Flashcards in Severe Childhood Malnutrition: Kwashiorkor and Marasmus Deck (34)
What childhood malnutrition diseases are associated with severe wasting due to severe malnutrition?
Kwashiorkor and Marasmus
What is the main difference between Kwashiorkor and Marasmus?
Kwashiorkor: has edema
Marasmus: severe wasting (less than 70% or less than 3SD from the mean)
Where is the best source of information on these childhood malnutrition diseases?
Patients with marasmus will have no obvious pathology. Kwashiorkor will have multiple pathologies, what are they?
1. Pitting edema (can mask the weight loss)
2. Dermatosis (lighter hair color, peeling/scaly skin)
3. Hypoalbuminemia (fatty liver)
4. Abnormal plasma AA
5. K + deficiency (Apathy and anorexia)
How is Kwashiorkor illness managed clinically (very simple and effective, but not widely known and can cause death)?
Treatment needs to be phased: high protein diets in the beginning can be fatal
---Resuscitate, Repair, and Replete
--tx the severe malnutrition
---repair the damaged cellular injury
---replete the obvious tissue deficits only after cells are repaired
Routine treatment, for Kwashiorkor, includes the following ten steps:
1. Prevent and Treat: hypoglycemia (Days 1-2), hypothermia (Days 1-2), dehydration (days 1-2), electrolyte imbalance (important throughout), infection (first week), and micronutrient deficiencies
---DO NOT GIVE ANY IRON THE FIRST WEEK start the second week
2. Special feeds for initial stabilization (1st week) followed by catch up growth (2nd week)
3. Provide loving care and stimulation (important throughout)
4. Follow up after discharge
Inappropriate high protein tube feeding on admission in Kwashiorkor patients will result in what?
In Kwashiorkor what is the goal for treatment/
An initial low protein low energy maintenance diet with antibiotics and selective supplements resolves the pathology.
In Kwashiorkor treatment week 1 is for stabilization. Infections in this stage is treated with what?
Treat infections with broad spectrum antibiotics (while addressing associated hypoglycemia and hypothermia)
In the first week how do you treat the dehydration?
Rehydration solution malnutrition (ReSoMal)
--it is possible to have edema with low blood volume
In the first week how do you treat K and Mg deficiencies?
with electrolyte supplementation low protein feeds
In Kwashiorkor, when the edema is cured, what returns?
What micronutrient is avoided in the first week of stabilization in Kwashiorkor children?
IRON (Start week 2)
Weeks 2-6 involves rehabilitation of Kwashiorkor children. What should these children be fed??
Feed large amounts of energy dense milk based feed with about 50% fat content
--full cream milk, sugar and oil with 10% protein
--include iron now
In weeks 2-6 rehab should you allow the Kwashiorkor patient to eat as they wish?
Allow patient to eat as much as they want and catch up growth is very successful
Is Kwashiorkor due to protein energy malnutrition?
---the myth began in the 30s stating that symptoms were cured by milk, it was due to a protein deficiency.
Usually the edema is explained by hypoalbuminemia, what are explanations for hypoalbuminemia?
1. Failure to adapt to a low protein diet
2. Cortisol inadequacy
4. Protein losing enteropathy
The idea that Kwashiorkor can be explained by a protein deficiency is inadequate. Why?
1. Protein deficiency in children in vary rare (requirements are very low --5% of calories) and symptoms can be cured by a low protein diet.
---even in countries where malnutrition is likely to occur, it is still difficult to develop a protein deficiency. Only when the diet is composed primarily of root vegetables does protein deficiency occur.
Breast milk only has 6% of protein content (aka low protein) ---- this indicates the initial level of protein that Kwashiorkor children begin with. Therefore catch up growth, children need how much protein content in diets?
Edema is gone before there is any change in what?
Serum albumin concentration
Hypoalbuminemia is not linked to any other symptoms besides what?
Patients with Kwashiorkor are malnourished with either a low protein or insufficient diet; growth stops and anorexia and weight loss occur. Patient are on their way to becoming stunted or wasted, when what happens?
when an additional noxious inflammatory insult causes marasmus or kwashiorkor to develop
What is the pathway for Kwashiorkor once the inflammatory insult happens?
Insult ----- increased ROS ---- poor diet causes inadequate protection (Vit E, A, C, SE, and Zinc, Mn and Sulpher) ---- Iron overload (Due to tissue breakdown without excretion) catalyses the formation of more ROS (formation of the superoxide radicals) ---- Inadequate repair (micronutrient deficiencies)---damages
When Kwashiorkor patients loss weight, what happens to the iron?
There is no mechanism for excretion of iron and as your blood volume goes down you reduce the amount of circulating hemoglobin and therefore you need to put the iron somewhere so it goes into stores in the body (aka in the liver and bone marrow)
--too much iron causes inflammation
Excess iron has what effect on the body?
Excess iron can damage membranes and proteins disrupting transport and ionic balances resulting in K+ loss and sodium entering
--these children dont have FA to repair
Increased oxidative stress has what effect on organs?
1. Kidney: impaired function contributes to edema
2. Liver: Impaired protein synthesis, decreased albumin and APOB100 secretion, damaged mitochondrial function. (decreased ATP production and fatty infiltration)
3. Skin: similar changes seen in a sunburn (photosensitivity) ---dermatitis appears like this
4. Hair: bleaching, black children have reddish hair. White children will have blonde
Free iron is extremely toxic and contributes to the formation of what?
When the plasma ferritin is elevated in the child what does this indicate?
Patient with Kwashiorkor may have similar symptoms to what?
Anemia of chronic disease (growth inhibition, tissue wasting, decreased blood volume and hemoglobin)
--this is because the iron is high, but it is locked up in storage (hepcidin)
--low RBC synthesis due to inflammatory cytokines