is diverted through a heart-lung machine (called on-pump coronary bypass surgery).
The surgeon makes an incision down the center of the chest, along the breastbone. The rib cage is spread open to expose the heart. After the chest is opened, the heart is temporarily stopped and a heart-lung machine takes over blood circulation to the body.
The surgeon takes a section of healthy blood vessel, often from inside the chest wall (the internal mammary artery) or from the lower leg, and attaches the ends above and below the blocked artery so that blood flow is diverted (bypassed) around the narrowed portion of the diseased artery.
There are other methods your surgeon may use if you're having coronary bypass surgery:
1. Off-pump or beating-heart surgery. This procedure allows surgery to be done on the still-beating heart using special equipment to stabilize or quiet the area of the heart the surgeon is working on. This type of surgery is challenging because the heart is still moving. Because of this, it's not an option for everyone. The long-term outcome of this type of procedure is not yet known, and there have been no proven benefits of this technique over standard coronary bypass using the heart-lung machine in the average patient.
2. Minimally invasive surgery. In this procedure, a surgeon performs coronary bypass through a smaller incision in the chest, often with the use of robotics and video imaging that help the surgeon operate in a small area. Variations of minimally invasive surgery may be called port-access or keyhole surgery.
Once you're anesthetized, a breathing tube is inserted through your mouth. This tube attaches to a ventilator, which breathes for you during and immediately after the surgery.
After the procedureCoronary bypass surgery is a major operation. Expect to spend a day or two in the intensive care unit after coronary bypass surgery. Here, your heart, blood pressure, breathing and other vital signs will be continuously monitored. Your breathing tube will remain in your throat for a few hours after surgery, so you won't be able to speak. You can communicate with hand gestures and notes. The breathing tube will be removed as soon as you are awake and able to breathe on your own.
Barring any complications, you'll likely be discharged from the hospital within a week, although even after you've been released, you may find it difficult to perform everyday tasks, or even walk a short distance. If, after returning home, you experience any of the following signs or symptoms, call your doctor. They could be warning signs that your chest wound is infected:
1. A fever higher than 100.4 F (38 C)
2. Rapid heart rate
3. New or worsened pain around your chest wound
4. Reddening, bleeding, or other discharge from your chest wound
Expect a recovery period of about six to 12 weeks. In most cases, you can return to work, begin exercising, and resume sexual activity after six weeks, but make sure you have your doctor's OK before doing so.

Results
After surgery, most people have improvement or complete relief of their symptoms and remain symptom-free for as long as 10 to 15 years. Over time, however, it's likely that other arteries or even the new graft used in the bypass will become clogged, requiring another bypass or angioplasty.
Although bypass surgery improves blood supply to the heart, it doesn't cure underlying coronary artery disease. Your results and long-term outcome will depend in part on following healthy lifestyle recommendations and taking your medication as directed. Healthy lifestyle recommendations include:
1. Stop smoking.
2. Follow a healthy-eating plan, such as the DASH diet.
3. Reduce cholesterol levels.
4. Maintain a healthy weight.
5. Control blood pressure.
6. Manage diabetes.
7. Exercise.

Ref: Mayo clinic

The Outcome of Anorexia Nervosa in the 20th Century

Review and Overview by Hans-Christoph Steinhausen, M.D., Ph.D

http://ajp.psychiatryonline.org/

Abstract

OBJECTIVE: The present review addresses the outcome of anorexia nervosa and whether it changed over the second half of the 20th century. METHOD: A total of 119 study series covering 5,590 patients suffering from anorexia nervosa that were published in the English and German literature were analyzed with regard to mortality, global outcome, and other psychiatric disorders at follow-up. RESULTS: There were large variations in the outcome parameters across studies. Mortality estimated on the basis of both crude and standardized rates was significantly high. Among the surviving patients, less than one-half recovered on average, whereas one-third improved, and 20% remained chronically ill. The normalization of the core symptoms, involving weight, menstruation, and eating behaviors, was slightly better when each symptom was analyzed in isolation. The presence of other psychiatric disorders at follow-up was very common. Longer duration of follow-up and, less strongly, younger age at onset of illness were associated with better outcome. There was no convincing evidence that the outcome of anorexia nervosa improved over the second half of the last century. Several prognostic features were isolated, but there is conflicting evidence. Most clearly, vomiting, bulimia, and purgative abuse, chronicity of illness, and obsessive-compulsive personality symptoms are unfavorable prognostic features. CONCLUSIONS: Anorexia nervosa did not lose its relatively poor prognosis in the 20th century. Advances in etiology and treatment may improve the course of patients with anorexia nervosa in the future.

Introduction
Anorexia nervosa received its present name only in the late 19th century (1). In the 20th century, critical analyses of epidemiological data showed that a true increase in the incidence and prevalence rates of anorexia nervosa over time was questionable (2, 3). Currently, the etiology of anorexia nervosa is not fully understood, with present models emphasizing its multifactorial origin, coupled with multiple determinants and risk factors and their interactions within a developmental framework (3).
Treatment of anorexia nervosa shifted in the second half of the 20th century from a purely medical approach that included reliance on neuroleptics in the 1950s and 1960s to a strong emphasis on individual psychotherapy (4), taking into account both a developmental and a biological framework (5) and the need for a multifaceted treatment approach (6). Later, both behavioral and cognitive interventions were added to treatment programs (7). In younger patients, the inclusion of family therapy has been advocated since the 1970s (3, 8). At the end of the 20th century, medications played a role in the treatment of some patients with anorexia nervosa, but they have been rarely used as the exclusive mode of intervention (9).
Selection criteria for the inclusion of studies in the present review were the following: 1) the study contained data on at least one of 15 outcome measures, and/or 2) the study contained data on any prognostic factor. Previous reviews of the outcome of anorexia nervosa by my associates and myself covered 45 studies (with 46 series of patients) published between 1953 and 1989 (10–56) and 23 additional follow-up studies (with 24 series of patients) published between 1981 and 1989 (57–80). Furthermore, Fichter and Quadflieg (81) discussed 22 additional series of anorectic patients (82–99; unpublished 1991 paper presented by Halmi). In addition to these three reviews, and based on a systematic search with PUBMED, I identified an additional 27 series of patients in outcome studies published between 1993 and 1999 (100–125). Thus, a total of 119 patient outcome series on anorexia nervosa were suitable for the present analysis. A preliminary and descriptive report on 108 patient outcome series published before 1996 (126) was used as a starting point for the present analysis. In addition to the 119 outcome series, there were five studies (127–131) that contained only data on prognostic factors suitable for the present review.

Study Characteristics

The 119 outcome series were composed of 5,590 patients (group size: mean=47.0, SD=30.8, range=6–151). There were considerable differences among the studies in design, group size, and methods. Few studies were prospectively organized. There was only one study based exclusively on male patients (65). Diagnostic categories changed considerably over the period of the studies, with virtually no official criteria existing at the time of the first study, to the appearance of the first research criteria, by Feighner et al. (132), and ending with more recent criteria offered by DSM-III, DSM-III-R, DSM-IV, and ICD-10.
Because of the global descriptions of age at onset in the studies, precise age parameters could not be computed. For the present review, the following two age groups were formed: 1) patient series containing only younger adolescent patients, i.e., no older than 17 years at illness onset (N=37), and 2) series containing both younger and older patients, i.e., adolescents and adults (N=82).
Duration of follow-up was also quite difficult to compute from the original studies. Besides missing data, this problem was due to variations in the definition of the starting point or to the general practice of providing only ranges instead of precise group parameters. Similarly, data on the follow-up period, which ranged from less than 1 year to a maximum of 29 years, did not allow a more precise calculation of group parameters. Almost all groups were characterized by a marked heterogeneity regarding the duration of follow-up. Thus, the present review classified not the mean but the entire range of follow-up duration for arrangement of the studies into the following groups: 1) 20 series with follow-up after less than 4 years, 2) 45 series with follow-up from 4 to 10 years later, 3) seven series with follow-up after more than 10 years to 20 years, 4) four series with follow-up after more than 20 years, and 5) 42 series with variable follow-up periods that did not fit into the other group). Because of low frequencies, groups 3 and 4 had to be collapsed for data analysis; because of the heterogeneity of data, group 5 was excluded from the analyses on the impact of duration of follow-up. There was one study with no clear description of the length of follow-up.
There were a general lack of control conditions and a scarcity of precise information on treatment in these studies. Different treatment and psychotherapeutic approaches were used. The diversity of interventions precluded any definite evaluation of treatment effects.

