MALNUTRITION / MedUrgent
MALNUTRITION
Introduction
Nutrition is the process by which the organism
utilizes food. The purpose is to maintain life, growth, normal functioning of organ, energy, and reproduction of species.
Malnutrition is any form of disordered
nutrition with a span from obesity to Protein Energy Malnutrition (PEM). The
latter can be endogenous due to of utilization, or exogenous due to defective
intake or both.
The PEM is range of pathological conditions
arising from coincident lack in varying of protein and calories, occurring most
frequently in infants and young children and commonly associated with severe
recurrent infection. PEM includes a variety of closely related syndromes
resulting from different deficiencies of calories and /or protein and is
governed by the age of the child and severity and duration of the deficiency.
The typical severe forms of PEM are known as Kwashiorkor and Marasmus, however,
intermediate or combined forms in different stages of development are also
observed. In all these conditions, there is low weight for age and low weight
for height. Kwashiorkor is characterized by oedema and low body weight for age.
It occurs commonly in the age group 1-3 years. Signs commonly seen include
muscle wasting, dermatitis, hepatomegaly, hair changes, diarrhea and mental
changes Marasmus is characterized by very low body weight for age, loss o
subcutaneous fat, gross muscle wasting and absence of oedema. It occurs
commonly in infants and very young children, although it may occur age and any
society. Etiology:
• High protein and energy requirement of the
rapidly growing child.
• Ignorance of parents concerning food needed
by the growing child.
• Starvation: insufficient amount of food
given due to unavailability, poverty, wrong believes, famine, food faddism and
taboos (a practice based on wrong believes, Customs or religious grounds).
• Prolonged exclusive breast feeding with
inadequate intake
• In availability or high cost of breast milk
substitutes and use of over diluted Cow's or formula milks.
• Use of thin gruels made out of cereals or
starchy products e.g. Cocked or wheat flour
•
Stopping food from children during diarrheal diseases with the concept that
food increases the duration and and frequency of the disease.
• Early weaning of young infants without
alternative or adequate resources for safe alternative artificial feeding.
• Poor distribution of available food within
the family.
• Acute infections such as measles, whooping
cough and others that have direct effect on weight loss
• Prematurity
•Chronic disease which are common problems
particularly in the developing world
•Congenital malformations, metabolic and
endocrine disorders
EPIDEMIOLOGY
1. Infections lead to PEM directly due to
reduced food intake during disease. Loss of appetite and stomatitis. Moreover,
diarrhea leads to decreased absorption and increased loss of nutrients and
pyrexia leads to high energy expenditure.
2. Low socioeconomic development of the
country and that of the family
3.Low level of education of the parents,
particularly the mother that leads to uneven distribution of available family
financial and other resources, and family priorities include expenses' other
than food.
4. Poor environmental sanitation
5. Ignorance that pre-school children have
higher nutritional requirements for body weight; in addition to their increased
incidence of diseases. They are commonly given less food to satisfy their
nutritional needs for different reasons.
6. Feeding and weaning practices. are major
contribute including early weaning practice milk substitutes , supplementation
with over-diluted milk and poor quantity and quality of food supplements lead
to severe malnutrition , Failure of breast feeding may be precipitated by
psychological factors of the mother including painful suckling of the infant
due to cracked or retracted nipple and breast infection. Additional factors
include responsibilities of the working mother, anxiety and the desire to
achieve a "modern lady". a Worse additional factor is speared of
media advertisements regarding types of artificial milks, foods and also body
style!
PATHOPHYSIOLOGY
Malnutrition occurs as a result of many other factors in the
body ir to the above mentioned; these include disturbances in:
1. Water, electrolytes and minerals: Decreased osmolality,
decreased glomerular filtration rate and impaired renal response to overload of
water. Total body sodium, potassium and magnesium are reduced.
