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Flashcards in 35 Nutritional Assessment and Undernutrition Deck (23):
1

Malnutrition

  • Malnutrition
  • optimized nutrition

  • Malnutrition
    • includes extremes of both underweight and overweight states.
    • affects > 50% of hospitalized patients (frequently with coexistent chronic illnesses)
    • contributes to significantly longer hospital stays, higher morbidity, and higher mortality rates among both medical and surgical patients
  • optimized nutrition
    • leads to improved clinical outcomes in patients with both medically- and surgically-treated conditions

2

Protein-energy malnutrition (PEM)

  • Protein-energy malnutrition (PEM)
  • Other terms used interchangeably with PEM
  • (PEM) and PCM are somewhat misleading terms implying that/
  • malnutrition is a more general term that encompass

  • Protein-energy malnutrition (PEM)
    • a form of malnutrition resulting from inadequate and/or inefficient nutrient availability in relation to tissue needs.
  • Other terms used interchangeably with PEM are protein-calorie malnutrition (PCM), undernutrition, or simply, malnutrition.
  • (PEM) and PCM are somewhat misleading terms implying that the clinical signs and symptoms of malnutrition are due only to energy (calories) and protein deficiencies.
    • deficiencies of vitamins, minerals and trace elements are equally important and often occur concurrently with macronutrient deficiencies (rarely with macronutrient excess).
  • malnutrition is a more general term that encompass a mismatch of both macro- and/or micronutrient stores compared to physiological needs.

3

Primary vs. Secondary Malnutrition

  • Primary malnutrition:
  • Secondary malnutrition:

  • Primary malnutrition:
    • exists when the caloric, vitamin, or mineral content of ingested food is not sufficient to meet the minimum daily need as defined by the Recommended Daily Allowance (RDA).
  • Secondary malnutrition:
    • occurs when an adequate diet is available and consumed, but the nutrients of the diet are unable to be digested, absorbed or assimilated because of illness.
    • can occur in the context of illnesses that markedly increase nutrient requirements such that even “normal” intake becomes insufficient to meet needs.
    • most common form in the United States, especially in acutely ill, hospitalized patients.

4

Two major patterns of severe malnutrition

  • Unstressed starvation
  • Stressed starvation

  • Unstressed starvation
    • generalized primary malnutrition resulting from slow, chronic semi-starvation (ingesting fewer nutrients than is required to meet daily needs) resulting in a severe total caloric deficiency that drives marked loss of body fat and protein stores.
  • Stressed starvation
    • an acquired, maladaptive state with primary protein deficiency typically seen during severe metabolic stress.
    • common in patients with both acute and chronic illnesses and leads to rapid muscle wasting, micronutrient deficiencies, decubitus ulcers, and life-threatening infections.

5

Common Etiologies of Malnutrition

  • Primary malnutrition
  • Common causes of secondary undernutrition 
    • Digestion
    • Absorption
    • Metabolism
    • excretion
    • nutritional requirements

  • Primary malnutrition
    • the most common form of malnutrition worldwide.
    • common in impoverished children in Third World countries where the increased nutrient needs during growth and development often exceed supply.
    • Other contributors to primary malnutrition include political unrest and displacement, famine, poverty, neglect, and lack of sanitation and infection.
    • also occurs in the United States, often in the context of individuals with ongoing gastrointestinal symptoms (e.g. gastroparesis, dysphagia), impaired deglutition (gingivitis, poor dentition, stroke), cancer-induced anorexia, alcoholism/drug abuse, eating disorders, and those with severe mental illness or dementia
  • Common causes of secondary undernutrition (i.e. malnutrition that occurs despite adequate oral intake) 
    • Digestion (cholestasis, disaccharidase deficiency, small bowel bacterial overgrowth, pancreatic insufficiency, cystic fibrosis, radiation enteritis, short bowel syndrome, AIDS, celiac disease, intestinal lymphoma)
    • Absorption (enteritis, short bowel syndrome, tropical sprue, celiac, Whipple’s disease)
    • Metabolism (AIDS, cancer, liver disease, renal disease, corticosteroid use, inborn errors of metabolism)
    • Increased nutrient excretion (diarrhea, protein losing enteropathy)
    • Increased nutritional requirements (burns, chronic infection, chronic lung disease, hyperthyroidism, major surgery, sepsis or trauma).