Outcome Measures

The majority of outcome studies on anorexia nervosa reported crude mortality rates; a small number of studies presented standard mortality ratios. The crude mortality rates may have been slightly inflated; not all studies reported the cause of death, so causes other than the eating disorder might have led to subject death. In the surviving patients, outcome was most frequently described as one or more of the following three categories: 1) global, 2) normalization of the core symptom characteristics of anorexia nervosa, i.e., involving weight, menstruation, and eating behavior, and 3) psychiatric diagnoses other than eating disorders.
The most common scheme of global outcome classification in anorexia nervosa was the trichotomy between good, fair, and poor outcome. Although the studies varied regarding criteria, there was a general agreement that a good outcome stands for recovery from all essential clinical symptoms of anorexia nervosa, whereas a fair outcome represents improvement with some residual symptoms, and a poor outcome is synonymous with chronicity of the disorder. A substantial number of studies used the criteria of Morgan and Russell (37), whereas other studies used more idiosyncratic definitions or did not report data for all three categories. The sum of the three categories did not necessarily round up to precisely 100%. In the present analysis, all reported data were included in calculations of the basic findings across studies. The original data that included mortality as a fourth outcome criterion in calculations of outcome percentages were adjusted into a three-category outcome, with mortality as a separate criterion. Thus, the potential inflation of crude mortality rates and the nonreported causes of death in some studies did not affect the outcome rates in the surviving patients.
In a substantial number of studies, psychiatric diagnoses in addition to eating disorders were mentioned. However, with the wide span of the dates of publication, a certain variation of criteria in the clinical assessment of psychiatric disorders other than the eating disorders needed to be accepted. The following eight psychiatric diagnoses were extracted from the outcome studies: 1) a broad category of affective disorders, 2) other neurotic disorders, including unspecified anxiety disorders and phobias, 3) obsessive-compulsive disorders, 4) schizophrenia, 5) histrionic personality disorder, 6) unspecified personality disorders, including borderline states, 7) obsessive-compulsive personality disorder, and 8) substance abuse disorders.

Statistical Analyses

A total of 15 outcome variables were calculated in percentages that were rounded to the nearest whole. In order to take into account the large variation of group sizes, weighted percentages were calculated by weighting each reported rate with the size of the study group. With the help of SPSS (SPSS, Chicago), data for all studies were converted into individual data for performance of statistical analyses. The following variables that may have influenced outcome were used in analyses of variance (ANOVAs): 1) dropout rate, 2) duration of follow-up, 3) age at illness onset, and 4) period effects. The ANOVAs were supplemented by post hoc comparisons and calculations of effect sizes by computing the percentage of variance (sum of squares between the groups divided by the total), according to the procedure introduced by Cohen (133). According to Cohen, 1.0%–5.9% variance is small, 6.0%–13.9% is medium, and >14.0% is large.

Results
Effects of Dropout Rates
In a large number of studies, conclusions were jeopardized by a relatively high dropout rate at follow-up. The mean dropout rate for the 105 patient series with some relevant information was 12.3% (SD=14.7, range=0–77). An analysis of dropout effects revealed an inconsistent pattern, with no clear indication that studies with high dropout rates tended to have better results because of nonparticipating patients with poor outcomes (data available on request).

Mortality and Global Outcome

Two important issues were considered. First, the sizes of the patient groups differed significantly for the various outcome measures, because not all variables were assessed in all studies. Second, for each measure, there were rather wide standard deviations with extreme ranges across the studies, so that the means reflected only a central trend.
The mean crude mortality rate was 5.0% (Table 1). In the surviving patients, on average, full recovery was found in only 46.9% of the patients, while 33.5% improved, and 20.8% developed a chronic course of the disorder. Outcome was slightly better for the core symptoms, with normalization of weight occurring in 59.6% of the patients, normalization of menstruation in 57.0%, and normalization of eating behavior in 46.8%. However, these slightly higher rates of normalization of the core symptoms, compared to the global outcome rating, may be largely due to the smaller total group sizes. Nevertheless, this gap remained, even after adaptation for group size (when only the studies that reported both global outcome ratings and normalization of the core symptoms were considered).

Other Psychiatric Disorders

The findings presented in Table 1 show that at follow-up a large proportion of anorectic patients suffered from additional psychiatric disorders. Frequent diagnoses at follow-up were neurotic disorders, including anxiety disorders and phobias, affective disorders, substance use disorders, obsessive-compulsive disorder (OCD), and unspecified personality disorders, including borderline states. A few studies reported a high rate of obsessive-compulsive personality disorder and a less pronounced rate of histrionic personality disorder. Schizophrenia was only rarely observed at follow-up.

Effect Variables

It was possible to control for three major factors that might have affected outcome. Their influence is reported only for mortality and the global outcome of the eating disorder in order to avoid conclusions that might be biased due to incomplete data or a markedly smaller group size for other outcome variables. Furthermore, only 61 studies that reported three global outcome categories (recovery, improvement, and chronicity) were considered for these analyses.
The first factor tested was duration of follow-up. Findings are shown in Table 2. All four outcome parameters were significantly affected by duration of follow-up, and all four effect sizes were large. With increasing duration of follow-up, mortality rates also increased. In the surviving patients, there was a strong tendency toward recovery with increasing duration of follow-up. The rate of recovery increased, while the rates of improvement and chronicity declined. With the exception of the test on improvement rates in groups 1 and 2, all post hoc tests indicated that group differences were significant. Given the significance of the follow-up duration, this variable was controlled in two-way ANOVAs in the additional analyses on the impact of age at onset of illness and the effects of period.

When I compared the group of patients with adolescent onset and the group with a much wider age range at onset of illness, there was a significantly lower mortality rate in the group with the younger patients, as shown in Table 3. The rates of recovery, improvement, and chro

nicity were more favorable in the group with the younger patients. However, in each instance, in addition to duration of follow-up, the interactions between duration of follow-up and each outcome variable were significant, as shown in Figure 1.

The interaction effects showed that the differences between the subgroups with different onsets of illness were wider or narrower or even inverted for the four outcome measures, depending on the duration of follow-up. A comparison of the two effect sizes, as shown in Table 3, indicates that the effect of age at onset was stronger for mortality, whereas the effect of duration of follow-up was stronger for recovery, improvement, and chronicity.

The third effect tested was a potential period effect or time trend. The studies were divided into large groups, as follows: 1) studies from 1950 to 1979, 2) studies from 1980 to 1989, and 3) studies from 1990 to 1999. Mortality showed a complex pattern associated with time trends (Table 4). It was absent both for very short and very extended study courses in the early studies (with only one study each), from 1950 through 1979, whereas it increased linearly in the studies from 1980 to 1989 and from 1990 to 1999, with the highest rate for the most extended studies reported for 1980–1989.

There were few differences between the studies for 1980–1989 and the studies for 1990–1999 on the other outcome measures—recovery, improvement, and chronicity—whereas the studies from 1950 to 1979 primarily stood out because of high recovery rates and low rates of improvement and chronicity during short-term courses For all four outcome measures, the effect sizes for duration of follow-up were markedly stronger than for time period.

Prognostic Factors

Knowledge of the identified prognostic factors for anorexia nervosa is summarized in Table 5. First, the findings were considerably heterogeneous for the majority of the prognostic factors. Most clearly, this interpretation applies to the ambiguous findings regarding age at onset of illness. Furthermore, most studies indicated that a short duration of symptoms before treatment resulted in a favorable outcome. The impact of the duration of inpatient treatment is unclear because of ambiguous findings across the outcome studies. Similarly, no definite conclusions could be drawn as to whether greater weight loss at presentation had long-term effects on outcome.

Although hyperactivity and dieting as weight-reduction measures did not have any prognostic significance, it is quite clear that vomiting, bulimia, and purgative abuse imply an unfavorable prognosis. A few studies also showed that premorbid developmental and clinical abnormalities, including eating disorders during childhood, carry the risk for a poor outcome of anorexia nervosa. In contrast, a good parent-child relationship may protect the patient from a poor outcome.
In addition, the data clearly show that chronicity leads to poor outcome, a finding that implies that there are cases of anorexia nervosa in which treatment is refractory. A substantial number of studies provided evidence that the features of histrionic personality disorder indicate a favorable outcome. In contrast to comorbid OCD, which has no effect on outcome (118), the features of coexisting obsessive-compulsive personality or compulsivity add to chronicity. Finally, no definite conclusions can be drawn from the outcome studies as to the relevance of socioeconomic status.

