Nutrition Assessment: Role of Laboratory Data

Nutrition Assessment: Role of Laboratory Data
Liz Hudson MPH, RD September, 21st 2016

Laboratory Assessment and Nutrition Care Process
Objective measure: diagnose diseases, support nutrition diagnoses, monitor medication effectiveness, and evaluate NCP interventions Many things are involved with interpretation Age Pt condition Medical condition Hydration Status Fasting status Interpretation with regard to nutrition can be tricky, but is essential for the nutrition expert So there were many directions I could have taken this lecture, but I wanted to focus on 2 particular areas that I think a nutrition expert really needs to understand. And the first starts with serum proteins as markers of nutritional status – an area we have come very far on, even since I started practicing, but is still somewhat of a battle for lack of better words The good thing about laboratory assessments is that they offer an objective measure However many factors influence their interpretation: acute illness or injury can have dramatic effects on lab test results, just as a chronic condition that develops slowly can influence lab tests in a different way

Biomarkers: Next big thing or buzzword?
“Precision medicine: (PM) is a medical model that proposes the customization of healthcare, with medical decisions, practices, and/or products being tailored to the individual patient.” wikipedia Biomarkers: often not that easy to interpret Not necessarily a better measure of what you are doing than just asking the person Well biomarkers arent exactly new, but as we are trying to move toward precision medicine, biomarkers seems to be popping up all the over place and there is lots of energy and money spent to identify new biomarkers According to NIH.gov and the precision medicine intiative president Obama announced last year, Precision medicine is an emerging approach for disease treatment and prevention that takes into account individual variability in genes, environment, and lifestyle for each person. That leads us to biomarkers a measurable substance in an organism whose presence is indicative of some phenomenon such as disease, infection, or environmental exposure. I was at a seminar talk last week where a physician and researcher was speaking about his research on caffeine intake during pregnancy. He was talking about discovering a biomarker for caffeine intake and how they initially thought this was greatest thing. However what he concluded was biomarkers have something to add, but should not be taken as the gold standard, and are often not that easy to interpret. He also said, they are not necessarily a better measure of what you are doing than just asking the person. The reason I bring this up is because as dietitians or future nutrition experts especially in a public health domain. The ability to interpret biomarkers in conjunction with a comprehensive nutrition assessment, is an invaluable skill. It really is, it will set you apart and truly make you an asset to any medical team or research team. No one else has these skills. The physician does not. We know how much nutrition training physicians get, very little.

Definition of Specimen Types
Whole blood: Used when entire content of blood is to be evaluated – no elements are removed Serum: The fluid obtained from blood after the blood has been clotted and then centrifuged to remove the clot and blood cells Plasma: liquid component of blood (water, blood proteins, inorganic electrolytes, clotting factors) Erythrocytes: red blood cells Leukocytes: white blood cells Other tissues: scrapings and biopsy samples Urine: random samples or timed collections Feces: random samples or timed collections Less common: saliva, nails, hair, sweat, breath tests

Interpretation of Routine Medical Laboratory Tests
Clinical chemistry panels Basic Metabolic Panel Comprehensive Metabolic Panel Complete Blood Count Urinanalysis Hydration Status Serum Proteins Vitamin D

Clinical Chemistry Panels
Basic Metabolic Panel Glucose Calcium Sodium Potassium CO2 (bicarbonate) Chloride BUN (blood urea nitrogen) Creatinine Comprehensive Metabolic Panel Glucose Calcium Sodium Potassium CO2 (bicarbonate) Chloride BUN (blood urea nitrogen) Creatinine Albumin Total Protein ALP ALT AST Bilirubin Mag, phos, lipid panel may also be ordered along with Comp panel

Examples

Considerations regarding interpretation: Electrolytes
Sodium (Na): 136 to 144 mEq/L Hyponatremia: most common electrolyte abnormality in hospitalized patients Usually caused by excessive hypotonic IV fluid intake and/or gastrointestinal losses of sodium-rich fluids (gastric suctioning, diarrhea, high ileostomy output) High serum glucose concentrations increase plasma osmolality to cause fluid shift from intracellular space to plasma – resulting in hyponatremia Hypernatremia: commonly the result of impaired water intake or relative water deficit

Potassium: mEq/L (minimally affected by diet) Hypokalemia: decreases can be seen in excessive GI losses (diarrhea), intracellular shift during refeeding, medications (loop and thiazide diuretics increase K+ losses) Hyperkalemia: decreased kidney function, medications (potassium-sparing diuretics, cyclosporine, tacrolimus)

Acid base disorders are usually caused by the patient’s underlying diseases and clinical condition(s) Chloride: mEq/L Hyperchloremic acidosis: may result from large and rapid infusion of normal saline fluids or significant bicarbonate losses from intestines or kidneys (can cause chloride retention) Bicarbonate or total Co2: 21-30mEq/L Metabolic alkalosis (increase in bicarbonate): prolonged vomiting, high gastric fluid suctioning, potassium wasting diuretic use

Blood Urea Nitrogen (BUN): 7-20mg/dL Increased inkidney disease, dehydration, excessive protein catabolism Decreased in liver failure, negative nitrogen balance, pregnancy (2nd or 3rd trimester) Creatinine: mg/dL Increased in: poor kidney function Decreased in: malnutrition

Calcium: mg/dL. Serum levels related to many factors Hypocalcemia: 45% of serum calcium is bound to serum albumin. A one gram decrease in serum albumin results in ~.8 mg decrease in serum calcium Corrected calcium: measured serum calcium (4-serum albumin) Ionized calcium (free calcium) is better measure of calcium status when albumin levels are low Hypercalcemia: rarely caused by excess calcium intake Common causes: malignancies, hyperparathyroidism, immobilization Related to many factors including vitamin D status, renal function, phosphorus status, parathyroid function, medications

