Deaths due to eating disorders per million persons in 2012 AN has the highest mortality rate of any psychological disorder. The mortality rate is 11 to 12 times greater than in the general population, and the suicide risk is 56 times higher. Half of women with AN achieve a full recovery, while an additional 20–30% may partially recover. Not all people with anorexia recover completely: about 20% develop anorexia nervosa as a chronic disorder. If anorexia nervosa is not treated, serious complications such as heart conditions and kidney failure can arise and eventually lead to death. The average number of years from onset to remission of AN is seven for women and three for men. After ten to fifteen years, 70% of people no longer meet the diagnostic criteria, but many still continue to have eating-related problems. Alexithymia influences treatment outcome. Recovery is also viewed on a spectrum rather than black and white. According to the Morgan-Russell criteria, individuals can have a good, intermediate, or poor outcome. Even when a person is classified as having a "good" outcome, weight only has to be within 15% of average, and normal menstruation must be present in females. The good outcome also excludes psychological health. Recovery for people with anorexia nervosa is undeniably positive, but recovery does not mean a return to normal. Complications Anorexia nervosa can have serious implications if its duration and severity are significant and if onset occurs before the completion of growth, pubertal maturation, or the attainment of peak bone mass. Complications specific to adolescents and children with anorexia nervosa can include the following: Growth retardation may occur, as height gain may slow and can stop completely with severe weight loss or chronic malnutrition. In such cases, provided that growth potential is preserved, height increase can resume and reach full potential after normal intake is resumed. Height potential is normally preserved if the duration and severity of illness are not significant or if the illness is accompanied by delayed bone age (especially prior to a bone age of approximately 15 years), as hypogonadism may partially counteract the effects of undernutrition on height by allowing for a longer duration of growth compared to controls. Appropriate early treatment can preserve height potential, and may even help to increase it in some post-anorexic subjects, due to factors such as long-term reduced estrogen-producing adipose tissue levels compared to premorbid levels. In some cases, especially where onset is before puberty, complications such as stunted growth and pubertal delay are usually reversible. Anorexia nervosa causes alterations in the female reproductive system; significant weight loss, as well as psychological stress and intense exercise, typically results in a cessation of menstruation in women who are past puberty. In patients with anorexia nervosa, there is a reduction of the secretion of gonadotropin releasing hormone in the central nervous system, preventing ovulation. Anorexia nervosa can also result in pubertal delay or arrest. Both height gain and pubertal development are dependent on the release of growth hormone and gonadotropins (LH and FSH) from the pituitary gland. Suppression of gonadotropins in people with anorexia nervosa has been documented. Typically, growth hormone (GH) levels are high, but levels of IGF-1, the downstream hormone that should be released in response to GH are low; this indicates a state of “resistance” to GH due to chronic starvation. IGF-1 is necessary for bone formation, and decreased levels in anorexia nervosa contribute to a loss of bone density and potentially contribute to osteopenia or osteoporosis. Anorexia nervosa can also result in reduction of peak bone mass. Buildup of bone is greatest during adolescence, and if onset of anorexia nervosa occurs during this time and stalls puberty, low bone mass may be permanent. Hepatic steatosis, or fatty infiltration of the liver, can also occur, and is an indicator of malnutrition in children. Neurological disorders that may occur as complications include seizures and tremors. Wernicke encephalopathy, which results from vitamin B1 deficiency, has been reported in patients who are extremely malnourished; symptoms include confusion, problems with the muscles responsible for eye movements and abnormalities in walking gait. The most common gastrointestinal complications of anorexia nervosa are delayed stomach emptying and constipation, but also include elevated liver function tests, diarrhea, acute pancreatitis, heartburn, difficulty swallowing, and, rarely, superior mesenteric artery syndrome. Delayed stomach emptying, or gastroparesis, often develops following food restriction and weight loss; the most common symptom is bloating with gas and abdominal distension, and often occurs after eating. Other symptoms of gastroparesis include early satiety, fullness, nausea, and vomiting. The symptoms may inhibit efforts at eating and recovery, but can be managed by limiting high-fiber foods, using liquid nutritional supplements, or using metoclopramide to increase emptying of food from the stomach. Gastroparesis generally resolves when weight is regained. Cardiac complications Anorexia nervosa increases the risk of sudden cardiac death, though the precise cause is unknown. Cardiac complications include structural and functional changes to the heart. Some of these cardiovascular changes are mild and are reversible with treatment, while others may be life-threatening. Cardiac complications can include arrhythmias, abnormally slow heart beat, low blood pressure, decreased size of the heart muscle, reduced heart volume, mitral valve prolapse, myocardial fibrosis, and pericardial effusion. Abnormalities in conduction and repolarization of the heart that can result from anorexia nervosa include QT prolongation, increased QT dispersion, conduction delays, and junctional escape rhythms. Electrolyte abnormalities, particularly hypokalemia and hypomagnesemia, can cause anomalies in the electrical activity of the heart, and result in life-threatening arrhythmias. Hypokalemia most commonly results in anorexic patients when restricting is accompanied by purging (induced vomiting or laxative use). Hypotension (low blood pressure) is common, and symptoms include fatigue and weakness. Orthostatic hypotension, a marked decrease in blood pressure when standing from a supine position, may also occur. Symptoms include lightheadedness upon standing, weakness, and cognitive impairment, and may result in fainting or near-fainting. Orthostasis in anorexia nervosa indicates worsening cardiac function and may indicate a need for hospitalization. Hypotension and orthostasis generally resolve upon recovery to a normal weight. The weight loss in anorexia nervosa also causes atrophy of cardiac muscle. This leads to decreased ability to pump blood, a reduction in the ability to sustain exercise, a diminished ability to increase blood pressure in response to exercise, and a subjective feeling of fatigue. Some individuals may also have a decrease in cardiac contractility. Cardiac complications can be life-threatening, but the heart muscle generally improves with weight gain, and the heart normalizes in size over weeks to months, with recovery. Atrophy of the heart muscle is a marker of the severity of the disease, and while it is reversible with treatment and refeeding, it is possible that it may cause permanent, microscopic changes to the heart muscle that increase the risk of sudden cardiac death. Individuals with anorexia nervosa may experience chest pain or palpitations; these can be a result of mitral valve prolapse. Mitral valve prolapse occurs because the size of the heart muscle decreases while the tissue of the mitral valve remains the same size. Studies have shown rates of mitral valve prolapse of around 20 percent in those with anorexia nervosa, while the rate in the general population is estimated at 2–4 percent. It has been suggested that there is an association between mitral valve prolapse and sudden cardiac death, but it has not been proven to be causative, either in patients with anorexia nervosa or in the general population. Relapse Rates of relapse after treatment range from 9–52% with many studies reporting a relapse rate of at least 25%. Relapse occurs in approximately a third of people in hospital, and is greatest in the first six to eighteen months after release from an institution.
symptom of Bird fancier's lung
symptoms of Bird fancier's lung
symptom of Aspiration pneumonia
symptom of Alpha-1 antitrypsin deficiency
symptom of Bronchiectasis
symptom of Peritonsillar abscess
symptom of Acute respiratory distress syndrome
symptom of Pulmonary heart disease