Discussion

Besides use of a more extended database than in previous reviews, the present review on the outcome of anorexia nervosa is the first to my knowledge that was not confined to descriptive statistics only. For the first time an attempt was made to analyze trends by use of inferential statistics in order to isolate factors that might have influenced the course of anorexia nervosa in the last century. Findings based on this large group of 5,590 patients contained in a large number of studies indicate that despite wide variations of all outcome parameters across studies, anorexia nervosa remains a mental illness with a serious course and outcome in many of the affected individuals. This conclusion is based on various parameters analyzed in the present review.
First, crude mortality rates were high and increased significantly with length of follow-up. Even stronger evidence comes from a series of studies that calculated standard mortality rates. A review of the standard mortality rate in 10 cohort studies (134) found standard mortality rates between 1.36 and 17.80, indicating a slight to an almost 18-fold increase in mortality in patients with anorexia nervosa, with a maximal standard mortality rate of 30 for female patients in the first year after presentation and a statistically significant increase for up to 15 years after presentation. The data suggest that there are more deaths from suicide and other and unknown causes and fewer deaths related to the eating disorder than have been previously reported.
Second, less than a half of the patients, or exactly 46%, fully recovered from anorexia nervosa, whereas a third improved with only partial or residual features of anorexia nervosa, and 20% remained chronically ill over the long term. This relatively poor global outcome is slightly obscured if one looks in isolation at the better outcome of the core symptoms of weight restoration (60%) and normalization of both menstruation (57%) and eating behavior (47%).
A third outcome indicator of the seriousness of the course of anorexia nervosa—namely, other psychiatric disorders—shows that exactly one-quarter of the anorexia nervosa patients had anxiety disorders and one-quarter had affective disorders. Substance use disorders, OCD, and obsessive-compulsive personality disorder were very common diagnoses at outcome. Furthermore, there was evidence that some of these comorbidities—that is, depression, anxiety disorder, phobias, and personality disorders—served as risk factors contributing to a less favorable outcome of anorexia nervosa (78, 94, 105, 106). However, so far, little is known about the comorbidity of these various psychiatric disorders among each other, their true coexistence with anorexia nervosa, and the sequential patterns across time. The two parameters of global outcome and other psychiatric disorders overlap greatly, so that at follow-up, more than 50% of the anorexia nervosa patients showed either a complete or a partial eating disorder in combination with another psychiatric disorder or another psychiatric disorder without an eating disorder. However, an exact figure could not be obtained from the present data set.
There are two main factors mitigating the problematic outcome of anorexia nervosa, namely, duration of follow-up and age at onset of the disorder. In contrast to the strong effect of the increasing crude mortality rate, the global outcome in the surviving patients clearly improves with increasing duration of follow-up. The data indicate with strong effect sizes that with increasing duration of follow-up, the illness course improved linearly if the patient survived. Thus, it is recommended that clinicians follow up with patients for extended periods.
Onset of the disorder during adolescence was associated with a lower mortality rate and a strong effect size that was clearly more important than the duration of follow-up. This finding simply reflects the probabilistic event that more deaths are to be expected with increasing age. Although the other three general outcome measures were affected by age at onset, indicating that younger age at onset was associated with better outcome, the duration of follow-up was a more influential factor. However, two limitations of the analyses have to be taken into consideration. First, the group with variable age at onset was not the most suitable contrast to the group with adolescent onset because of the wide variation in age. A group of patients with adult onset only would be more appropriate for comparison. However, such a contrasting group was not available for study. Second, it must also be kept in mind that onset of anorexia nervosa before puberty has a very poor outcome (135).
Trends over five decades of outcome research are less clear. The early studies, from 1950 to 1979, provided evidence for lower mortality during long-term follow-up (>10 years) and higher recovery rates with short-term follow-up which were introduced in 1975. Accordingly, the reliability of outcome measurement in the early studies may be questionable. With these caveats and the relatively small effect sizes in mind, there was only limited evidence that the outcome of anorexia nervosa has improved significantly across these five decades.
Research on the outcome of anorexia nervosa has also analyzed a large list of prognostic factors and produced both conflicting and clear evidence of their significance. There is clear and almost unanimous evidence from a sizable number of studies that vomiting, bulimia and purgative abuse, chronicity, and features of obsessive-compulsive personality represent unfavorable prognostic factors, whereas hysterical personality features represent the only favorable prognostic factors that have not been documented with conflicting evidence. The favorable functions of many other prognostic factors are obscured by the fact that besides some positive evidence, there are also a sizable number of studies that found these factors to be of no significance. These factors include early age at onset, short duration of symptoms before treatment, short duration of inpatient treatment, good parent-child relationship, and high socioeconomic status. Similarly, there was no clear evidence that major weight loss and premorbid abnormalities serve as unfavorable factors. Both the variability in findings on prognostic factors and the likely nature of the data preclude any delineation of rules as to individual prognosis in a patient suffering from anorexia nervosa.
So far, one of the major questions of developmental psychopathology as to the continuity and discontinuity of psychiatric disorder has received little attention in studies on the course of anorexia nervosa. Most of the studies have concentrated on outcome, leaving aside the process of course. Study of the latter requires prospective designs that have emerged only in the recent past. Some of these more recent studies have analyzed time trends of certain features of anorexia nervosa based on the survival-analysis model (116, 131, 136). Finally, the descriptive nature of data on treatment, the lack of rigorous evaluation of interventions in the majority of outcome studies, and the scarcity of randomized intervention studies with sufficient evaluation of outcome do not allow any definite statement as to the role and function of treatment for long-term course.

Footnotes

Received May 18, 2001; revision received Oct. 30, 2001; accepted Jan. 28, 2002. From the Department of Child and Adolescent Psychiatry, University of Zurich. Address reprint requests to Dr. Steinhausen, Department of Child and Adolescent Psychiatry, University of Zurich, Neumünsterallee 9, Postfach, CH-8032 Zurich, Switzerland; steinh@kjpd.unizh.ch '//-->(e-mail). The author thanks C. Winkler Metzke for assistance with data analysis.

