Why does kwashiorkor happen

Ashworth A. Nutrition, food security, and health. In: Kliegman RM, St. Nelson Textbook of Pediatrics. Philadelphia, PA: Elsevier; chap Manary MJ, Trehan I. Protein-energy malnutrition. Goldman-Cecil Medicine. Updated by: Neil K. Editorial team.

Kwashiorkor is most common in areas where there is: Famine Limited food supply Low levels of education when people do not understand how to eat a proper diet This disease is more common in very poor countries.

Poor weight gain. Slowing of linear growth. Behavioral changes - Irritability, apathy, decreased social responsiveness, anxiety, and attention deficits. What happens in beri beri? Beriberi is a disease caused by a vitamin B-1 deficiency, also known as thiamine deficiency. Wet beriberi affects the heart and circulatory system. In extreme cases, wet beriberi can cause heart failure. Dry beriberi damages the nerves and can lead to decreased muscle strength and eventually, muscle paralysis. Who needs protein?

Every cell in the human body contains protein. The basic structure of protein is a chain of amino acids. You need protein in your diet to help your body repair cells and make new ones. Protein is also important for growth and development in children, teens, and pregnant women. Who malnutrition 10 steps? There are ten essential steps: 1. Correct electrolyte imbalance. Days Weeks What is protein deficiency called? This misconception has influenced the recommendations for treating children with severe acute malnutrition.

There are close pathophysiological parallels between kwashiorkor and Finnish congenital nephrotic syndrome CNS pre-nephrectomy; both develop protein-energy malnutrition and hypoalbuminaemia, which predisposes them to intravascular hypovolaemia with consequent sodium and water retention, and makes them highly vulnerable to develop hypovolaemic shock with diarrhoea.

In CNS this is successfully treated with intravenous albumin boluses. It is time to trial intravenous bolus albumin for the treatment of children with kwashiorkor and shock. Malnutrition in young children may lead to severe wasting alone marasmus , or may be associated with oedema kwashiorkor.

The high mortality of severe acute kwashiorkor has changed little 1 since it was first described in , 2 and about half of children who present today with shock still die. The World Health Organisation WHO recommend treating marasmus and kwashiorkor with the same fluid regimen when it is associated with shock, 3 as if they shared precisely the same pathophysiology.

During the s it was recognised that the presence of oedema in kwashiorkor was correlated with a very low plasma albumin concentration, presumably related to a dietary lack of protein. The relationships between the plasma albumin concentration in children with severe malnutrition and a the percentage chance of them having signs of oedema, and b their mortality risk, as identified by Whitehead 5 and Hay 7 in the early s.

Albumin is a relatively small protein, so it contributes disproportionately to the plasma oncotic pressure, and in health is its major contributor. Starling's equation 14 explains how the movement and distribution of water between the plasma and tissue spaces of all tissues is physically regulated by the balance of hydrostatic and oncotic pressures across capillary blood vessel walls.

However, Golden ruled out this mechanism as the primary cause for oedema in kwashiorkor by demonstrating that children who he treated with a relatively low protein diet showed marked clinical improvement and lost their oedema before their plasma albumin concentrations had risen.

By scanning and enlarging the figure and constructing a grid from the y-axis to obtain the numerical data, and re-plotting these values with a conventional aspect ratio and horizontal text Fig. Paired values can be discerned for six of the 13 cases denoted by filled circles , and by combining the remaining seven cases in every possible way, paired t -tests show that the true P -value was somewhere between 0. Graphs of the changes in plasma albumin concentrations in children on dietary treatment for kwashiorkor before, during and after the disappearance of oedema, from Golden et al, Albumin concentrations can be measured accurately by using specific immunological assays that only respond to that particular protein, even at very low levels.

These methods rely on the fact that proteins have negatively charged surfaces that bind readily to certain positively charged dyes such as bromcresol-green BCG , and that gram-for-gram, albumin binds more avidly than most of the globulins. However, globulins do bind with BMG, so when the albumin levels are very low this causes the measurements to be disproportionately high.