6

Subjective Nutritional Assessment

  • Typical diet, with attention to any medical restriction or self-imposed limits (i.e. low sodium, diabetic diet, vegan, Atkins, Kosher, lactose intolerance, etc.)
  • Food allergies
  • Use of vitamins/minerals and over-the-counter supplements
  • Appetite changes
  • Difficulties/barriers to normal intake (i.e. poor fitting dentures, tooth pain, etc.)
  • Gastrointestinal symptoms such as dysphagia, abdominal pain, bloating, early satiety, nausea, vomiting or diarrhea
  • Living situation / activities of daily living
    • elderly patients living alone are at high risk for malnutrition due to loss of independence with restricted mobility, driving, or access to shopping.
    • Nursing home residents with dementia or mental retardation may not be able to communicate or recognize hunger or thirst.

7

Objective Nutritional Assessment

  • In the clinical nutritional assessment,
    • important to identify/
    • undernutrition can be expected if a patient develops/
  • nutritional risk

  • In the clinical nutritional assessment,
    • important to identify recent changes in dietary intake and/or body weight, new or chronic gastrointestinal symptoms, levels of functional activity and diseases that may affect nutritional status.
    • undernutrition can be expected if a patient develops an unintentional weight loss of > 10% IBW (ideal body weight) within the preceding 3 months, if the patient’s body weight is < 90% of IBW or if the body mass index (BMI = Weight (kilograms) / Height (meters squared)) is < 18.5.
  • patients can be placed at high, moderate or low nutritional risk based on either the current % of ideal body weight (IBW), or by using the body mass index (BMI).

8

Objective Nutritional Assessment

  • In clinical practice,
    • ideal body weight
    • Women
    • Men
  • Undernutrition: Severity
    • Low
    • Moderate
    • High
    • Incompatible with life
  • Weight Categories
    • Underweight
    • Normal
    • Overweight
    • Class I obese
    • Class II obese
    • Class III obese

  • In clinical practice,
    • ideal body weight of an adult is often estimated using a simple calculation that considers only a person’s height and gender:
    • Women: 100 lbs + (# of inches greater than 5 feet in height) x 5 lbs = IBW
    • Men: 110 lbs + (# of inches greater than 5 feet in height) x 6 lbs = IBW
  • Undernutrition: Severity
    • Low: BW< 90% IBW for HT
    • Moderate: BW< 85% IBW for HT
    • High: BW< 70% IBW for HT
    • Incompatible with life: BW< 60% IBW for HT
  • Weight Categories
    • Underweight: BMI< 18.5 kg/m²
    • Normal: BMI 18.5 – 24.9 kg/m²
    • Overweight: BMI 25 – 29.9 kg/m²
    • Class I obese: BMI 30 – 34.9 kg/m²
    • Class II obese: BMI 35 – 39.9 kg/m²
    • Class III obese: BMI ≥40 kg/m²

9

Objective Nutritional Assessment (p.5-7+24)

  • Physical signs of malnutrition include:
    • General
    • Mouth
    • Head/neck
    • Hands
    • Abdomen
    • Skin
  • Classic signs of micronutrient deficiency:
    • Glossitis
    • Cheilosis/Angular Stomatitis
    • Pellagra (Dermatitis)
    • Koilonychia (Spoon Nails)

  • Physical signs of malnutrition include:
    • General: obesity (with attention to distribution to thighs/buttocks vs. abdominal), cachexia, or anasarca
    • Mouth: condition of teeth, lips, gums, tongue
    • Head/neck: temporal wasting, visible bony prominences, hair changes
    • Hands: interosseus/thenar/hypothenar muscle wasting, nail bed deformities
    • Abdomen: ascites, adiposity, presence of a gastrostomy/jejunostomy tube
    • Skin: xanthomas, rash, edema
  • Classic signs of micronutrient deficiency:
    • Glossitis -- Thiamine, Niacin, or B12 Deficiency
    • Cheilosis/Angular Stomatitis -- Riboflavin and/or Folic Acid Deficiency
    • Pellagra (Dermatitis) - Niacin Deficiency
    • Koilonychia (Spoon Nails) –Severe Iron Deficiency