References
Silverman JA: Anorexia nervosa: historical perspective on treatment, in Handbook of Treatment for Eating Disorders, 2nd ed. Edited by Garner DM, Garfinkel PE. New York, Guilford, 1997, pp 3-10
Fombonne E: Anorexia nervosa: no evidence of an increase. Br J Psychiatry 1995; 166:462-471[Abstract/Free Full Text]
Steinhausen HC: Anorexia and bulimia nervosa, in Child and Adolescent Psychiatry: Modern Approaches, 4th ed. Edited by Rutter M, Taylor E. Oxford, UK, Blackwell Scientific, 2002
Bruch H: Eating Disorders: Obesity, Anorexia Nervosa and the Person Within. New York, Basic Books, 1978
Crisp AH: Anorexia Nervosa: Let Me Be. London, Academic Press, 1980
Russell GFM: Anorexia nervosa: its identity as an illness and its treatment, in Modern Trends in Psychological Medicine, 2nd ed. Edited by Price JH. London, Butterworths, 1970, pp 131-164
Bemis KMM: The present status of operant conditioning for the treatment of anorexia nervosa. Behav Modif 1987; 11:432-463[Abstract]
Vandereycken W: The place of family therapy in the treatment of eating disorders, in Eating Disorders in Adolescence: Anorexia and Bulimia Nervosa. Edited by Steinhausen HC. New York, Walter de Gruyter, 1995, pp 287-300
Garfinkel PE, Walsh BT: Drug therapies, in Handbook of Treatment for Eating Disorders, 2nd ed. Edited by Garner DM, Garfinkel PE. New York, Guilford Press, 1997, pp 372-382
Steinhausen HC, Glanville K: Follow-up studies of anorexia nervosa—a review of research findings (editorial). Psychol Med 1983; 3:239-249
Kay DW: Anorexia nervosa: a study in prognosis. Proc R Soc Med 1953; 46:669-674
Beck JC, Brøchner-Mortensen K: Observations on the prognosis in anorexia nervosa. Acta Med Scand 1954; 149:409-430
Williams E: Anorexia nervosa: a somatic disorder. Br Med J 1958; 2:190-195
Lesser LI, Ashenden BJ, Debushey M, Eisenberg L: Anorexia nervosa in children. Am J Orthopsychiatry 1960; 30:572-580[Medline]
Thomä H: Anorexia Nervosa. Bern, Switzerland, Huber, 1961
Blitzer JR, Rollins N, Blackwell A: Children who starve themselves: anorexia nervosa. Psychosom Med 1961; 23:369-383[Abstract/Free Full Text]
Meyer JE: Das Syndrom der Anorexia nervosa: Katamnestische Untersuchungen. Arch Psychiatr Nervenkr 1961; 202:31-59[CrossRef]
Tolstrup K: Die Charakteristika der jüngeren Fälle von Anorexia nervosa, in Anorexia Nervosa. Edited by Meyer JE, Feldmann H. Stuttgart, Germany, Thieme, 1965, pp 51-59
Frahm H: Ergebnisse einer systematisch durchgeführten somatisch orientierten Behandlungsform bei Kranken mit Anorexia nervosa. Ibid, pp 64-70
Frazier SH: Anorexia nervosa. Dis Nerv Syst 1965; 26:155-159
Kay DW, Shapira K: The prognosis in anorexia nervosa, in Anorexia Nervosa. Edited by Meyer JE, Feldman H. Stuttgart, Germany, Thieme, 1965, pp 113-127
Crisp AH: Some aspects of the evolution, presentation and follow-up of anorexia nervosa. Proc R Soc Med 1965; 58:814-820[Medline]
Farquharson RF, Hyland HH: Anorexia nervosa: the course of 15 patients treated from 20 to 30 years previously. Can Med Assoc J 1966; 96:411-419
Dally PJ, Sargant W: Treatment and outcome of anorexia nervosa. Br Med J 1966; 2:793-795
Warren W: A study of anorexia nervosa in young girls. J Child Psychol Psychiatry 1968; 9:27-40[Medline]
Seidensticker J, Tzagournis M: Anorexia nervosa—clinical features and long-term follow-up. J Chronic Dis 1980; 21:366-367
Browning CH, Miller SI: Anorexia nervosa: a study in prognosis and management. Am J Psychiatry 1968; 124:1128-1132[Abstract/Free Full Text]
Ziegler R, Sours J: A naturalistic study of patients with anorexia nervosa admitted to a university medical center. Compr Psychiatry 1968; 9:644-651[CrossRef][Medline]
Dally PJ: Anorexia Nervosa. London, Heinemann Medical Books, 1969
Theander S: Anorexia nervosa: a psychiatric investigation of 94 female patients. Acta Psychiatr Scand Suppl 1970; 214:1-194[Medline]
Valanne EH, Taipale V, Larkio-Miettinen AK, Morén R, Aukee M: Anorexia nervosa: a follow-up study. Psychiatria Fennica 1972, pp 265-269
Halmi KA, Brodland G, Loney J: Prognosis in anorexia nervosa. Ann Intern Med 1973; 78:907-909
Bruch H: Outcome and outlook, in Eating Disorders. Edited by Bruch H. New York, Basic Books, 1973, pp 377-387
Bhanji S, Thompson J: Operant conditioning in the treatment of anorexia nervosa. Br J Psychiatry 1974; 124:166-172[Medline]
Niskanen P, Jääskeläinen J, Achté K: Anorexia nervosa: treatment results and prognosis. Psychiatria Fennica 1974, pp 257-263
Silverman JA: Anorexia nervosa: clinical observations in a successful treatment plan. J Pediatr 1974; 84:68-73[CrossRef][Medline]
Morgan HG, Russell GFM: Value of family background and clinical features as predictors of long-term outcome in anorexia nervosa: four-year follow-up study of 41 patients. Psychol Med 1975; 5:355-371[Medline]
Brady JP, Rieger W: Behavioral treatment of anorexia nervosa, in Applications of Behavior Modification. Edited by Thompson T, Dockens WS III. New York, Academic Press, 1961, pp 45-63
Pierloot RA, Wellens W, Houben ME: Elements of resistance to a combined medical and psychotherapeutic program in anorexia nervosa. Psychother Psychosom 1975; 26:101-117[Medline]
Niederhoff H, Wiesler B, Kuenzer W: Somatisch orientierte Behandlung der Anorexia nervosa. Monatsschr Kinderheilkd 1975; 123:343-344[Medline]
Beumont PJV, George GCW, Smart DE: "Dieters" and "vomiters and purgers" in anorexia nervosa. Psychol Med 1976; 6:617-622[Medline]
Halmi KA, Brodland G, Rigas C: A follow-up study of seventy-nine patients with anorexia nervosa: an evaluation of prognostic factors and diagnostic criteria, in Life History Research in Psychopathology, vol 4. Edited by Winokur G, Roff M, Wirt RD. Minneapolis, University of Minnesota Press, 1976, pp 290-300
Willi J, Hagemann R: Langzeitverläufe von Anorexia nervosa. Schweizerische Med Wochenschrift 1976; 106:1459-1465
Rosman BL, Minuchin S, Liebman R, Baker L: Input and outcome of family therapy in anorexia nervosa, in Successful Psychotherapy. Edited by Claghorn JL. New York, Brunner/Mazel, 1976, pp 128-139
Goetz PL, Succop RA, Reinhart JB, Miller A: Anorexia nervosa in children: a follow-up study. Am J Orthopsychiatry 1977; 47:597-603[Medline]
Sturzenberger S, Cantwell PD, Burroughs J, Salkin B, Green JK: A follow-up study of adolescent psychiatric inpatients with anorexia nervosa. J Am Acad Child Psychiatry 1977; 16:703-715[Medline]
Cantwell DP, Sturzenberger S, Burroughs J, Salkin B, Green J: Anorexia nervosa—an affective disorder? Arch Gen Psychiatry 1977; 34:1087-1093[Abstract]
Stonehill E, Crisp AH: Psychoneurotic characteristics of patients with anorexia nervosa before and after treatment and at follow-up 4-7 years later. J Psychosom Res 1977; 16:703-715
Garfinkel PE, Moldofsky H, Garner DM: The outcome of anorexia nervosa: significance of clinical features, body image and behavior modification, in Anorexia Nervosa. Edited by Vigersky RA. New York, Raven Press, 1977, pp 315-329
Pertschuk MJ: Behavior therapy: extended follow-up. Ibid, pp 305-314
Cremerius J: Zur Prognose der Anorexia nervosa. Z Psychosom Med Psychoanal 1978; 24:56-69[Medline]
Ziolko HU: Zur Katamnese der Pubertätsmagersucht. Arch Psychiatr Nervenkr 1978; 225:117-125[CrossRef][Medline]
Petzold E: Familienkonfrontationstherapie bei Anorexia nervosa. Göttingen, Germany, Verlag für medizinische Psychologie Dr CJ Hogrefe, 1979
Hsu LKG, Crisp AH, Harding B: Outcome of anorexia nervosa. Lancet 1979; 1:61-65[Medline]
Schütze G: Anorexia Nervosa. Bern, Switzerland, Huber, 1980
Rollins N, Piazza E: Anorexia nervosa: a qualitative approach to follow-up. J Am Acad Child Psychiatry 1981; 20:167-183[Medline]
Steinhausen HC, Rauss-Mason C, Seidel R: Follow-up studies of anorexia nervosa: a review of four decades of outcome research. Psychol Med 1991; 21:447-454[Medline]
Becker H, Körner P, Stöffler A: Psychodynamics and therapeutic aspects of anorexia nervosa: a study of family dynamics and prognosis. Psychother Psychosom 1981; 36:8-16[Medline]
Bassøe HH, Eskeland I: A prospective study of 133 patients with anorexia nervosa—treatment and outcome. Acta Psychiatr Scand 1982; 65:127-133[Medline]
Kohle K, Mall H: Follow-up study of 36 anorexia nervosa patients treated on an integrated internistic-psychosomatic ward. Int J Eat Disord 1983; 2:215-219
Colligan RC, Ferdinande RJ, Lucas AR, Duncan JW: A one-year follow-up study of adolescent patients hospitalized with anorexia nervosa. J Dev Behav Pediatr 1983; 4:278-279[Medline]
Morgan HG, Purgold J, Welbourne J: Management and outcome in anorexia nervosa—a standardized prognostic study. Br J Psychiatry 1983; 143:282-287[Abstract/Free Full Text]
Steinhausen HC, Glanville K: Retrospective and prospective follow-up of adolescent anorexia nervosa. Acta Psychiatr Scand 1983; 68:1-10[Medline]
Hall A, Slim E, Hawker F, Salmond C: Anorexia nervosa—long-term outcome in 50 female patients. Br J Psychiatry 1984; 145:407-413[Abstract/Free Full Text]
Burns T, Crisp AH: Outcome of anorexia nervosa in males. Br J Psychiatry 1984; 145:319-325[Abstract/Free Full Text]
Touyz SW, Beumont PJV: Anorexia nervosa: a follow-up investigation. Med J Aust 1984; 141:219-222[Medline]
Nussbaum M, Shenker IR, Baird D, Saravay S: Follow-up investigation in patients with anorexia nervosa. J Pediatr 1985; 106:835-840[CrossRef][Medline]
Tolstrup K, Brinch M, Isager T, Nielsen S, Nystrup J, Severin B, Olesen NS: Long-term outcome of 151 cases of anorexia nervosa. Acta Psychiatr Scand 1985; 71:380-387[Medline]
Martin FE: The treatment and outcome of anorexia nervosa in adolescents: a prospective study and five-year follow-up. J Psychiatr Res 1985; 19:509-514[CrossRef][Medline]
Theander S: Outcome and prognosis in anorexia nervosa and bulimia: some results of previous investigations, compared with those of a Swedish long-term study. J Psychiatr Res 1985; 19:493-508[CrossRef][Medline]
Suematsu H, Kuboki T, Itoh T: Statistical studies on the prognosis of anorexia nervosa. Psychother Psychosom 1985; 43:104-112[Medline]
Hawley RM: The outcome of anorexia nervosa in younger subjects. Br J Psychiatry 1985; 146:657-660[Abstract/Free Full Text]
Toner BB, Garfield PE, Garner DM: Long-term follow-up of anorexia nervosa. Psychosom Med 1986; 48:520-529[Abstract/Free Full Text]
Santonastaso P, Favaretto G, Canton G: Anorexia nervosa in Italy: clinical features and outcome in a long-term follow-up study. Psychopathology 1987; 20:8-17[Medline]
Engel K: Prognostic factors in anorexia nervosa. Psychother Psychosom 1988; 49:137-144[Medline]
