30 - Clinical Manifestation of Malnutrition Flashcards
Malnutrition
Condition resulting from a diet in which certain nutrients are lacking, in excess or in the wrong proportions
Hunger, and its associated malnutrition
Greatest single threat to the world’s public health
Protein-Energy Malnutrition (PEM)
Body’s needs for:
Protein
Energy fuels
or
Both
cannot be satisfied by diet
Protein-Energy Malnutrition (PEM) Syndromes
Kwashiorkor (edematous) - Predominant Protein Deficiency
Marasmus - Predominant Energy Deficiency
Marasmic Kwashiorkor (edematous) - Chronic Energy Deficiency PLUS acute or chronic Protein Defiiciency
Edematous PEM
Kwashiorkor
Marasmic Kwashiorkor
Secondary PEM - Causes
Diseases causing poor intake - Anorexia of disease
Inadequate nutrient absorption or utilization with increased losses - IBD, Celiac, CF
Increased nutritional requirements - CF, Lung, Heart, Kidney
Increasd nutrient losses - CF, Celiac
Where do most malnourished patitents live?
Developing countries
30% in Africa and Far East
15% in Latin America and Near East
33% o chidlren
PEM - Social & Economic Factors
Poverty - Low food availability, overcrowding, unsanitary conditions Ignorance Decline in practice and duration of breast feeding Inadequate weaning practices Abuse Deprivation Abandonment Dependence Taboo Fads Migration
PEM - Biologic Factors
Maternal Malnutrition
Infectious Diseases:
Measles
Diarrhea
Respiratory
Diets
PEM - Environmental Factors
Overcrowding
Unsanitary living conditions
Agricultural patterns: Droughts Floods Wars Forced migration
PEM - Age
Increased frequency in infants and young children
Older kids experience milder forms
Pregnant and lactating women have increased nutritional requirements that can lead to PEM
Elderly and unable to care for themselves also experience PEM
Adolescents, adult men, non-pregnant, non-lactating women have a low prevalence of PEM
Marasmus - Age
Most common form of PEM in children
Kwashiorkor - Age
More frequent in children >18 mo
PEM - Pathophysiology
Develops gradually over weeks to months
Series of metabolic and behavioral adjustments:
Decreased nutrient demands and nutritional equilibrium compatible with lower level of nutrient availability
The slower PEM develops, the better adaptation to current nutritional status - Maintain a less fragile metabolic equilibrium.
PEM - Adaptive mechanisms
Energy mobilization and expenditure Protein breakdown and synthesis Endocrine changes Hematologic changes Cardiovascular and renal function changes Immune changes Monokines Electrolytes GI function CNS & PNS
PEM - Energy mobilization and expenditure
Decreased energy intake
Decreased energy expenditure (body fat mobilized)
Decreased adiposity with weight loss as subQ fat is reduced
Protein catabolism with muscle wasting
PEM - Energy mobilization and expenditure - Marasmic Patients
Visceral protein usually preserved
Increased basal O2 consuption
Increased basal metabolic rate
More severe:
Decreased basal metabolic rate
Blood glucose usually normalized by glycerol from fats & gluconeogenesis of AA
PEM - Energy mobilization and expenditure - Kwashiorkor Patients
Early visceral depletion of amino acids
Decreased basal O2 consumption
Decreased basal energy expenditure/unit body mass
PEM - Protein Breakdown & Synthesis
Poor availability of dietary proteins
Decreased protein synthesis
Initial adaptations:
Sparing body protein and essential protein dependent functions
PEM - Protein Breakdown & Synthesis - Long term deficits
Loss of skeletal muscle
Increased loss of visceral protein
Death
PEM - Amino Acid Recycling
90 - 95% of dietary AAs are recycled (normal metabolism is 75%)
Proportional decrease in AA catabolism (normally 25%)
Decrease in urea synthesis
Decrease in urinary nitrogen excretion.
PEM - Albumin
Decreased rate of synthesis and breakdown
Shift of albumin from extravascular to intravascular to maintain oncotic pressure
Severe depletion: Adaptive mechanisms fail Decreased serum protein Decreased intravascular oncotic pressure Outflow of water into extravascular space Edema of Kwashiorkor
PEM - Cardiovascular & Renal Function
Decreased Cardiac Output
Decreased Heart Rate
Decreased Blood Pressure
Central circulation takes precedence over peripheral circulation
Altered cardiovascular reflexes
Postural hypotension
Decreased venous return
Severe: Peripheral circulatory failure Hemodynamic compensation Tachycardia Decreased renal plasma flow & GFR (secondary to decreased cardiac output)
Normal water clearance with normal concentration and acidification of urine
PEM - Immune System
Depletion of T-Lymphocytes from Thymus
Atrophy of Thymus gland
Decrease in complement production
Increased susceptibility to Gram (-) sepsis
Decreased functional activity of the complement system
Increased susceptibility to Gram (-) sepsis
Decreased opsonic activity of serum
Increased susceptibility to Gram (-) sepsis
Decreased phagocytosis
Decreased chemotaxis
Decreased intracellular killing
Possible defects in secretory IgA
Increased predisposition to infections and severe complications from otherwise less-important infectious diseases.