The impact of using corrected albumins instead of BCG or electrophoresis values can be seen in Figure 2c , which demonstrates just how severely hypoalbuminaemic these children actually were on arrival. Finally, the true impact on their plasma albumin levels of feeding these children is most obvious when its increase is plotted for the period when they lost their oedema Fig. Both plots demonstrate just how low the true plasma albumin concentrations are in kwashiorkor.

Figure 3a shows that in each study which included children with both marasmus and kwashiorkor, the mean albumin concentrations were consistently lower in kwashiorkor. Though there is some overlap between different studies, this may in part be owing to technical differences, such as measurement variations. The corrected albumin concentrations measured in children with kwashiorkor a compared to children with marasmus in 12 studies, and b before and after feeding in 10 studies, four of which tested two different milks.

Figure 3b shows that the plasma albumin rises promptly when appropriate milk feeds are introduced, with a mean daily increase of about 1. This compares to a mean daily increase of 0. Some, but not all, of the reports indicated how long it took for the oedema to disappear, and these intervals were typically in the range of 6—12 days.

These data provide no support for the hypothesis that the oedema resolved before the albumin rose. The evidence I have reviewed thus far points to the pathophysiology of kwashiorkor being a combination of severe malnutrition and a low plasma oncotic pressure due to extreme hypoalbuminaemia.

This closely resembles the pathophysiology of untreated Finnish congenital nephrotic syndrome CNS , though of course the mechanism leading to them acquiring protein-energy malnutrition is very different. Infants with CNS simply cannot retain albumin, nor the smaller globulins, and waste vast quantities of energy.

Today, children with CNS are managed very actively in developed countries, with drug treatment or unilateral nephrectomy to limit their proteinuria, 37 or bilateral nephrectomy to stop it, 38 followed by dialysis and transplantation.

However, before this CNS was universally fatal by 18 months of age; children failed to thrive, and died of protein-energy malnutrition before they were old enough to develop renal failure. Like children with kwashiorkor, 40 they had markedly increased platelet stickiness.

Low-dose aspirin is used to counter this in CNS, but of course if the same mechanism was responsible in kwashiorkor it would correct as the albumin rises with nutritional treatment.

The two conditions also share similarly altered hormonal profiles. Much attention has been drawn towards the low glutathione levels seen in kwashiorkor but not in marasmus. It was argued that the oedema of kwashiorkor could not be a consequence of hypoalbuminaemia as glutathione levels were said to be normal in nephrotic patients. The major feature common to both kwashiorkor and CNS, however, is their disordered fluid balance physiology. Children with persistent nephrotic syndrome lose plasma water into the interstitium because of their low oncotic pressure, and as a consequence have chronic intra-vascular hypovolaemia.

This induces avid water retention by an increased secretion of arginine vasopressin antidiuretic hormone in a non-osmolar response to hypovolaemia, and avid sodium retention by increased plasma renin activity and consequent secondary hyperaldosteronism, as well as by suppression of the release of the natriuretic peptides. This therefore leads to fluid retention and oedema, which is exacerbated if the child receives greater quantities of salt.

The presence of oedema increases the interstitial pressure which therefore slows the accumulation of more oedema by balancing the Starling forces. Children with kwashiorkor are also markedly hypovolaemic and respond hormonally to this in the same way as nephrotic children. Viart demonstrated that children with severe malnutrition had a reduced blood volume compared to controls by re-injecting them with their own 51 Cr-labelled red blood cells.

Women over the age of 50 have increased needs for several vitamins and minerals. Here are the 10 best multivitamins for women over Health Conditions Discover Plan Connect. What Is Kwashiorkor? Medically reviewed by Natalie Butler, R. What causes kwashiorkor? What are the symptoms of kwashiorkor? How is kwashiorkor diagnosed? How is kwashiorkor treated? What are the complications of kwashiorkor?

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