Engel K, Wilfarth B: Therapy results and follow-up of an integrated treatment for severe cases of anorexia nervosa. Psychother Psychosom 1988; 50:5-14[CrossRef][Medline]
Remschmidt H, Wienand F, Wewetzer C: Der Langzeitverlauf der Anorexia nervosa. Monatsschr Kinderheilkd 1988; 136:726-731[Medline]
Bryant-Waugh R, Knibbs J, Fosson A, Kaminski Z, Lask B: Long-term follow-up of patients with early onset anorexia nervosa. Arch Dis Child 1988; 63:5-9[Abstract]
Deter HC, Petzold E, Hehl FJ: Differenzierung der Langzeitwirkungen einer stationären psychosomatischen Therapie von Anorexia-nervosa-Patienten. Z Psychosom Med 1989; 35:68-91
Willi J, Limacher B, Nussbaum P: Zehnjahres-Katamnese der 1973-75 im Kanton Zürich erstmals hospitalisierten Anorexien. Schweizerische Med Wochenschrift 1989; 119:147-159
Fichter MM, Quadflieg N: Comparative studies on the course of eating disorders in adolescents and adults: is age at onset a predictor of outcome? in Eating Disorders in Adolescence: Anorexia and Bulimia Nervosa. Edited by Steinhausen HC. New York, Walter De Gruyter, 1995, pp 301-337
Arroyo D, Tonkin R: Adolescents with bulimic and nonbulimic eating disorders. J Adolesc Health Care 1985; 6:21-24[CrossRef][Medline]
Calvo Sagardoy R, Fernandez Ashton A, Ayuso Mateos JL, Bayon Perez C, Santo-Domingo Carrasco J: Between 5 and 9 years follow-up in the treatment of anorexia nervosa. Psychother Psychosom 1989; 52:133-139[Medline]
Crisp AH, Callender JS, Halek C, Hsu LKG: Long-term mortality in anorexia nervosa: a 20-year follow-up of the St George’s and Aberdeen cohorts. Br J Psychiatry 1992; 161:104-107[Abstract/Free Full Text]
Deter HC, Herzog W, Petzold E: The Heidelberg-Mannheim study: long-term follow-up of anorexia nervosa patients at the University Medical Center—background and preliminary results, in The Course of Eating Disorders: Long-Term Follow-Up Studies of Anorexia and Bulimia Nervosa. Edited by Herzog W, Deter HC, Vandereycken W. Berlin, Springer, 1992, pp 71-84
Greenfeld DG, Anyan WR, Hobart M, Quinlan DM, Plantes M: Insight into illness and outcome in anorexia nervosa. Int J Eat Disord 1991; 10:101-109
Higgs JF, Goodyer IM, Birch J: Anorexia nervosa and food avoidance emotional disorder. Arch Dis Child 1989; 64:346-351[Abstract]
Jenkins ME: An outcome study of anorexia nervosa in an adolescent unit. J Adolesc 1987; 10:71-81[CrossRef][Medline]
Kreipe RE, Churchill BH, Strauss J: Long-term outcome of adolescents with anorexia nervosa. Am J Dis Child 1989; 143:1322-1327[Abstract]
Ratnasuriya RH, Eisler I, Szmukler GI, Russell GFM: Anorexia nervosa: outcome and prognostic factors after 20 years. Br J Psychiatry 1991; 158:465-502
Rosenvinge JH, Mouland SO: Outcome and prognosis of anorexia nervosa: a retrospective study of 41 subjects. Br J Psychiatry 1990; 156:92-97[Abstract/Free Full Text]
Santonastaso P, Pantano M, Panarotto L, Silvestri A: A follow-up study on anorexia nervosa: clinical features and diagnostic outcome. Eur Psychiatry 1991; 6:177-185
Steiner H, Mazer C, Litt IF: Compliance and outcome in anorexia nervosa. West J Med 1990; 157:133-139[Medline]
Steinhausen HC, Seidel R: Outcome in adolescent eating disorders. Int J Eat Disord 1993; 14:487-496[Medline]
Walford G, McCune N: Long-term outcome in early-onset anorexia nervosa. Br J Psychiatry 1991; 159:383-389[Abstract/Free Full Text]
Fichter MM, Quadflieg N, Rief W: The German Longitudinal Bulimia Nervosa Study I, in The Course of Eating Disorders: Long-Term Follow-Up Studies of Anorexia and Bulimia Nervosa. Edited by Herzog W, Deter HC, Vandereycken W. Berlin, Springer, 1992, pp 133-149
Herzog DB, Sacks NR, Keller MB, Lavori PW, Ranson KB, Gray HM: Patterns and predictors of recovery in anorexia nervosa and bulimia nervosa. J Am Acad Child Adolesc Psychiatry 1993; 32:835-842[Medline]
Vandereycken W, Pieters G: A large-scale longitudinal follow-up study of patients with eating disorders: methodological issues and preliminary results, in The Course of Eating Disorders: Long-Term Follow-Up Studies of Anorexia and Bulimia Nervosa. Edited by Herzog W, Deter HC, Vandereycken W. Berlin, Springer, 1992, pp 182-197
Norring CEA, Sohlberg SS: Outcome, recovery, relapse and mortality across six years in patients with clinical eating disorders. Acta Psychiatr Scand 1993; 87:437-444[Medline]
Smith C, Feldman SS, Nasserbakht A, Steiner H: Psychological characteristics and DSM-III-R diagnoses at 6-year follow-up of adolescent anorexia nervosa. J Am Acad Child Adolesc Psychiatry 1993; 32:1237-1245[Medline]
Deter HC, Herzog W: Anorexia nervosa in a long-term perspective: results of the Heidelberg-Mannheim Study. Psychosom Med 1994; 56:20-27[Abstract/Free Full Text]
van der Ham T, van Strien DC, van Engeland H: A four-year prospective follow-study of 49 eating-disordered adolescents: differences in course of illness. Acta Psychiatr Scand 1994; 90:229-235[Medline]
Wonderlich SA, Fullerton D, Swift WJ, Klein MH: 5-year outcome from eating disorders—relevance of personality disorders. Int J Eat Disord 1994; 15:233-244[Medline]
Gillberg C, Råstam M, Gillberg IC: Anorexia nervosa 6 years after onset, 1: personality disorders. Compr Psychiatry 1995; 36:61-69[CrossRef][Medline]
Eckert ED, Halmi KA, Marchi P, Grove W, Crosby R: Ten-year follow-up of anorexia nervosa: clinical course and outcome. Psychol Med 1995; 25:143-156[Medline]
Herpertz-Dahlmann BM, Wewetzer C, Schulz E, Remschmidt H: Course and outcome in adolescent anorexia nervosa. Int J Eat Disord 1996; 19:335-345[Medline]
Theander S: Anorexia nervosa with an early onset: selection, gender, outcome, and results of a long-term follow-up study. J Youth Adolesc 1996; 25:419-429[CrossRef]
Bryant-Waugh R, Hankins M, Shafran R, Lask B, Fosson A: A prospective follow-up of children with anorexia nervosa. J Youth Adolesc 1996; 25:431-437[CrossRef]
Steinhausen HC, Boyadjieva S: The outcome of adolescent anorexia nervosa: findings from Berlin and Sofia. J Youth Adolesc 1996; 25:473-481[CrossRef]
Kreipe RE, Piver Dukam C: Outcome of anorexia nervosa related to treatment utilizing an adolescent medicine approach. J Youth Adolesc 1996; 25:483-497[CrossRef]
Casper RC, Jabine LN: An eight-year follow-up: outcome from adolescent compared to adult-onset anorexia nervosa. J Youth Adolesc 1996; 25:499-517[CrossRef]
Sunday SR, Reeman IM, Eckert E, Halmi KA: Ten-year outcome in adolescent onset anorexia nervosa. J Youth Adolesc 1996; 25:533-544[CrossRef]
Fichter MM, Quadflieg N: Course and two-year outcome in anorexic and bulimic adolescents. J Youth Adolesc 1996; 25:545-562[CrossRef]
North C, Growers S, Byram V: Family functioning and life events in the outcome of adolescent anorexia nervosa. Br J Psychiatry 1997; 171:545-549[Abstract/Free Full Text]
Schulze U, Neudörfli A, Krill A, Warnke A, Remschmidt H, Herpertz-Dahlmann B: Verlauf und Heilungserfolg der frühen Anorexia nervosa. Z Kinder Jugendpsychiatr 1997; 25:5-16
Strober M, Freeman R, Morrell W: The long-term course of severe anorexia nervosa in adolescents: survival analysis of recovery, relapse, and outcome predictors over 10-15 years in a prospective study. Int J Eat Disord 1997; 22:339-360[Medline]
Finzer P, Haffner J, Müller-Küppers M: Zu Verlauf und Prognose der Anorexia nervosa: Katamnese von 41 Patienten. Prax Kinderpsychol Kinderpsychiatr 1998; 47:302-313[Medline]
Thiel A, Züger M, Jacoby GE, Schüssler G: Thirty-month outcome in patients with anorexia or bulimia nervosa and concomitant obsessive-compulsive disorder. Am J Psychiatry 1998; 155:244-249[Abstract/Free Full Text]
Sullivan PF, Bulik CM, Fear JL, Pickering A: Outcome of anorexia nervosa: a case-control study. Am J Psychiatry 1998; 155:939-946[Abstract/Free Full Text]
Saccomani L, Savoini M, Cirrincione M, Ravera G: Long-term outcome of children and adolescents with anorexia nervosa: study of comorbidity. J Psychosom Res 1998; 44:565-571[CrossRef][Medline]
Deter HC, Köpp W, Zipfel S, Herzog W: Männliche Anorexia-nervosa-Patienten im Langzeitverlauf. Nervenarzt 1998; 69:419-426[CrossRef][Medline]
Jarman FC, Rickards WS, Hudson L: Late adolescent outcome of early-onset anorexia nervosa. J Paediatr Child Health 1991; 27:221-227[Medline]
Fichter MM, Quadlieg N: Six-year course and outcome of anorexia nervosa. Int J Eat Disord 1999; 26:359-385[Medline]
Pla C, Toro J: Anorexia nervosa in a Spanish adolescent sample: an 8-year longitudinal study. Acta Psychiatr Scand 1999; 100:441-446[Medline]
Wentz Nilsson E, Gillberg C, Gillberg IC, Råstam M: Ten-year follow-up of adolescent-onset anorexia nervosa: personality disorders. J Am Acad Child Adolesc Psychiatry 1999; 38:1389-1395[CrossRef][Medline]
Steinhausen HC: Eating disorders, in Risks and Outcomes in Developmental Psychopathology. Edited by Steinhausen HC, Verhulst F. Oxford, UK, Oxford University Press, 1999, pp 210-330
Sohlberg S, Norring C, Holmaren S, Rosmark B: Impulsivity and long-term prognosis of psychiatric patients with anorexia nervosa/bulimia nervosa. J Nerv Ment Dis 1989; 177:249-258[Medline]
Crisp AH, Harding G, McGuiness B: Anorexia nervosa: psychoneurotic characteristics of parents: relationship to prognosis. J Psychosom Res 1974; 18:167-173[CrossRef][Medline]
Kalucy RS, Crisp AH, Harding B: A study of 56 families with anorexia nervosa. Br J Med Psychol 1977; 50:381-395[Medline]
Rollins N, Blackwell A: The treatment of anorexia nervosa in children and adolescents: stage 1. J Child Psychol Psychiatry 1968; 9:81-91[Medline]
Herzog DB, Dorer DJ, Keel PK, Selwyn SE, Ekeblad ER, Flores A, Greenwood DN, Burwell RA, Keller MB: Recovery and relapse in anorexia and bulimia nervosa: a 7.5-year follow-up study. J Am Acad Child Adolesc Psychiatry 1999; 38:829-837[CrossRef][Medline]
Feighner JP, Robins E, Guze SB, Woodruff RA Jr, Winokur G, Muñoz R: Diagnostic criteria for use in psychiatric research. Arch Gen Psychiatry 1972; 26:57-63[Medline]
Cohen J: Statistical Power Analysis for the Behavioral Sciences, revised ed. New York, Academic Press, 1977
Nielsen S, Møller-Madsen S, Isager T, Jørgensen J, Pagsberg K, Theander S: Standardized mortality in eating disorders—a quantitative summary of previously published and new evidence. J Psychosom Res 1998; 44:413-434[CrossRef][Medline]
Russell GFM: Anorexia nervosa of early onset and its impact on puberty, in Feeding Problems and Eating Disorders in Children and Adolescents. Edited by Cooper PJ, Stein A. Chur, Switzerland, Harwood Academic, 1992, pp 85-112
Steinhausen HC, Seidel R, Winkler Metzke C: Evaluation of treatment and intermediate and long-term outcome of adolescent eating disorder. Psychol Med 2000; 30:1089-1098

