The following symptomatology is evident in acute or chronic phase of Kwashiorkor:

General appearance: Kwashiorkor patients show apathy and lethargy as acute signs. They may appear with signs of easy irritability which are all attributed to low energy levels due to lack of protein. They are generally thin with cachexia due to the absence of muscle mass with defective protein synthesis.

Integumentary system: Hair may appear with different shades of light and dark bands referred to as the “flag sign”. The different hues in the hair represents the different periods of impaired nutrition. The skin will appear flaky due incompetent connective tissues formed from a defective protein synthesis process.

Cardiovascular and respiratory system: The heart may present with mild murmur due to micronutrient deficiency anemia or impending heart failure in the late stages. Pericardial effusion may present with severe PEM in children [7]. Breathing may be shallow due to metabolic acidosis.

Abdomen: The abdomen may be protuberant or enlarged due to ascites. The liquid damming in the abdominal cavity is due to the hypoalbuminemia effect on osmosis. Hepatomegaly may ensue with chronic fatty liver disease. Intestinal parasitism may not be infrequent with severe malnutrition.

Extremities: The limbs will generally convey weakness because of the lack of energy from proteins. Bipedal non-pitting edema may occur in the legs due to the osmotic imbalance.

Patients with Kwashiorkor are often subjected to these following tests:

• Complete blood count to determine state of anemia and inflammatory processes with infections.
• Arterial blood gases to determine extent of metabolic acidosis of the patient.
• BUN and Creatinine are accurate markers for the kidney’s health.
• Serum potassium determination guides management of hypokalemia.
• Total protein albumin and globulin determination to assess the levels of hypoalbuminemia and hypoglobulinemia.
• Urinalysis will show ketone bodies due to improper protein metabolism.

The early intervention of fulfilling protein caloric deficiency in Kwashiorkor will greatly improve patient’s outlook. Dietary replacement therapy are arbitrarily dependent on the severity of the disease. Caloric replacement will usually start with carbohydrates and simple sugars until the patient is able to achieve adequate energy.

By then protein infusion may be necessary along with supplemental vitamins and minerals. Patients who underwent prolonged starvation may not be immediately infused with protein because it may trigger a Refeeding Syndrome (RS) which leads to the uncontrolled catabolic action of insulin [8]. Kwashiorkor patients with superimposed infections treated with antibiotics should be reevaluated for the kidney’s clearance of the drugs used because it is usually impaired in PEM [9].

Patients received in shock will benefit from the immediate transfusion with plasma expanders and fluids. Oral enzymatic replacement with lactase may be helpful in cases of lactose intolerance.

Kwashiorkor and other protein energy malnutrition is considered a metabolic emergency. Patients who get medical care early have a good outlook in the clinical course of the disease.

However, those treated at the later stage of the disease may still be alleviated but permanent conditions like mental and growth retardation may occur. Patients who demonstrated lipids and ketones in the urine may have a poorer prognosis with PEM [5].

Kwashiorkor and PEM carries a grim prognosis when it occurs in patients below 5 years of age and in elderly people beyond 55 years old [6].

Complications

The primary protein energy state in Kwashiorkor may give rise to these complications:

• Sepsis: The dermatologic manifestation of generalized ulceration may invite a host of pathogenic bacteria to the ailing body. Defective protein synthesis will impair antibody production which may hamper significantly the body’s immune response against invading microorganism.
• Coma: The state of continuous carbohydrate breakdown in the light of a limited supply of protein may lead to a system condition of metabolic acidosis. The rapid decline of pH and the increased acidity of the plasma may incapacitate the brain into a vegetative state of coma.
• Hypovolemic shock: The incompetent fatty liver in Kwashiorkor will decrease the albumin production and decrease the osmotic gradient in the intracellular spaces. Progressive dehydration due to an incompetent osmotic gradient within the vessels may lead to hypovolemic shock.
• Mental and physical disability: Uncontrolled metabolic imbalance that afforded chronic insults to the brain may result in a permanent mental retardation and physical incapacities.
• Death: The severe forms of these PEMs may culminate with liver failure, heart failure or renal failure that can eventually lead to death.

The basic etiology in Kwashiorkor is the limited or meager supply of food available in the community. This condition is greatly influenced by drought, famine, war, and political unrest which are common in some countries in Africa and Central America.