10

Laboratory data

  • Measurement of plasma proteins levels
  • The measurement of visceral proteins needs to be taken in a physiological context.
    • In a steady state
    • systemic inflammatory states
    • during states of acute systemic inflammatory illness

  • Measurement of plasma proteins levels
    • an objective method of nutritional assessment of macronutrient status.
    • Serum albumin, prealbumin, transferrin, and retinol binding protein are the most commonly used “visceral” proteins used in nutritional assessment.
    • equally important to assess the status of micronutrients when suspected by the history and/or physical examination.
  • The measurement of visceral proteins needs to be taken in a physiological context.
    • In a steady state (without significantly active systemic disease), the levels of these proteins can be a useful readout of actual nutritional status.
    • systemic inflammatory states associated with acute illness or trauma rapidly reorient the hepatic synthesis of core visceral proteins due to the impact of circulating inflammatory cytokines.
      • Although true malnutrition clearly can occur simultaneously with acute illness, it becomes more difficult to use the absolute value of any one of the circulating visceral proteins as a direct measure of current nutritional state during systemic inflammatory states.
      • measurement of C-reactive protein (CRP) levels is typically integrated into the nutritional assessment as a measure of systemic inflammation.
    • during states of acute systemic inflammatory illness, there is a significant inverse correlation between albumin/prealbumin and CRP levels.
      • The trend of these measurements serves as an invaluable tool in assessing both the progression of clinical disease and the underlying nutritional state.

11

Visceral Proteins in Nutritional Assessment:
For each: normal values, half-life, increased in, and decreased in

  • Albumin
  • Prealbumin (transthyretin)
  • Retinol Binding Protein
  • Transferrin

  • Albumin
    • Normal values: 3.5-5.2 g/dl
    • Half-life: 3 weeks
    • Increased: Dehydration
    • Decreased: Chronic malnutrition, Nephrotic syndrome, Severe liver disease, Inflammation/Malignancy, Fluid overload, Pregnancy
  • Prealbumin (transthyretin)
    • Normal values: 19-43 mg/dl
    • Half-life: 3 days
    • Increased: Dehydration, Renal failure
    • Decreased: Acute and chronic malnutrition, Cancer/Inflammatory response, Fluid overload, Hyperthyroidism, Severe liver injury, Pregnancy
  • Retinol Binding Protein
    • Normal values: 2.1-6.4 mg/dl
    • Half-life: 12 hours
    • Increased: Renal Failure, Alcoholism
    • Decreased: Acute and Chronic malnutrition, Chronic Liver disorders, Hyperthyroidism, Vitamin A deficiency, Zinc deficiency
  • Transferrin
    • Normal values: 200-400 mg/dl
    • Half-life: 1 week
    • Increased: Iron deficiency, Estrogens/oral contraceptives, Acute hepatitis, Pregnancy
    • Decreased: Malnutrition, Inflammatory response, Nephrotic syndrome, Marked liver disease

12

Laboratory data

  • Serum Albumin:
    • Normal levels
    • synthesized by
    • Half-life
    • Negative acute phase reactant
  • Prealbumin (transthyretin):
    • Normal levels
    • Synthesized in
    • Half-life
    • Negative acute-phase reactant
    • Useful in monitoring
  • Other indirect measures of nutritional status:
    • BUN
      • Normal
      • Reflects
      • Can be elevated in
      • Can be decreased in 
    • Creatinine
      • Normal 
      • In a steady state (euvolemia) and with normal renal function
    • Hemoglobin / Hematocrit:

  • Serum Albumin:
    • Normal levels 3.5 – 5.2 g/dl
    • synthesized by the liver, and is the most abundant plasma protein, providing 80% of the oncotic pressure
    • Half-life 21 days; therefore albumin is a lagging indicator of poor nutritional status
    • Negative acute phase reactant (decreases rapidly with inflammation)
  • Prealbumin (transthyretin):
    • Normal levels 19-43 mg/dl
    • Synthesized in the liver
    • Half-life: 2 days; therefore it is generally a good indicator of recent changes in nutritional status (typically measured weekly)
    • Negative acute-phase reactant
    • Useful in monitoring improvements in protein-energy status especially when a baseline value is obtained; increasing values correlate with improved nutritional status
  • Other indirect measures of nutritional status:
    • BUN:
      • Normal 7 – 20 mg/dl
      • Reflects protein breakdown
      • Can be elevated in catabolic state or with high protein intake
      • Can be decreased in low metabolic states or with very low protein intake
    • Creatinine:
      • Normal 0.5 – 1.1 mg/dl
      • In a steady state (euvolemia) and with normal renal function, creatinine levels reflect lean muscle mass (higher creatinine with greater lean body mass; creatinine can be nearly undetectable in those with severe cachexia).
    • Hemoglobin / Hematocrit:
      • Anemia and mean corpuscular volume (MCV) can be indicative of iron (low MCV), or B12 / folate deficiencies (high MCV)