Lymphedema

Definition
Lymphedema refers to swelling that occurs most often in your arms or legs. It may affect just one arm or leg, but sometimes lymphedema can involve both arms or both legs.
The swelling occurs when a blockage in your lymphatic system prevents the lymph fluid in your arm or leg from draining adequately. As the fluid accumulates, the swelling continues.
No cure for lymphedema exists. But lymphedema can be controlled. Controlling lymphedema involves diligent care of your affected limb.

Symptoms
Lymphedema is a type of abnormal swelling of an arm or leg. Swelling ranges from mild, hardly noticeable changes in the size of your limb to extreme swelling that can make it impossible to use the affected arm or leg.
Lymphedema symptoms include:
1. Swelling of part of your arm or your entire arm or leg, including your fingers or toes
2. A feeling of heaviness or tightness in your arm or leg
3. Restricted range of motion in your arm or leg
4. Aching or discomfort in your arm or leg
5. Recurring infections in your affected limb
6. Hardening and thickening of the skin on your arm or leg

Causes
Your lymphatic system is crucial to keeping your body healthy. It circulates protein-rich lymph fluid throughout your body, collecting bacteria, viruses and waste products. Your lymphatic system carries these through your lymph vessels, which lead to lymph nodes. The wastes are then filtered out by lymphocytes — infection-fighting cells that live in your lymph nodes — and ultimately flushed from your body.
Lymphedema occurs when your lymph vessels are unable to adequately drain lymph fluid from your arm or leg. Lymphedema can be either primary or secondary. This means it can occur on its own (primary lymphedema) or it can be caused by another disease or condition (secondary lymphedema).

Causes of primary lymphedema

Primary lymphedema is a rare, inherited condition caused by problems with the development of lymph vessels in your body. Primary lymphedema occurs most frequently in women and usually affects the legs, rather than the arms. Specific causes of primary lymphedema include:
Milroy disease (congenital lymphedema). This is an inherited disorder that begins in infancy and causes a malformation of your lymph nodes, leading to lymphedema.
Meige disease (lymphedema praecox). This hereditary disorder causes lymphedema in childhood or around puberty. It causes your lymph vessels to form without the valves that keep lymph fluid from flowing backwards, making it difficult for your body to properly drain the lymph fluid from your limbs.
Late-onset lymphedema (lymphedema tarda). This occurs rarely and usually begins after age 35.

Causes of secondary lymphedema

Any condition or procedure that damages your lymph nodes or lymph vessels can cause lymphedema. Causes include:
1. Surgery can cause lymphedema to develop if your lymph nodes and lymph vessels are removed or severed. For instance, surgery for breast cancer may include the removal of one or more lymph nodes in your armpit to look for evidence that cancer has spread. If your remaining lymph nodes and lymph vessels can't compensate for those that have been removed, lymphedema may result in your arm.
2. Radiation treatment for cancer can cause scarring and inflammation of your lymph nodes or lymph vessels, restricting flow of the lymph.
Cancer cells can cause lymphedema if they block lymphatic vessels. For instance, a tumor growing near a lymph node or lymph vessel could become large enough to obstruct the flow of the lymph fluid.
3. Infection can infiltrate your lymph vessels and lymph nodes, restricting the flow of lymph fluid and causing lymphedema. Parasites also can block lymph vessels. Infection-related lymphedema is most common in tropical and subtropical regions of the globe and is more likely to occur in undeveloped countries.
4. Injury that damages your lymph nodes or lymph vessels also can cause lymphedema.

When to seek medical advice
Make an appointment with your doctor if you notice any persistent swelling in your arms, legs or lymph nodes.

Tests and diagnosis
Your doctor may try to rule out other causes of swelling in order to arrive at a diagnosis of lymphedema. Swelling can have many causes, including a blood clot or an infection that doesn't involve your lymph nodes.
If you're at risk of lymphedema — for instance, if you've recently had cancer surgery involving your lymph nodes — your doctor may assume you have lymphedema based on your signs and symptoms.
If the cause of your lymphedema isn't as obvious, your doctor may order imaging tests to determine what's causing your signs and symptoms. To get a look at your lymphatic system, your doctor may use an imaging technique, such as:
1. Radionuclide imaging of your lymphatic system (lymphoscintigraphy). During this test you're injected with a radioactive dye and then scanned by a machine. The resulting images show the dye moving through your lymph vessels, highlighting areas where the lymph fluid is blocked.
2. Magnetic resonance imaging (MRI). This scan gives your doctor a better look at the tissues in your arm or leg. He or she might be able to use an MRI to see characteristics of lymphedema.
3. Computerized tomography (CT). A CT scan produces images of your arm or leg in cross sections.
4. Doppler ultrasound. This variation of the conventional ultrasound assesses blood flow and pressure by bouncing high-frequency sound waves (ultrasound) off red blood cells.

Complications
Lymphedema in your arm or leg can lead to serious complications, such as:
1. Infections. Lymphedema makes your affected arm or leg particularly vulnerable to infections, including cellulitis and lymphangitis. Any injury to your arm or leg provides an entry point for an infection.
2. Elephantiasis. This condition occurs when your arm or leg becomes so hardened with thickened skin that you have difficulty moving it. Elephantiasis may make the skin on your arm or leg very weak, leading to chronic ulcers and repeated infections.
3. Lymphangiosarcoma. This rare form of soft tissue cancer can result from the most severe cases of untreated lymphedema. Lymphangiosarcoma originates in the lymph nodes and lymph vessels.

Treatments and drugs
Lymphedema can't be cured. Treatment focuses on minimizing the swelling and controlling the pain. Lymphedema treatments include:
1. Exercises. Light exercises that require you to move your affected arm or leg may encourage movement of the lymph fluid out of your limb. These exercises shouldn't be strenuous or make you tired. Instead, they should focus on gentle contraction of the muscles in your arm or leg. Exercises help pump the lymph fluid out of your affected limb. Your doctor or a physical therapist can teach you exercises that may help.
2. Wrapping your arm or leg. Bandages wrapped around your entire limb encourage lymph fluid to flow back out of your affected limb and toward the trunk of your body. When bandaging your arm or leg, start by making the bandage tightest around your fingers and toes. Wrap the bandage more loosely as you move up your arm or leg. A lymphedema therapist can show you how to wrap your limb.
3. Massage. A special massage technique called manual lymph drainage may encourage the flow of lymph fluid out of your arm or leg. Manual lymph drainage involves special hand strokes on your affected limb to gently move lymph fluid to healthy lymph nodes, where it can drain. Massage isn't for everyone. Avoid massage if you have a skin infection, active cancer, blood clots or congestive heart failure. Also avoid massage on areas of your body that have received radiation therapy.
4. Pneumatic compression. If you receive pneumatic compression, you'll wear a sleeve over your affected arm or leg. The sleeve is connected to a pump that intermittently inflates the sleeve, putting pressure on your limb. The inflated sleeve gently moves lymph fluid away from your fingers or toes, reducing the swelling in your arm or leg.
5. Compression garments. Compression garments include long sleeves or stockings made to compress your arm or leg to encourage the flow of the lymph fluid out of your affected limb. Once you've reduced swelling in your arm or leg through other measures, your doctor may suggest you wear compression garments to prevent your limb from swelling in the future. Obtain a correct fit for your compression garment by getting professional help — ask your doctor where you can buy compression garments in your community. Some people will require custom-made compression garments.
In cases of severe lymphedema, your doctor may consider surgery to remove excess tissue in your arm or leg. While this reduces severe swelling, surgery can't cure lymphedema.

