If oedema is detected when the patient first presents clinically, or if it develops without a preceding improvement in food intake, the underlying mechanisms should be carefully investigated in order to avoid the risks of congestive cardiac failure and pulmonary oedema. By the time peripheral oedema is detectable, the amount of fluid retained in the body contributes several kilograms to the patient's weight, thereby concealing the true loss of weight. There is a common misconception that peripheral oedema is usually due to a lowering of plasma albumen, but this is uncommon in anorexia nervosa. Therefore the clinician must look for other reasons.
1. A fall in interstitial fluid pressure has been proposed whereby water seeps from the blood into the interstitial spaces (86) whereas the total exchangeable sodium is likely to remain within the normal range.
2. 'Rebound' oedema following hyponatraemia due to abuse of laxatives or diuretics.
3. Wet beri-beri: vitamin deficiency in anorexia nervosa is uncommon because many patients continue to eat vegetables and fruit. Nevertheless a lack of vitamin B 1 (thiamine) may occur in patients who eat a stereotyped diet, and Wernicke's encephalopathy may follow. (8)) Vitamin B, deficiency may also manifest itself in congestive cardiac failure with severe oedema from a nutritional cardiomyopathy, precipitated by refeeding without thiamine.
4. Congestive heart failure and pulmonary oedema may occur as a result of general undernutrition leading to a decreased cardiac mass, cardiac output, and volume.
Severe hypoglycaemia with plasma glucose levels as low as 1.0 mmol/l is rare in anorexia nervosa but is recognized as a cause of death. Hypoglycaemia may go unrecognized, as a lack of sympathetic nervous response may mask the classical symptoms and signs.
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