SEVERE CHILDHOOD UNDERNUTRITION (SCU)

Protein energy malnutrition Protein energy malnutrition (PEM)(PEM)

GIT Lec. 6GIT Lec. 6

ByDr. Athal HumoDr. Athal Humo

Severe childhood undernutrition (SCU)• To know the cause of SCU.• To know its types.• To define marasmus.• To distinguish its manifestation.• To define kwashiorkor.• To distinguish its manifestation.• To know the complication of PEM• To know the treatment of PEM

Protein energy Protein energy malnutrition (PEM)malnutrition (PEM)

Marasmus was thought to result primarily from inadequate energy intake, whereas kwashiorkor was thought to result primarily from inadequate protein intake.

Marasmic kwashiorkor, has features of both disorders (wasting and edema).

ETIOLOGY:✎ primary malnutrition :

malnutrition resulting from inadequate food intake

✎ secondary malnutrition :• increased nutrient needs.•decreased nutrient absorption.• increased nutrient losses.

MARASMUS (Non-edematous SCU)

Can be defined as: Emaciation with body weightBelow 60 % of median (50th percentile) for age

OrBelow 70% of the ideal weight for height

AndDepleted body fat store Loss of muscle mass and subcutaneous fat stores

is confirmed by inspection or palpation and quantified by anthropometric measurements.

MARASMUS

MARASMUS

CLINICAL MANIFESTATIONS:• Growth chart criteria.• Mental changes: irritability, listlessness, may be apathetic & weak• failure to gain weight, weight loss, until emaciation results.• Skin: dry ,thin, loses turgor and becomes wrinkled and loose as

subcutaneous fat disappears. Loss of fat from the sucking pads of the cheeks often occurs late in the course of the disease; thus, the infant's face may retain a relatively normal appearance compared with the rest of the body, but this, too, eventually becomes shrunken and wizened.

Head: may appear large but proportional to length• Hair: thin sparse easily pulled Tongue: atrophy of filliform papilli, monilial stomatitis• Muscles: atrophy and resultant hypotonia Abdomen may be distended or flat, and the intestinal pattern may

be readily visible.• temperature usually becomes subnormal and the pulse slows. • Constipation but may develop starvation diarrhea with frequent

small stool containing mucous• Infections and parasitic infestations are common.

Kwashiorkor Edematous SCU

Hypoalbuminemic, edematous malnutrition may become evident from early infancy to about 5 yr of age, usually after weaning from the breast.

Can be defined as: ☯Body weight of the child ranges from

60-80% of expected weight for age ☯With edema.

CLINICAL MANIFESTATIONS: • Growth chart criteria.• Mental changes: especially irritability and apathy, are

common. Stupor, coma, and death may follow• Hair:

– often sparse and thin, easily plucked, appears dull brown, red, or yellow-white.

– nutritional repletion restores hair color, leaving a band of hair with altered pigmentation followed by a band with normal pigmentation (flag sign).

• Face: facial edema result in moon facies• Skin: a relative maintenance of subcutaneous adipose tissue,

skin changes are common and may include:– Hyperpigmented hyperkeratosis– Erythematous macular rash (pellagroid) on the trunk and extremities.

Darkening of the skin appears in irritated areas but not in those exposed to sunlight, a contrast to the situation in pellagra

– In the most severe form of kwashiorkor, a superficial desquamation occurs over pressure surfaces ("flaky paint" rash).

Flaky paint” dermatosis on the thighs

Flaky paint” dermatosis

Diffuse fine scale in a reticulated pattern over the abdomen

Kwashiorkor

Kwashiorkor, apathy and misery

• Edema:– Varies from a minor pitting of the dorsum of the foot to

generalized edema with involvement of the eyelids and scrotum– Edema usually develops early; failure to gain weight may be

masked by edema, which is often present in internal organs before it can be recognized in the face and limbs.

• Muscle :marked atrophy of muscle mass.

• Tongue and mouth: Angular cheilosis, atrophy of the filiform papillae of the tongue, and monilial stomatitis are common

• Abdomen: may reveal an enlarged, soft liver with an indefinite edge. The abdomen is distended, and bowel sounds tend to be hypoactive

• GIT: anorexia ,vomiting, diarrhea.Others: Lymphatic tissue commonly is atrophic. Infections and parasitic infestations are common

COMPLICATIONS of PEM➷ Infection :Infection : Malnourished children are more susceptible to infection,

especially sepsis, pneumonia, and gastroenteritis. because:

☯ Malnutrition causes defects in host defenses.