Prevention
If you're at risk of developing secondary lymphedema, you can take measures to help prevent it. If you've had or are going to have cancer surgery, ask your doctor whether your particular procedure will involve your lymph nodes or lymph vessels. Ask if your radiation treatment will be aimed at any of your lymph nodes, so you'll be aware of the possible risks.
To reduce your risk of lymphedema, try to:
1. Protect your arm or leg. Avoid any injury to your affected limb. Cuts, scrapes and burns can all invite infection, which can cause lymphedema. Protect yourself from sharp objects. For example, shave with an electric razor, wear gloves when you garden or cook, and use a thimble when you sew. If possible, avoid medical procedures, such as blood draws and vaccinations, in your affected limb.
2. Rest your arm or leg while recovering. After cancer treatment, avoid heavy activity with that limb. Early exercise and stretching are encouraged, but avoid strenuous activity until you've recovered from surgery or radiation.
3. Avoid heat on your arm or leg. Don't apply heat, such as with a heating pad, to your affected limb.
4. Elevate your arm or leg. When you get a chance, elevate your affected limb.
Avoid tight clothing. Avoid anything that could constrict your arm or leg, such as tightfitting clothing and, in the case of your arm, blood pressure readings. Ask that your blood pressure be taken in your other arm.
5. Keep your arm or leg clean. Make skin care and nail care high priorities. Inspect the skin on your arm or leg every day, keeping watch for changes or breaks in your skin that could lead to infection.

Coping and support
It can be frustrating to know that no cure exists for lymphedema. But if you find yourself getting down about the daily bandaging or constant need to protect your affected limb, know that you can control some aspects of lymphedema. To help you cope, try to:
1. Find out all you can about lymphedema. Knowing what lymphedema is and what causes it helps you better understand the signs and symptoms you experience. The more you know, the better you can communicate with your doctor or physical therapist.
2. Take care of your affected limb. Do your best to prevent complications in your arm or leg. Clean your skin daily, looking over every inch of your affected limb for signs of trouble, such as cracks and cuts. Apply lotion to prevent dry skin.
3. Take care of your whole body. Eat a diet full of fruits and vegetables. Exercise daily, if you can. Reduce the stress in your life that you can control. Try to get enough sleep so that you wake up refreshed each morning. Taking care of your body gives you more energy, encourages healing and helps you control your lymphedema.
4. Get support from others with lymphedema. Whether you attend support group meetings in your community or participate in online message boards and chat rooms, it helps to talk to people who understand what you're going through. Contact the National Lymphedema

5. Network to find support groups in your area. They can also put you in touch with other people with lymphedema with whom you can connect via e-mail or letter.
If you feel frustrated or overwhelmed by lymphedema, talk to your doctor or other health care provider about how you feel. He or she may be able to address your concerns.

Reference: Mayoclinic.com

Low blood pressure (hypotension)

Definition
Low blood pressure, also called hypotension, would seem to be something to strive for. After all, high blood pressure (hypertension) is a well-known risk factor for heart disease and other problems. In fact, in recent years there has been an ongoing downward revision of what is considered a normal blood pressure reading. A blood pressure less than 120/80 millimeters of mercury (mm Hg) is now considered normal and optimal for good health.
So, it's easy to understand why you might assume the lower the better when it comes to blood pressure. And it's true that for some people — those who exercise and are in top physical condition — low blood pressure is a sign of health and fitness. But that's not always the case.
For many people, low blood pressure can cause dizziness and fainting or indicate serious heart, endocrine or neurological disorders. Severely low blood pressure can deprive the brain and other vital organs of oxygen and nutrients, leading to a life-threatening condition called shock.

Symptoms
Some people with low blood pressure are in peak physical condition with strong cardiovascular systems and a reduced risk of heart attack and stroke. But low blood pressure can also signal an underlying problem, especially when it drops suddenly or is accompanied by signs and symptoms such as:
Dizziness or lightheadedness
Fainting (syncope)
Lack of concentration
Blurred vision
Nausea
Cold, clammy, pale skin
Rapid, shallow breathing
Fatigue
Depression
Thirst

Causes
Blood pressure is a measurement of the pressure in your arteries during the active and resting phases of each heartbeat. Here's what the numbers mean:
Systolic pressure. The first number in a blood pressure reading, this is the amount of pressure your heart generates when pumping blood through your arteries to the rest of your body.
Diastolic pressure. The second number in a blood pressure reading, this refers to the amount of pressure in your arteries when your heart is at rest between beats.
Although you can get an accurate blood pressure reading at any given time, blood pressure isn't static. It can vary considerably in a short amount of time — sometimes from one heartbeat to the next, depending on body position, breathing rhythm, stress level, physical condition, medications you take, what you eat and drink, and even time of day. Blood pressure is usually lowest at night and rises sharply on waking.
Blood pressure: How low can you go?
Current guidelines identify normal blood pressure as lower than 120/80 — many experts think 115/75 is optimal. Higher readings indicate increasingly serious risks of cardiovascular disease. Low blood pressure, on the other hand, is much harder to quantify.
Some experts define low blood pressure as readings lower than 90 systolic or 60 diastolic — you need to have only one number in the low range for your blood pressure to be considered lower than normal. In other words, if your systolic pressure is a perfect 115, but your diastolic pressure is 50, you're considered to have lower than normal pressure.
Yet this can be misleading because what's considered low blood pressure for you may be normal for someone else. For that reason, doctors often consider chronically low blood pressure too low only if it causes noticeable symptoms.
On the other hand, a sudden fall in blood pressure can be dangerous. A change of just 20 mm Hg — a drop from 130 systolic to 110 systolic, for example — can cause dizziness and fainting when the brain fails to receive an adequate supply of blood. And big plunges, especially those caused by uncontrolled bleeding, severe infections or allergic reactions can, be life-threatening.
Causes of low blood pressure varyAthletes and people who exercise regularly tend to have lower blood pressure than do people who aren't as fit. So, in general, do nonsmokers and people who eat well and maintain a normal weight.
But in some instances, low blood pressure can be a sign of serious, even life-threatening disorders.
The American Heart Association considers the following as possible causes of low blood pressure:
Pregnancy.
Because a woman's circulatory system expands rapidly during pregnancy, blood pressure is likely to drop. In fact, during the first 24 weeks of pregnancy, systolic pressure commonly drops by five to 10 points and diastolic pressure by as much as 10 to 15 points.
Medications.
Many drugs can cause low blood pressure, including diuretics and other drugs that treat high blood pressure; heart medications such as beta blockers; drugs for Parkinson's disease; tricyclic antidepressants; sildenafil (Viagra), particularly in combination with nitroglycerine; narcotics; and alcohol. Some over-the-counter medications can cause low blood pressure when taken in combination with medications used to treat high blood pressure.
Heart problems.
Some heart conditions that can lead to low blood pressure include extremely low heart rate (bradycardia), heart valve problems, heart attack and heart failure. These conditions may cause low blood pressure because they prevent your body from being able to circulate enough blood.
Endocrine problems.
An underactive thyroid (hypothyroidism) or overactive thyroid (hyperthyroidism) can cause low blood pressure. In addition, other conditions, such as adrenal insufficiency (Addison's disease), low blood sugar (hypoglycemia), and in some cases, diabetes, can trigger low blood pressure.
Dehydration.
When you become dehydrated, your body loses more water than it takes in. Even mild dehydration can cause weakness, dizziness and fatigue. Fever, vomiting, severe diarrhea, overuse of diuretics and strenuous exercise can all lead to dehydration. Far more serious is hypovolemic shock, a life-threatening complication of dehydration. It occurs when low blood volume causes a sudden drop in blood pressure and a corresponding reduction in the amount of oxygen reaching your tissues. If untreated, severe hypovolemic shock can cause death within a few minutes or hours.
Blood loss.
Losing a lot of blood from major injury or severe internal bleeding reduces the amount of blood in your body, leading to a severe drop in blood pressure.
Severe infection (septicemia).
Septicemia can happen when an infection in the body enters the bloodstream. Lung, abdomen or urinary tract infections are usually the cause of septicemia. These conditions can lead to a life-threatening drop in blood pressure called septic shock.
Allergic reaction (anaphylaxis).
Anaphylaxis is a severe and potentially life-threatening allergic reaction. Common triggers of anaphylaxis include foods, certain medications, insect venoms and latex. Anaphylaxis can cause breathing problems, hives, itching, a swollen throat and a drop in blood pressure.
Nutritional deficiencies.
A lack of the vitamins B-12 and folate can cause anemia, a condition in which your body doesn't produce enough red blood cells. In addition to making you feel tired because you're not getting enough oxygen, anemia can lead to low blood pressure.