PEM - Monokines
Peptide/glycoprotein mediators of the body’s response to injury.
Decreased IL-1 - Poor febrile response and decreased leukocyte counts in infection
Increased TNF - Anorexia, muscle wasting, lipid abnormalities
PEM - Electrolytes
Decrease of total body potassium
Altered cellular exchange Na+ and K+ loss
Potassium loss
Increased intracellular Na+
Intracellular overhydration
PEM - GI Function
Impaired absorption of:
Lipids
Disaccharides
Glucose
Decreased gastric, pancreatic & bile production
Normal - low enzyme and conjugated bile
Further impairment of absorption
Diarrhea
Irregular intestinal motility
Diarrhea
Bacterial overgrowth
Diarrhea
PEM - CNS & PNS
Severe PEM at early age:
Decreased brain growth
Decreased nerve myelination
Decreased neurotransmitter production
Decreased velocity of nerve conduction
PEM - Hormones
Gonadotropins - Decreased
Hypothalamic - Pituitary Axis & Medulla Oblongata are preserved, so patients can still respond to stress. Epi and corticosteroids can still go up in response to stress.
PEM - Classifications (Severity)
Normal (90 - 110% weight for height)
Mild (80 - 89% weight for height)
Moderate (70 - 79% weight for height)
Severe (
PEM - Classifications (Course-based)
Acute
Chronic
Acute w/chronic background
PEM - Classifications (Main defect)
Protein
Energy
Both
Anthropometric Measurements
Weight/Height - Index of CURRENT nutritional status
Height/Age - Index of PAST nutritional history
Wasting - Deficit weight/height
Stunting - Deficit height/age
4 Anthropometric Categories
Normal
Wasted (acute PEM)
Wasted and stunted (acute and chronic PEM)
Stunted (Past PEM)
Intensity of wasting
Calculate as percent of reference median wt/ht
% Weight/Heigh = Observed Weight/Reference weight/height
% Height/Age = Observed height/Reference height/age
BMI = Weight/Height^2
Recommended for adolescents and adults
PEM - BMI
> = 18.5 - Normal
- 0 - 18.4 - Mild
- 0 - 16.9 - Moderate
Mild/Moderate PEM - Clinical Features
Weight Loss
Decreased SubQ fat
Decreased adiposity (
Extreme Marasmus - Physical Findings
Severely wasted Shorter Look wasted/ill Irritable Apathetic Look of anxiety Sunken cheeks (monkey) Hair dry and brittle Hair pulls out without pain Hypothermia Slow pulses Eye infections (Vitamin A deficiency) Respiratory infections Diarrhea
Extreme Kwashiorkor - Physical Findings
Edema (face, perineum, legs, feet, arms, hands)
Growth not as stunted as marasmic patients
Apathetic
Irritable
Look ill
Hair turns lifeless & dull
Color of hair turns to yellowish white, dull brown or red
Irritation and skin lesions in areas of edema.
Depigmented skin
Hyperkeratotic skin
Scales of dermis coming off in large patches
Big bellies
Hepatomegaly
Fatty liver
Vitamin deficiencies
Extreme Marasmus - Labs
Everything is normal or slightly reduced
EXCEPT glucose
Glucose is much lower than in Kwashiorkor patients
Total body water high
Extracellular water high
Total body protein low
Extreme Kwashiorkor - Labs
Everything is reduced or markedly reduced
Total body water high
Extracellular water higher
Total body protein low
Liver fatty infiltration severe
Flag Sign
During malnutrition, hair becomes depigmented
Hair is pigmented, then not pigmented, then pigmented. Not pigmented signifies malnutrition period.
Mild/Moderate PEM - Prognosis
Good
Patients normalize signs of malnutrition quickly
Maintain normal wt/height
May take longer for height to reach normal, or they may never reach normal height.
Decreased work capacity
Behavioral problems
Decreased capacity for social interaction and creativity.