2. Carbohydrates: Hypoglycemia may occur and it is one of
the causes of death in severe malnutrition due to:
• Impaired glucose absorption and metabolism
• decreased insulin level with poor response to intravenous
glucose, decreased gluconeogenesis. Decreased G-6-Phosphatase in the liver
leading to failure of breakdown of glycogen to glucose
• Decreased disaccharides level in the intestinal mucosa
leads to accumulation of sugars and water in the intestinal lumen that can lead
to osmotic diarrhea.
3. Hormonal disturbances:
Low thyroid functions compared to normal children, but this
is thought to be due to adaptation as there is no functional impairment upon
stimulation High level of Growth Hormone High level of plasma epinephrine
• High level of plasma Cortisol
4. Fats:
• Colonization of proximal part of the small intestines with
bacteria high levels of free bile acids and failure of esterification and on of
fat. Free fatty acids may distort the intestinal villi
• Decreased pancreatic lipase
• Decreased Ć-lipoprotein formation in the liver leads to
failure of fat from the liver to other organs
• Decreased Retinol-binding protein leads to accumulation of
vitamin A in the liver and results in low serum vitamin A
• Development of fatty liver due to increased fat transport
from adipose tissue, increased liver lipogenesis and decreased B-lipoprotein
synthesis
5. Protein and Amino Acids:
• In bwashiorkor, hypoproteinemia due to
hypoalbuminemia resulting from decreased synthesis
• Low B-globulin and Increased level of a1,
a2-globulins and y-globulins • low plasma amino acids except phenylalanine .
• Loss of fecal nitrogen during diarrhea
Decreased urea synthesis
Biochemical changes:
A. Serum protein and albumin:
• Serum albumin level is <_ 3 gm/100ml (a
reduction of _> 20% of serum albumin indicates early malnutrition) and the
albumin/globulin ratio is low. During recovery, the albumin level rises early
before changes in the clinical picture and can be used as an indicator
• B-globulins level decreases while y-globulin
rises
• Both transferrin and pre-albumin are reduced
early.
B. Amino acids:
• Essential amino acids are reduced especially
the branched chain amino acids (except phenylalanine and lysine), while non-essential
amino acids are not affected or raised
C. Glucose:
°May be decreased to _< 30mg% in severely malnourished children.
D. Urine:
The hydroxyproline Index which is measured
according to the following equation: (umol Hydroxyproline/ml) / (umol Creatinine/ml/kg)
The urinary Hydroxyproline excretion is an
indicator of growth in children the index is markedly reduced in PEM.
Age is excluded from the Index because it is usually unknown in poor unities and therefore, the test is not age-dependent.
•
Creatinine excretion decreases with the decrease of muscle mass:
• creatinine clearance per square meter surface area equals height (m) x 0.43 serum creatinine: Normal range is 80-120 mg E. Water and Electrolytes: Total body water is increased in both kwashiorkor and marasmus though there may be evidence of dehydration.
• There is a compensated hyperchloremic acidosis with normal pH hich Chloride and low CO2 Pathology:
Pathological changes that are commonly seen in
PEM include:
Hair and skin changes:
In Kwashiorkor, the hair is silky, sparse and
easily pluckable. Areas of hypopigmentation corresponding to the periods of
deficiency (flag sign). The skin shows areas of erythema, and areas of
hypopigmentation, hyperpigmentation, excoriation and hyperkeratosis. Skin may
atrophy and there are areas which peel off easily (flaky paint rash), and
secondary infection may occur.
• Fat:
Preserved in Kwashiorkor and consumed by lipolysis and gluconeogensis in Marasmus.
- Muscles: Are atrophied, and this is related to energy deficit.
• Gastrointestinal Tract: In kwashiorkor,
atrophy of intestinal mucosa is minimal where the villous size is reduced and
villi are both normal and slightly reduced, while in marasmus villi are short
and there is also atrophy of brush boarders. Decreased levels of intestinal
disaccharides, dipeptidases and lipases have been documented
• Liver: Fatty changes in kwashiorkor, starts in periportal areas and then spreads centrally. This is reversible with nutritional treatment.