Types of low blood pressureDoctors often break down low blood pressure (hypotension) into different categories, depending on the causes and other factors. Some types of low blood pressure include:
Low blood pressure on standing up (postural or orthostatic hypotension).
This is a sudden drop in blood pressure when you stand up from a sitting position or if you stand up after lying down. Ordinarily, blood pools in your legs whenever you stand, but your body compensates for this by increasing your heart rate and constricting blood vessels, thereby ensuring that enough blood returns to your brain. But in people with postural hypotension, this compensating mechanism fails and blood pressure falls, leading to dizziness, lightheadedness, blurred vision and even fainting.
Postural hypotension can occur for a variety of reasons including dehydration, prolonged bed rest, pregnancy, diabetes, heart problems, burns, excessive heat, large varicose veins and certain neurological disorders. A number of medications can also cause postural hypotension, particularly drugs used to treat high blood pressure — diuretics, beta blockers, calcium channel blockers and angiotensin-converting enzyme (ACE) inhibitors — as well as antidepressants and drugs used to treat Parkinson's disease and erectile dysfunction.
Postural hypotension is especially common in older adults, with as many as 20 percent of those over age 65 experiencing postural hypotension. But postural hypotension can also affect young, otherwise healthy people who stand up suddenly after sitting with their legs crossed for long periods or after working for a time in a squatting position.
Low blood pressure due to nervous system damage (multiple system atrophy with orthostatic hypotension).
Also called Shy-Drager syndrome, this rare disorder causes progressive damage to the autonomic nervous system, which controls involuntary functions such as blood pressure, heart rate, breathing and digestion. Although multiple system atrophy can be associated with muscle tremors, slowed movement, problems with coordination and speech, and incontinence, its main characteristic is severe orthostatic hypotension in combination with very high blood pressure when lying down. Multiple system atrophy can't be cured and usually proves fatal within seven to 10 years of diagnosis.
Low blood pressure after eating (postprandial hypotension).
A problem that almost exclusively affects older adults, postprandial hypotension is a sudden drop in blood pressure after eating. Just as gravity pulls blood to your feet when you stand, a large amount of blood flows to your digestive tract after you eat. Ordinarily, your body counteracts this by increasing your heart rate and constricting certain blood vessels to help maintain normal blood pressure. But in some people these mechanisms fail, leading to dizziness, faintness and falls. Postprandial hypotension is more likely to affect people with high blood pressure or autonomic nervous system disorders such as Parkinson's disease. Lowering the dose of blood pressure drugs and eating small, low-carbohydrate meals may help reduce symptoms.
Low blood pressure from faulty brain signals (neurally mediated hypotension).
Unlike orthostatic hypotension — which occurs when you stand up from a sitting or lying position — this disorder causes blood pressure to drop after standing for long periods, leading to symptoms such as dizziness, nausea and fainting. Although the end result is similar, neurally mediated hypotension differs from orthostatic hypotension in other important respects: It primarily affects young people, for instance, and rather than resulting from failed blood pressure regulation, it seems to occur because of a miscommunication between the heart and the brain. When you stand for extended periods, your blood pressure falls as blood pools in your legs. Normally, your body then makes adjustments to normalize your blood pressure. But in people with neurally mediated hypotension, nerves in the heart's left ventricle actually signal the brain that blood pressure is too high, rather than too low, and so the brain lessens the heart rate, decreasing blood pressure even further. This causes more blood to pool in the legs and less blood to reach the brain, leading to lightheadedness and fainting.

Risk factors
Low blood pressure (hypotension) can happen to anyone, though certain types of low blood pressure are more common depending on your age or other factors:
Age. Drops in blood pressure on standing or after eating occur primarily in older adults. Orthostatic hypotension happens after standing up, while postprandial hypotension happens after eating a meal. Neurally mediated hypotension happens as a result of a miscommunication between the brain and heart. It primarily affects children and younger adults.
Medications. People who take certain medications, such as high blood pressure medication, have a greater risk of low blood pressure.
Certain diseases. Parkinson's disease and some heart conditions put you at a greater risk of developing low blood pressure.

When to seek medical advice
In many instances, low blood pressure isn't serious. If you have consistently low readings but feel fine, your doctor is likely to monitor you during routine exams. Even occasional dizziness or lightheadedness may be relatively minor — the result of mild dehydration, low blood sugar or too much time in the sun or a hot tub, for example. In these situations, it's not a matter so much of how far, but of how quickly, your blood pressure drops. Still, it's important to see your doctor if you experience any signs or symptoms of hypotension because they sometimes can point to more serious problems. It can be helpful to keep a record of your symptoms, when they occur and what you were doing at the time. If these occur at times that may endanger you or others, you should talk to your doctor.

Tests and diagnosis
The goal in evaluating low blood pressure is to find the underlying cause. This helps determine the correct treatment and identify any heart, brain or nervous system problems that may be responsible for lower than normal readings. To help reach a diagnosis, your doctor may recommend one or more of the following:
Blood tests. These can provide a certain amount of information about your overall health as well as whether you have low blood sugar (hypoglycemia) or a low number of red blood cells (anemia), both of which can cause lower than normal blood pressure.
Electrocardiogram (ECG, EKG). This noninvasive test, which can be performed in your doctor's office, detects irregularities in your heart rhythm, structural abnormalities in your heart, and problems with the supply of blood and oxygen to your heart muscle. It can also tell if you're having a heart attack or if you've had a heart attack in the past. Sometimes you may be asked to wear a 24-hour Holter monitor to record your heart's electrical activity as you go about your daily routine.
Echocardiogram. Using the same technology that allows you to view a fetus in the womb, an echocardiogram uses sound waves to produce images of your heart that may show abnormalities in your heart muscle or valves.
Stress test. Some heart problems which can cause low blood pressure are easier to diagnose when your heart is working harder than when it's at rest. During a stress test, you'll exercise, such as walking on a treadmill. (Or, you may be given medication to make your heart work harder if you're unable to exercise.) When your heart is working harder, your heart will be monitored with electrocardiography or echocardiography. Your blood pressure also may be monitored.
Valsalva maneuver. This noninvasive test checks the functioning of your autonomic nervous system by analyzing your heart rate and blood pressure after several cycles of a type of deep breathing: You take a deep breath and then force the air out through your lips, as if you were trying to blow up a stiff balloon.
Tilt-table test. If you have low blood pressure on standing, or from faulty brain signals (neurally mediated hypotension), your doctor may suggest a tilt-table test, which evaluates how your body reacts to changes in position. During the test, you lie on a table that's tilted to raise the upper part of your body, which simulates the movement from a prone to a standing position.

Complications
Even moderate forms of low blood pressure can seriously affect quality of life, leading not only to dizziness and weakness but also to fainting and a risk of injury from falls. And severely low blood pressure from any cause can deprive your body of enough oxygen to carry out its normal functions, leading to damage to your heart and brain.

Treatments and drugs
Low blood pressure that doesn't cause signs or symptoms rarely requires treatment. In symptomatic cases, the appropriate therapy depends on the underlying cause, and doctors usually try to address the primary health problem — dehydration, heart failure, diabetes or hypothyroidism, for example — rather than low blood pressure itself. When low blood pressure is caused by medications, treatment usually involves changing the dose of the medication or stopping it entirely.
If it's not clear what's causing low blood pressure or no effective treatment exists, the goal is to raise your blood pressure and reduce signs and symptoms. Depending on your age, health status and the type of low blood pressure you have, this may be accomplished in several ways:
Use more salt. Experts usually recommend limiting the amount of salt in your diet because sodium can raise blood pressure, sometimes dramatically. But for people with low blood pressure, that can be a good thing. But because excess sodium can lead to heart failure, especially in older adults, it's important to check with your doctor before upping your salt intake.
Drink more water. Although nearly everyone can benefit from drinking enough water, this is especially true if you have low blood pressure. Fluids increase blood volume and help prevent dehydration, both of which are important in treating hypotension.
Use compression stockings. The same elastic stockings and leotards commonly used to relieve the pain and swelling of varicose veins may help reduce the pooling of blood in your legs.
Medications. Several medications, either used alone or together, can be used to treat low blood pressure that occurs when you stand up (orthostatic hypotension). For example, the drug fludrocortisone is often used to treat this form of low blood pressure. This drug helps boost your blood volume, which raises blood pressure. Doctors often use the drug midodrine to raise standing blood pressure levels in people with chronic orthostatic hypotension. It works by restricting the ability of your blood vessels to expand, which raises blood pressure. Other drugs, such as pyridostigmine, nonsteroidal anti-inflammatory drugs (NSAIDs), caffeine and erythropoietin are sometimes used, too, either alone or with other drugs.

Lifestyle and home remedies
Depending on the reason for your low blood pressure, you may be able to take certain steps to help reduce or even prevent symptoms. Some suggestions include:
Drink more water, less alcohol. Alcohol is dehydrating and can lower blood pressure, even if you drink in moderation. Water, on the other hand, combats dehydration and increases blood volume.
Follow a healthy diet. Get all the nutrients you need for good health by focusing on a variety of foods, including whole grains, fruits, vegetables, and lean chicken and fish. If your doctor suggests increasing your sodium intake but you don't like a lot of salt on your food, try using natural soy sauce — a whopping 1,200 milligrams of sodium per tablespoon — or adding dry soup mixes, also loaded with sodium, to dips and dressings.
Go slow. You may be able to reduce the dizziness and lightheadedness that occurs with low blood pressure on standing by taking it easy when you move from a prone to a standing position. Before getting out of bed in the morning, breathe deeply for a few minutes and then slowly sit up before standing. Sleeping with the head of your bed slightly elevated also can help fight the effects of gravity. If you begin to get symptoms while standing, cross your thighs in a scissors fashion and squeeze or put one foot on a ledge or chair and lean as far forward as possible. These maneuvers encourage blood to flow from your legs to your heart.
Eat small, low-carb meals. To help prevent blood pressure from dropping sharply after meals, eat small portions several times a day and limit high-carbohydrate foods such as potatoes, rice, pasta and bread. Drinking caffeinated coffee or tea with meals may temporarily raise blood pressure, in some cases by as much as 3 to 14 millimeters of mercury (mm Hg). But because caffeine can cause other problems, check with your doctor before increasing your caffeine intake.


Reference: MayoClinic.com