13

Pathophysiology of Malnutrition / Undernutrition (p.17)

  • People lose weight when:
  • Body Composition
    • The human body stores
    • The remaining fat-free mass (FFM)
    • In addition to body fat, energy reserves are provided by
    • The BCM

  • People lose weight when:
    • the intake or gastrointestinal assimilation of dietary calories is insufficient to meet normal energy expenditure
    • the expenditure of body energy stores is greater than the energy normally consumed or assimilated
    • the metabolism of energy, protein, and other nutrients is impaired by a disease process
  • Body Composition
    • The human body stores between 15 and 25% of its energy as fat (generally greater in women than men), which becomes available for metabolism of endogenous fatty acids (FAs) during starvation.
    • The remaining fat-free mass (FFM) is composed of extracellular and intracellular water, the bony skeleton, glycogen and cellular visceral proteins.
    • In addition to body fat, energy reserves are provided by intracellular glycogen and protein, which together with intracellular water constitute the body cell mass (BCM).
    • The BCM, particularly from muscle stores, provides reserve protein for energy production via gluconeogenesis during metabolic stress.

14

Metabolic Responses to Starvation and Stress

  • The rate of changes in various fluid compartments and body stores of energy 
  • unstressed starvation
  • stressed starvation

  • The rate of changes in various fluid compartments and body stores of energy (fat, glycogen, protein) differs during unstressed starvation and stressed starvation.
  • General unstressed starvation slowly decreases the size of all body compartments,
  • stressed starvation more specifically reduces BCM (mostly via rapid muscle protein catabolism), increases extracellular water, and has variable effects on body fat.

15

Unstressed Starvation:
Metabolic adaptations to unstressed starvation

  • Early starvation (<24 hours):
  • Medium-term starvation (days to less than 3 weeks):
  • Late starvation (> 3 weeks):

  • Early starvation (<24 hours):
    • Glycogen stores are used to provide circulating glucose;
    • insulin concentrations decrease as glycogen is depleted;
    • glucagon concentrations increase;
    • amino acids (AAs) are released from muscle for gluconeogenesis;
    • fatty acids (FAs) are released from adipose tissue for additional energy.
  • Medium-term starvation (days to less than 3 weeks):
    • Glycogen is depleted,
    • glucose is derived solely from gluconeogenesis.
    • Protein breakdown occurs at a high rate to provide substrate for gluconeogenesis.
    • Lipolysis provides the primary energy source (via ketone bodies from FA metabolism).
    • After about one week, the brain can adapt to use both glucose and ketones for energy.
  • Late starvation (> 3 weeks):
    • Ketone body production (from lipid metabolism) accelerates
    • blood levels of ketone bodies rise, facilitating transfer into brain (which has adapted to use ketones for energy).
    • less need for gluconeogenesis,
    • reduction in the rate of protein breakdown.
    • Hormonal adaptations include: increased levels of growth hormone, TSH, free cortisol, renin, aldosterone, and ADH; decreased levels of glucagon, insulin, LH, FSH, T4, T3, prolactin, IGF-1 (somatomedin C).