☯ Conversely, infection increases the metabolic needs of the patient and often is associated with anorexia.

☯ Children with FTT may suffer from a malnutrition-infection cycle, in which recurrent infections exacerbate malnutrition, which leads to greater susceptibility to infection. Children with FTT must be evaluated and treated promptly for infection and followed closely. Treatment regimens should be appropriate for the infection.

Noma

➷ Refeeding syndrome:Refeeding syndrome:

• With the rapid reinstitution of feeding after starvation, fluid and electrolyte homeostasis may be lost, and the body may be unable to maintain normal serum concentrations of vital electrolytes.

• Changes in serum electrolyte concentrations and the associated complications resulting from these changes are collectively termed refeeding syndrome.

• These changes typically cause decrease in phosphorus, potassium, calcium, and magnesium and can result in life-threatening cardiac or neurological problems.

• Serum phosphate levels of ≤0.5 mmol/L can produce weakness, rhabdomyolysis, neutrophil dysfunction, cardiorespiratory failure, arrhythmias, seizures, altered level of consciousness, or sudden death.

• Refeeding syndrome can be avoided by slow institution of nutrition for children with severe malnutrition, close monitoring of serum electrolytes during the initial days of feeding, and prompt replacement of depleted electrolytes.

➷ Hypoglycemia Hypoglycemia is common after periods of severe fasting, but also may be a sign of sepsis.

➷ HypothermiaHypothermia may signify infection or, with bradycardiabradycardia, may signify a decreased metabolic rate to conserve energy. Bradycardia and poor cardiac output predispose the malnourished child to heart failure, which is exacerbated by acute fluid or solute loads.

➷ Micronutrient deficienciesMicronutrient deficiencies also can complicate malnutrition. Vitamin A and zinc deficiencies are common in the developing world and are an important cause of altered immune response and increased morbidity and mortality.

➷ Depending on the age at onset and the duration of the malnutrition, malnourished children may have

– Permanent growth stunting Permanent growth stunting – Delayed development Delayed development

Treatment:

In general the simples and least coasty approach is recommendedThe usual approach to treatment of PEM includes three phases.

1 .stabilization phase: The first relatively brief phase (1-7 days) . During this

phase, ☯ Dehydration, if present, is corrected and ☯ Antibiotic therapy is initiated to control infection. Because of the difficulty of estimating hydration, oral

rehydration therapy is preferred. If intravenous therapy is necessary, estimates of dehydration should be assessed frequently, particularly during the first 24hr of therapy.

☯ Treat or prevent hypothermia, hypoglycemia, electrolyte imbalances.

☯ Oral feedings are also started with specialized high-calorie formula, that can be made with simple ingredients. The initial phase of oral treatment is with the F75 diet (75 kcal or 315 kg/100 mL).

2 .Rehabilitation phase 2nd phase last (2-6weeks): includes• Continued antibiotic therapy with appropriate changes if the

initial combination was not effective and• Diet :providing maintenance requirements of energy and protein

along with adequate electrolytes, trace minerals, and vitamins. Nutritional management similar to FTT

• The rehabilitation diet is with the F100 diet (100 kcal or 420 kg/100 mL). Feedings are initiated with higher frequency and smaller volumes; over time, the frequency is reduced from 12 to 8 to 6 feedings/24 hr.

• If the infant is unable to take the feedings from a cup or bottle, administration of feedings by nasogastric tube rather than by the parenteral route is preferred.

• Iron supplements are not recommended during the acute rehabilitation phase, especially for children with kwashiorkor, for whom ferritin is often high. Additional iron may pose an oxidative stress, and iron supplementation has been associated with higher morbidity and mortality.

By the end of the second phase:

☢ Any edema that was present has usually been mobilized.

☢ Infections are under control.

☢ The child is becoming more interested in his or her surroundings, and his or her appetite is returning.

3 .the final follow-up phase

Which consists of feeding to cover catch-up growth as well as the provision of emotional and sensory stimulation. The child should be fed ad libitum.

The child should be switched gradually to a recovery diet providing up to 150kcal/kg/24hr

ூ� In all phases, parental education is crucial for continued effective treatment as well as prevention of additional episodes.

Time Frame for the Management of a Child with Severe

Malnutrition