These don’t persist if you “give them good stimulation when you treat them”
Severe PEM - Prognosis
40% die without proper treatment
10% die with proper treatment
Severe PEM - Markers for poor prognosis
Younger child Poor wt/height Infection (measles) Hemorrhagic tendencies Mental status changes Electrolyte disturbances Low serum protein Severe anemia
Mild/Moderate PEM - Treatment
Treat in ambulatory setting
GOAL - 2 times protein, 1.5 times energy requirements
Food supplements: Appetizing Easy to prepare Feed others in household No commercial value
Avoid decrease in breast feeding
Vitamin and mineral supplements
Severe PEM - Treatment
Home vs. Hospital Care
Probably hospital
Resolve life threatening conditions
Restore nutritional status without disrupting homeostasis
Ensure nutritional rehabilitation.
Severe PEM - Fluid/Electrolyte Disturbances
Hypoosmolarity
Moderate hyponatremia
Metabolic acidosis
Increased tolerance to hypocalcemia
Decreased body potassium without hypokalemia
Decreased body magnesium without hypomagnesemia
Severe PEM - Infection
Clinical manifestations may be mild
Antigen antibody reactions may be impaired
False negative skin tests
Altered drug metabolism & detoxification mechanisms
Severe PEM - Hemodynamic alterations
Cardiac failure secondary to anemia, fluids or improper treatment
Pulmonary edema
Severe PEM - Other conditions to resolve
Severe anemia Hypothermia Hypoglycemia (impaired thermoregulatory mechanisms) Severe vitamin A deficiency
Severe PEM - Treatment - Homeostatic restoration of nutritional status
Replace nutrient tissue deficits
Begin to slowly avoid metabolic disruptions
LIquid formula best (PO/NG) in small frequent feeds
Marasmus - Larger amounts of dietary energy needed
Increased mortality with TPN
K+, Na+, Ca, Mg, Zn, Folic acid, Vitamin A supplementation
Add iron after 1 week of diet therapy
Protein source of high biologic value, and easily digested
Cow, goat, ewe, buffalo, camel milk
Eggs, meat, fish, soy/vegetable mixtures are good too…
If you feed these patients too quickly, you get
Refeeding syndrome!!!!
Refeeding Syndrome
Fluid, electrolyte & metabolic abnormalities:
Chronic malnutrition - Body stores of nitrogen, phosphorous, magnesium & potassium are depleted, but serum levels are near normal
Refeeding - Proteins synthesized and insulin released. Increased cellular uptake of these cations, so HUGE drops in serum concentration!!!!
Common pathway ascribed to hypophosphatemia, but may include fluxes in K+, Mg+, Na+
Patients at risk for refeeding syndrome
Anorexia nervosa Classic Kwashiorkor Classic Marasmus Chronic malnutrition (underfeeding) Chronic alcoholism Morbid obesity with massive weight loss Unfed patient 7 - 10 days with evidence of stress and depletion Prolonged fasting Prolonged IV hydration Cancer cachexia
How to avoid refeeding syndrome
Test for electrolyte abnormalities before initiating nutrition support. Follow these values!
Judiciously restore circulatory volume
Increase caloric delivery slowly
Administer vitamins routinely
Monitor: Phosphorous Potassium Magnesium Glucose Urinary electrolytes
Ensuring Nutritional Rehabilitation
Introduction of traditional foods High calories High protein Emotional and physical stimulation Seek underlying cause of persistent or recurrent diarrhea or other health problems
Criteria for recovery from PEM
Weight gain
Adequate wt/ht
Normal CHI 0.9
PEM - Prevention and Control
Food production and distribution Preventative medicine Education Social development Economic improvement
Vitamin A Deficiency
Dry skin Decreased resistance to infection Night blindness Decreased hair growth 1/3 of all children on earth under 5 500,000 deaths yearly
Rickets
Vitamin D deficiency OR Calcium deficiency OR Phosphate deficiency
Softening/weakening of bones Bone pain or tenderness Dental deformities Impaired growth Bone fractures Skeletal deformities
Beriberi
Vitamin B1 (Thiamine) deficiency Common in alcoholics
CHF Fluid in lungs Tachycardia Swelling of legs Memory loss Delusions Coordination problems Death
Wet Beriberi
Dyspnea
Tachycardia
Swelling
Dry Beriberi
Difficulty walking Loss of sensation Nystagmus Tingling Vomiting
Wernicke-Korsakoff Syndrome
Brain disorder secondary to thiamine deficiency
Pellegra
Vitamin B3 (Niacin) deficiency
Diarrhea
Dermatitis
Dementia
Death
Scurvy
Vitamin C deficiency Lethargy Skin spots Bleeding gums Loss of teeth Fever Death
Treat with horse meat and citrus fruits
Ariboflavinosis
Vitamin B2 (Riboflavin) deficiency
Malnourished and alcoholics
Bright pink tongues Cracked lips Throat swelling Bloodshot eyes Low RBC count
Vitamin K Deficiency
Half of all newborns worldwide affected
Alcoholics, bulimics, dieters, CF
Bleeding