16

Unstressed Starvation:
Organ function adaptations to prolonged starvation

  • Metabolic/behavioral changes
  • Temperature
  • Cardiovascular changes
  • Renal function changes
  • Respiratory function changes
  • Gastrointestinal function changes
  • Immune system changes
  • Changes in body composition

  • Metabolic/behavioral changes: decrease in resting energy expenditure (REE) including decreased physical activity
  • Hypothermia
  • Cardiovascular changes: decreased cardiac output, blood pressure and heart rate
  • Renal function changes: decreases in urine output and glomerular filtration rate (GFR)
  • Respiratory function changes: decreased ventilation leading to increased risk of infections (pneumonia, bronchitis)
  • Gastrointestinal function changes: decreases in enterocyte villus height and brush border enzyme levels (e.g. lactase)
  • Immune system changes: decreased delayed cutaneous hypersensitivity (DCH), generalized impaired immune function (increased predisposition to infections)
  • Changes in body composition:
    • Increased water and sodium (Na+) retention
    • Increased extracellular and decreased intracellular water
    • Decreased total body potassium (K+) and magnesium (Mg++)
    • Decreased total body fat and increased fatty liver (due to increased circulating fatty acids)

17

Stressed Starvation

  • Starvation with significant metabolic stress (sepsis, trauma, surgery, burns) results in:
  • When untreated, body protein catabolism/

  • Starvation with significant metabolic stress (sepsis, trauma, surgery, burns) results in:
    • Hypermetabolism -- increased basal metabolic rate (BMR)
    • Increased rates of skeletal and visceral proteolysis to provide amino acid substrates for gluconeogenesis, and tissue/wound repair
    • High levels of circulating catecholamines, glucagon, cortisol and cytokines including tumor necrosis factor (TNF) alpha and interleukins 1 and 6
    • Insulin resistance and hyperglycemia
    • Increases in total body extracellular water (edema)
  • When untreated, body protein catabolism of up to 240 g/d during an acute illness can deplete 50% of a typical body’s protein stores within 2-3 weeks.

18

Consequences of Malnutrition

  • Growth retardation / Delayed puberty
  • Amenorrhea
  • Reduced IQ
  • Decreased physical activity / Reduced work capacity
  • Increased risk of infection
  • Increased risk of anemia
  • Increased operative risk
  • Increased length of hospital stay
  • Decubitus ulcers / wound dehiscence
  • Death / mortality
    • Immediate causes are usually infections (pneumonia, local and systemic infections due to gut/skin breakdown), and diarrhea with dehydration or worsening of secondary diseases.
    • Contributing factors are starvation-induced immune deficiency, hypothermia, anemia and other micronutrient deficiencies.
    • Cardiac arrhythmias may result in death.

19

Treatment

  • In principle, to treat malnutrition, one must /
    • Primary malnutrition
    • When nutrition is provided to previously starved patients
    • refeeding syndrome.
  • small amounts of energy (glucose, fat, protein) should be given to undernourished patients for the first few days, accompanied by/
    • Water
    • Some malabsorption of enteral nutrients

  • In principle, to treat malnutrition, one must provide enough nutrition to replace losses and to initiate and maintain growth and health.
    • Primary malnutrition develops slowly and severely malnourished patients are fragile, as their metabolic and hormonal milieu has adapted in order to minimize energy and nutrient losses.
      • these patients in particular cannot tolerate a large load of nutrients delivered immediately.
    • When nutrition is provided to previously starved patients, anabolism is quickly induced and a rapid shift of minerals (from extracellular to intracellular compartments) occurs.
      • Hypokalemia, hypomagnesemia and hypophosphatemia frequently ensue.
      • The need for vitamins increases and subclinical vitamin deficiencies become apparent (particularly thiamine).
      • Such abnormalities may result in organ failure (heart, lung, cardiac arrhythmias) and/or death if not anticipated and managed carefully.
    • Collectively, this dramatic response to the reintroduction of nutrition after periods of prolonged starvation is known as the refeeding syndrome.
  • small amounts of energy (glucose, fat, protein) should be given to undernourished patients for the first few days, accompanied by abundant amounts of potassium (K+), magnesium (Mg2+), phosphate (PO42-), vitamins and trace elements.
    • Water is needed to correct dehydration, but excessive amounts of sodium and water should be avoided to decrease the risk of developing congestive heart failure.
    • Some malabsorption of enteral nutrients is anticipated early in refeeding syndrome due to chronic blunting of mucosal villi and decreased expression of enteral digestive enzymes; this typically recovers in several days.

20

Choosing a Mode of Feeding

  • preferred route
  • trophic effect (i.e. “gut stimulation” effect)
  • There are some situations where using the gut is not feasible.