Kwashiorkor may also prevail in communities with no access to protein-rich foods like meat and poultry and are solely dependent on carbohydrates from grains and vegetables.

The incidence of Kwashiorkor in the US is relatively low but PEM is somewhat prevalent among hospitalized patients. The World Health Organization in 2000 announced that there at least 181.9 million children suffering from severe malnutrition especially in developing countries. Statistics in Central Asia and Eastern Africa reveal that approximately half of the children have some form of growth retardation due to protein energy malnutrition.

About 5 million children deaths in the developing countries are related to PEM and Kwashiorkor. Mortality rates in Kwashiorkor decrease with increasing age of its onset. The dark skinned races have more incidence of Kwashiorkor due to the relatively poor socio-economic situation in their country that affects dietary input.

Mediated by some complex mechanism, children suffering from sickle cell anemia are predisposed to PEM and Kwashiorkor [1].

Kwashiorkor as a protein energy malnutrition state in children happens with adequate carbohydrate nutrition but devoid of protein sources.

This condition will lower the body’s drive to produce its own visceral protein leading to poor energy supply. In Kwashiorkor, low protein substrates (raw materials) can lead to hypoalbuminemia that causes the extravasation of fluid to the extracellular space manifesting as edema.

Consequently, this low protein state may impair the production of B-lipoproteins that results in a fatty liver [2]. The inadequate production of transfer proteins may lead to micronutrient deficiency like zinc.

The concurrent zinc deficiency is implicated as the main cause of skin diseases like ulcerations in Kwashiorkor patients. Kwashiorkor is seen to affect glucose clearance in the blood causing a dysfunction in the beta-cells of the pancreas [3]. Pregnant mothers with PEM may affect inherent metabolic physiology of the fetus that my result to marasmus or Kwashiorkor when the baby is born [4].

1. Hyacinth HI, Adekeye OA, Yilgwan CS. Malnutrition in Sickle Cell Anemia: Implications for Infection, Growth, and Maturation. J Soc Behav Health Sci. Jan 2013; 1:7(1).
2. Bandsma RH, Spoelstra MN, Mari A, Mendel M, van Rheenen PF, Senga E, van Dijk T, Heikens GT. Impaired glucose absorption in children with severe malnutrition.J Pediatr. 2011; 158(2):282-7.e1 
3. Spoelstra MN, Mari A, Mendel M, et al. Kwashiorkor and marasmus are both associated with impaired glucose clearance related to pancreatic beta-cell dysfunction. Metabolism. Mar 2 2012;
4. Forrester TE, Badaloo AV, Boyne MS, Osmond C, Thompson D, Green C, et al. Prenatal factors contribute to the emergence of kwashiorkor or marasmus in severe undernutrition: evidence for the predictive adaptation model. PLoS One. 2012; 7(4):e35907.
5. Badaloo AV, Forrester T, Reid M, Jahoor F. Lipid kinetic differences between children with kwashiorkor and those with marasmus. Am J Clin Nutr. 2006; 83(6):1283-8 
6. Demling RH. The incidence and impact of pre-existing protein energy malnutrition on outcome in the elderly burn patient population. J Burn Care Rehabil. Jan-Feb 2005; 26(1):94-100.
7. Ahmad S, Ellis J, Nesbitt A, Molyneux E. Pericardial effusions in children with severe protein energy malnutrition resolve with therapeutic feeding: a prospective cohort study. Arch Dis Child. 2008; 93(12):1033-6 
8. Walmsley RS. Refeeding syndrome: screening, incidence, and treatment during parenteral nutrition. J Gastroenterol Hepatol. Dec 2013; 28 Suppl 4:113-7.
9. Oshikoya KA, Sammons HM, Choonara I. A systematic review of pharmacokinetics studies in children with protein-energy malnutrition. Eur J Clin Pharmacol. 2010; 66(10):1025-35 
10. Dorner TE, Lackinger C, Haider S, Luger E, Kapan A, Luger M, et al. Nutritional intervention and physical training in malnourished frail community-dwelling elderly persons carried out by trained lay "buddies": study protocol of a randomized controlled trial. BMC Public Health. Dec 2013; 13(1):1232.