• Pancreas: There is atrophy of acini and loss of zymogens granules. Decrease of endocrine and occasionally exocrine secretions which are reversible with treatment.
· Urinary Tract: tubules Hyalinization of
glomeruli and fatty degeneration of the convoluted tubules
• Thymus:
Is atrophied and there may be fatty
degeneration of lymphoid tissue
. Hormonal changes
Thyroid gland: Severe forms of PEM may lead to
decreased levels of thyroxin-binding globulin (TBG) and thyroxin-binding
pre-albumin (TBPA). Prolonged PEM leads to sluggish feedback mechanism between
thyroxin level and TSH.
Moderate hypoglycemia is commonly seen in all
forms of PEM during infection and hypothermia.
Low BMR is due to deficiency of diet and not
thyroxin.
Insulin: PEM is associated with impaired
insulin release resulting in impaired glucose tolerance test. Raised levels of
plasma fatty acids and growth hormone lead to normal or high levels of blood
glucose through gluconeogenesis.
The role of glucagon is not yet defined.
Adrenal glands may become smaller in size and
hormone output and metabolism are slowed down and the levels of steroids could
be normal or high. Urinary steroids excretion is low and rate of degradation of
cortisol is impaired.
Aldosterone level is raised leading to
hypokalemia There is marked sodium loss in urine because of decreased
reabsorption and inappropriate ADH secretion.
Pituitary: The feedback of
Hypothalamic-pituitary axis is essentially normal, though slow.
• Immune System
1-Humoral Immunity: B cells number is normal
or elevated IgA, IgG, IgM levels in the circulation are normal or elevated.
Secretory IgA level is reduced leading to increased susceptibility to gram
negative bacterial infections of the respiratory system and gastrointestinal
tract. IgE and IgD levels are elevated.
Antibody response to Yellow Fever vaccine,
Typhoid vaccine and Influenza Vaccine is impaired; however, the antibody
response to antigens of Measles, Poliomyelitis, Tetanus and Diphtheria Toxoid
is normal Complement proteins are all decreased except C4
2-Cellular Immunity: Thymus is atrophic with
fibrous tissue replacing its normal lymphoid tissue and Hassel's corpuscles.
Chemotaxis, phagocytosis and degranulation of
polymorphs are normal but the killing function is defective.
Enzymes of polymorphs (pyrovate kinase and
peroxidase) are normal.
Normal resting reduction of NBT dye test
Synergism of PEM and infectious diseases
Effect of malnutrition on infections
• Deficient intake of protein and
micronutrients adversely affect body defense mechanisms. • Protein deficiency
leads to poor wound healing, poor fibroblastic response to trauma, poor abscess
wall development, poor collagen formation and poor antibody formation.
• Vitamin A deficiency leads to decreased
macrophage activity, decreased activity of lysozymes in tears, sweat, saliva
and body fluids and disturbed tissue and mucus protective mechanisms.
• Vitamin B deficiency leads to decreased
antibody formation, decreased macrophage activity and decreased interferon
formation. • Vitamin C deficiency leads to decreased hydroxyproline formation
resulting in poor collagen formation and poor wound healing.
Effect of infection on nutritional status:
•
Infection and stressful conditions adversely affect the nutritional status by
loss of appetite and decreased tolerance to food.
• The tendency to change the patient diet
during disease from solid to liquid leads to decreased amount of protein taken.
• Fever and stressful conditions leads to high
BMR, loss of nutrients sweat and excess nitrogen excretion in urine.
• Stressful conditions lead to high insulin
and cortisone secretion, increase gluconeogenesis from body proteins.
• During infection, vit.A level is lowered and
may precipitate xerophthalm
• During infection there is loss of Na, K, Mg
and CI.
•Chronic infection leads to simple chronic
anemia. hook worm leads iron deficiency anemia and viral infections can
precipitate pancytopenia
•Diarrhea leads to loss of nutrients in stools
and decreased absorption of fat.
