Kwashiorkor, the classical example of severe acute malnutrition, is characterised by the presence of oedema. In addition to oedema, the hallmarks of the condition include dermatosis, diarrhoea, and fatty liver (1). Typically there are skin lesions (pigmented or depigmented areas with or without ulceration), scanty lustreless hair, an enlarged fatty liver, loss of interest in the surroundings, and loss of appetite. Oedema may even progress to generalised swelling or anasarca. Fluid homeostasis in the body is altered resulting in excess accumulation of fluid in the extracellular space. Cicely Willliams first introduced the name kwashiorkor in 1935, which in the Ga language of West Africa means “the disease of the deposed child” (2). This literally refers to the child who develops oedema after being weaned with starchy gruels following the birth of a sibling who is breastfed. Kwashiorkor, which occurs mostly in children 1-3 yr of age, results from a deficiency of dietary protein and is usually associated with an infection (3). However in India, Gopalan did not find any difference in diets of children developing marasmus or kwashiorkor (4). In response to infection, amino acids are used for the production of acute phase reactants at the expense of visceral protein synthesis. There is a decrease in blood albumin level, which is partly responsible for development of oedema (5). Beta-lipoprotein is not produced in adequate amounts, resulting in impaired transport of fat from the liver, accumulation of fat and an enlarged fatty liver (6). There is no population-based data on prevalence of oedematous malnutrition. This is due to the fact that large-scale health and nutrition surveys do not make any attempts to detect oedema. Case fatality, however, is very high among children hospitalised with oedematous malnutrition. These observations indicate the need for better information on the global, regional and national prevalence of kwashiorkor and other forms of oedematous malnutrition (7).