  • The oral or enteral route is always the preferred route for nutrition repletion.
  • There is inherently a trophic effect (i.e. “gut stimulation” effect) in the gut mucosa when it is exposed to nutrients.
    • Thus enteral feeding in of itself is protective and maintains a tight barrier.
    • Gut breakdown during malnutrition leads to bacterial translocation and typically sepsis.
  • There are some situations where using the gut is not feasible.
    • in intestinal obstruction, gut ischemia, profound ileus (i.e. absence of motility), or gut loss (trauma, multiple bowel resections or gut necrosis) the gut may need to be bypassed.
    • In these cases, nutrition can be given via IV, ultimately as total parenteral nutrition (requires central venous access).

21

Enteral Nutrition (p.40-41)

  • If possible
  • If oral intake is not feasible
  • If oral intake is restricted on a longer term (i.e. 6+ weeks) and more durable enteral access is needed
  • Enteral
  • Enteral tube feeds
  • Comparatively

  • If possible, oral intake is best
  • If oral intake is not feasible (sedated patient; dysphagia and aspiration risk), then direct infusion of nutrient liquids into the gut can be accomplished via a feeding tube.
    • Typical routes include a nasogastric or nasojejunal feeding tube
  • If oral intake is restricted on a longer term (i.e. 6+ weeks) and more durable enteral access is needed, typically a gastrostomy tube (PEG – endoscopically placed; or a directly placed, surgically- or interventional radiologically-placed G-tube)
  • Enteral is always the preferred route for nutritional delivery (trophic effect of enteral nutrition maintains gut barrier integrity, with benefits in preventing gut bacterial translocation / sepsis)
  • Enteral tube feeds are started a slow rates and steadily increased to a goal rate
  • Comparatively inexpensive

22

Peripheral / Total Parenteral Nutrition (TPN) (p.43-44)

  • Peripheral parenteral nutrition
  • Total parenteral nutrition
  • Both PPN and TPN
  • Multiple chronic complications

  • Peripheral parenteral nutrition – a lower osmotic solution (900 Osm or less) with mix of amino acids, dextrose, and lipids + vitamins and mineral salts (can be given via peripheral IV)
  • Total parenteral nutrition – a high osmotic solution (>900 Osm) with mix of amino acids, dextrose, and lipid emulsion + vitamins and mineral salts (can ONLY be given via central venous access)
  • Both PPN and TPN requires daily monitoring of lab values during initiation
    • Very costly
  • Multiple chronic complications: central line infections, hepatic steatosis, cholestasis, and bone metabolic complications

23

Calculating Fluid and Caloric Requirements

  • In research settings, highly accurate estimates of nutrient requirements can be made using/
  • in clinical settings, a few simple empiric formulas are commonly used and this approach comes fairly close to estimating/
  • Daily fluid requirements
  • Daily total calorie requirements
  • Daily total protein requirements
  • An additional consideration is given to clinical state – in systemic inflammatory illnesses/

  • In research settings, highly accurate estimates of nutrient requirements can be made using complex predictive equation (i.e. Harris-Benedict equation) and/or the use of direct and indirect calorimetry.
  • in clinical settings, a few simple empiric formulas are commonly used and this approach comes fairly close to estimating a patient’s true fluid and nutrient needs, both in health and disease.
  • Daily fluid requirements -- Based on age and IBW
    • 16-30 yrs: 40 ml/kg IBW
    • 30-55 yrs: 35 ml/kg IBW
    • 55-75 yrs: 30 ml/kg IBW
    • >75 yrs: 25 ml/kg IBW
  • Daily total calorie requirements – Based on BMI category and IBW
    • BMI < 25 (normal or underweight) – 25-35 kcal / kg IBW
    • BMI 25-29.9 (overweight) – 20-25 kcal/kg IBW
    • BMI 30-34.9 (obese) – 15-20 kcal / kg IBW
    • BMI 35+ (morbidly obese) – ~15 kcal / kg IBW
  • Daily total protein requirements – 1.2–1.5 g/kg IBW
  • An additional consideration is given to clinical state – in systemic inflammatory illnesses, the estimated daily protein requirements increase with severity of illness.
    • Acute infection (pneumonia, etc.) / Surgery – 1.6-1.8 g/kg IBW
    • Severe trauma / burns – 1.9-2.5 g/kg IBW