CLASSIFICATION OF PEM
Classification of PEM (originally called Protein-calorie
malnutrition by lelliffe D.B. in 1959), differs according to the objectives to
be achieved. A quantitative classification that is suitable for field studies
might not fulfill the requirement of a qualitative clinical study where the
type, severity and duration of the condition are important. An acceptable
classification must be simple, practical and applicable in different areas used
by different workers. The most widely used index in PEM classification is
weight for age as it indicates the condition of the child compared to a
standard at the same age. However it is not always possible to obtain the exact
age especially in poorer illiterate societies. Weight for height is an index of
the current nutritional status and is often used in surveys. Height for age
gives a picture of the past nutritional history; accordingly, descriptive terms
like stunting (deficit in height for age) and wasting (deficit in weight for
height) are used. No classification, so far, is ideal because it is impossible
to define "normal"; instead, the "Reference Standard” is used.
1. Gomez's classification (1956): using Harvard fiftieth percentile as a standard
First degree PEM: 90- 75% centile
Second degree PEM: 75-60% centile
Third degree PEM: less than 60% centile
2. Jelliffe classification (1966): (using Harvard fiftieth percentile as a standard)
First degree : 90- 80% centile
Second degree : 80- 70% centile
Third degree : 70-60% centile
Fourth degree : less than 60% centile
3. Garrow's classification (1966): (using Harvard fiftieth percentile as a standard)
Kwashiorkor: wt. 70 -60% +oedema +hepatomegaly
or dermatosis
Marasmus: Wt. 560% no oedema or hepatomegaly
or dermatosis Marasmic kwashiorkor: Wt._< 60% + oedema hepatomegaly or
dermatosisŲ²
Laboratory Tests:
1. Blood glucose: <54mg/dl indicates
hypoglycemia
2. Blood film for malaria should be done in
endemic areas
3. Hemoglobin: <4gm/dl indicates very severe
anemia
4. Packed cell volume: <12% indicates very
severe anemia
5. Urine general and culture: Presence of
bacteria on microscopy or culture
(or 10 leucocytes per high power field)
indicates infection
6. Stools microscopy: Blood for dysentery and
giardia cysts or trophozoites for infestation
7. Chest x-ray: patchy pneumonic
consolidations (pneumonia), pulmonary congestion (heart failure) and rachitic
changes in bones
8. Mantoux Test: Often negative
MANAGMENT
1. Hypothermia: If child's rectal temperature
is <35.5 C (95 F), the child should be put in a Kangaroo position on
mother's chest and actively warmed by proper covering and heating.
2. Hypoglycemia: If child's blood glucose is
<3 mmol/, a bolus of 10% glucose or sucrose (oral or NG) should be given. If
blood glucose <3 mmol/l and the patient is lethargic, unconscious or
convulsing, sterile 10% glucose should be given intravenously in a dose of
5ml/kg; and 50 ml bolus by NG tube should be administered. Alternatively, you
can use 25%Dextrose (2ml/kg) or 50%Dextrose (1 ml/kg)
3. Anemia: If Hb. <40gm/l or PCV <12%,
either whole fresh blood in a dose of 10ml/ kg or 5-7 ml/kg packed cells should
be given slowly over 3 hours.
4. Eye signs: If the patient has purulent
conjunctivitis evidenced by pus, redness or swelling of the eye, this should be
treated by chloramphenicol drops or tetracycline ointment in addition to
atropine drops. Prophylactic dose of oral vitamin A drops or tablets is given
according to age. If there are Bitot spots or ulcerations, give vitamin A in
therapeutic doses on day 1, 2, 14 Vitamin A dose according to age is as such:
5. Feeding: Nutritional treatment is divided into 3 phases:
Phase I: (Initiation phase)
As severely malnourished children cannot handle large
quantities of dietary protein, fat or Na, feeding is commenced by F-75 formula
(i.e. low energy and low protein) as soon as possible. If the child is
dehydrated. rehydrate initially and the patient is reweighed before determining
the amount of feeds. An NG tube may be used if the child cannot complete the
calculated amount. Night feeds are important to prevent hypoglycemia and feeds
are given 2 hourly. If hypoglycemia is determined by a random blood sugar, then
feeding should be 14 of this amount given every half hour for the first 2
hours, and continue this regimen until blood glucose reaches 3 mmol/l.
Phase 2: (Transition phase) When the appetite returns, oedema starts to subside, and the medical complications are treated and this usually takes about 3 days or more, feeding with F-100 formula (i.e. high energy and high protein) should be offered and given according to body weight. Feeds should be increased by 10 ml until patient refuses. The patient should be weighed daily and monitored for signs of fluid overload and heart failure.
Phase 3: (Rehabilitation phase) Once the child tolerates large amounts of feeds, referral to an nutrition rehabilitation center is indicated where his weight is every 2 weeks, health education regularly given, and monitoring is done.
6. Shock:
If there are signs of shock including lethargy,
unconsciousness, cold hands, slow capillary refill >3 seconds or has weak
fast pulse, administration of IV normal saline or Ringer's lactate in of 15
ml/kg in one hour should be started immediately. If there is no improvement,
the same amount should be repeated until signs of shock disappear. This is followed
by giving alternate ResoMal and F-75 for up
If there is no improvement
on IV fluids, the patient should be transfused with whole fresh blood (10ml/kg)
given in a relatively fast rate. 7. Dehydration: Treatment of severe
dehydration should be commenced using IV normal saline or Ringer's lactate
infusions according to weight until it disappears. This is followed by ReSoMal
by NG tube in a dose of 5 ml/kg every 12 hour for 2 hours, thereafter on
alternate hours and in addition F-75 liquid formula should be given in a
similar dose. 8. Dermatosis:
If there is evidence of severe dermatosis, the
patient should receive a bath with 1% potassium permanganate solution, or
Gentian violet solution may be applied on the skin. If there is fungal
infection, Nystatin is added. Oral zinc solution can speed up recovery
(10mg/day for 10 days).
Management of Malnutrition in infants
Infants less than 6 months of age and children
with body weight of s 4kg are treated separately, though the same rules of
phase management are applied.
At this age group malnutrition may result from lack of breast feeding inadequate breast feeding or failure of breast feeding due to congenital malformations or developmental problems. Indications for hospital admission Include visible wasting (SD Score cannot be applied to this age group), bilateral pitting oedema and failure of breast feeding.
Start with dilute F100, but if there is
oedema, start with F75. Dilute F100 is formed of one sachet of powder (one
liter size) and add water to make 1350ml. volume to be given in the Initial
Phase is 130ml/kg/day and should be increased regularly by 5 ml/feed if the
infant is accepting and finishing the offered feed or not gaining wieight properly.
Supplementary Suckling Technique i.e. breast feeding and formula feed together,
offers the infant
Phenomena encountered during the Rehabilitation phase
These phenomena are not very well understood,
however micro- and macronutrient imbalance play an important role in their
appearance
1-Pseudotumor Cerebri: Presents with clinical
picture of increased intracranial pressure with normal ventricular size,
anatomy and position
2-Encephalitis-like syndrome: Presents with
unexplained drowsiness and loss of consciousness
3-Rickets: Presents with clinical picture of
rickets as bones start to grow as bones start to grow
4- Kahn Syndrome: the syndrome presented with
Parkinsonism-like picture (tremors, rigidity, bradykinesia and myoclonus)
around the 6th day after the day after therapy.
5-Micronutrient Deficiency Presents with
clinical picture of specific micronutrient deficiency e.g. zinc vit E,
SELENIUM....
6-Anemia: Presents with a
blood picture of hypochromic microcytic, megaloblastic or dimorphic anemia
7-Gomez Syndrome: Presents with clinical
picture of a decompensating liver (hepatomegaly, ascites, collaterals, parotid
enlargement, hypertrichosis, gynaecomastia and eosinophilia) Each might need
relevant or specific treatment as the clinical picture dictates.
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