Corrected Calcium Serum Calcium = 8.1 Serum Albumin = 3.0
( ) = 8.9

Considerations regarding interpretation: phosphorus (normal: 2. 7-4
Considerations regarding interpretation: phosphorus (normal: mg/dL) Serum phos a poor reflection of body stores because <1% is in ECF Bones serve as a reservoir Hypophosphatemia: <2.7 mg/dL Impaired absorption (diarrhea, Vitamin D deficiency, impaired metabolism) Medications: phosphate binding antacids, sucralfate, insulin, corticosteroids) Alcoholism, especially during withdrawal Intracellular shifts such as in refeeding syndrome Increased losses: hyperparathyroidism, DKA recovery, hypomagnesemia

Hyperphosphatemia >4.5 mg/dL
Decreased renal excretion: acute or chronic renal failure; hypoparathyroidism Sign of excessive dietary intake in patients on hemodialysis Increased cellular release: tissue necrosis, tumor lysis syndrome Increased exogenous phosphorus load or absorption, phosphorus containing laxatives or enemas, vitamin D excess

Magnesium (normal: 1.3-2.5 mEq/L)
Magnesium homeostasis is maintained by the intestines, bone and the kidneys. Hypermagnesemia: decreased kidney function can cause magnesium accumulation Hypomagnesemia: common causes include diarrhea, high ileostomy fluid losses, medications (loop and thiazide diuretics, immunosuppressants) Adequate correction of hypomagnesemia essential for correction of hypokalemia

Clinical Chemistry Panels: Complete Blood Count (CBC)
Red blood cells Hemoglobin concentration Hematocrit Mean cell volume (MCV) Mean cell hemoglobin (MCH) Mean cell hemoglobin concentration (MCHC) White blood cell count (WBC) Differential: indicates percentages of different kinds of WBC

Example of CBC

Laboratory Data to assess for nutritional anemias
Classification of Anemia need to distinguish Iron deficiency anemia Microcytic anemia: most often association with true iron deficiency Important discriminating features are a low serum ferritin concentration, an increased total iron binding capacity (transferrin), and low serum iron concentration Macrocyctic anemia: generally due to deficient utilization of folate or B12 by the blood cells Pernicious anemia: not enough red blood cells due to lack of B12 Megaloblastic anemia: folate deficiency Anemia of chronic disease: (normocystic)  does not respond to iron supplementation

Tests for Iron Deficiency Anemias
Hemoglobin and hematocrit: below normal in all nutritional anemias. Not sensitive for iron, vitamin B12, or folate deficiencies Are sensitive to hydration status Serum Ferritin: Primary intracellular Fe-storage, serum levels parallel iron stores Increases during inflammatory response even when iron stores are not adequate Not useful in anemia of chronic disease Serum Iron: reflects recent iron intake, very insensitive index of total iron stores Total Iron Binding Capacity (TIBC): Increases when iron stores are depleted Transferrin Saturation: decreased when iron stores depleted; low vitamin B6 and low transferrin saturation seen in aplastic anemia Aplastic anemia develops when damage occurs to your bone marrow, slowing or shutting down the production of new blood cells.

Tests for Macrocytic Anemias from B vitamin Deficiencies
Folate and B12 tests are not sensitive or specific to actual levels Mean corpuscular volume or mean cell volume (MCV) is the average volume of red cells. Decreased in iron deficiency Increased in setting of vitamin B12 or folate deficiency

Urinanalysis Screening or diagnostic tool to detect substances or cellular material in the urine associated with different metabolic and kidney disorders Often involves visual examination, dipstick test, and microscopic examination

Urinanalysis Acidity (pH): Abnormal pH levels may indicate a kidney or urinary tract disorder. Concentration. A measure of concentration, or specific gravity, shows how concentrated particles are in your urine. Higher than normal concentration often is a result of not drinking enough fluids. Protein: larger amounts may indicate a kidney problem. Sugar: Any detection of sugar on this test usually calls for follow-up testing for diabetes. Ketones: Positive in poorly controlled DM, fever, anorexia, starvation Bilirubin: product of red blood cell breakdown. Bilirubin in urine may indicate liver damage or disease. Evidence of infection: If either nitrites or leukocyte esterase — a product of white blood cells — is detected in your urine, it may be a sign of a urinary tract infection Blood: it may be a sign of kidney damage, infection, kidney or bladder stones, kidney or bladder cancer, or blood disorders

Types of Assays Static assays: measures the actual level of the nutrient in the specimen (serum iron, white blood cell ascorbic acid) Do not reflect the amount of that substance stored in the body Highly influenced by recent dietary intake Functional Assays: measure a biochemical or physiological activity that depends on the nutrient of interest (serum ferritin, TIBC) Functional assays are not always specific to the nutrient (many biologic and physiologic functions involved) This might be changes in the activities of enzymes dependent on a given nutrient

Assessment of Hydration Status: two main fluid compartments
Total body water: fluid that occupies the intracellular and extracellular spaces Intracellular fluid compartment: fluid within the cells of the body (~2/3) Extracellular fluid compartment: Body’s internal environment and the cell’s external environment (~1/3) 2 parts: interstitial fluid and plasma Interstitial fluid: fluid in the spaces between cells Plasma: fluid portion of the blood

Assessment of hydration status
The distribution of body water varies under different circumstancesusually remains fairly constant Water consumed during the day (food, drink) is balanced by water lost (urination, perspiration, feces, respiration)

General Principles of disorders of water balance
Disorders of water balance and sodium balance are common, but the pathophysiology is frequently misunderstood Example: plasma sodium concentration is regulated by changes in water intake and excretion, not by changes in sodium balance.

General Principles of disorders of water balance
hyponatremia is primarily due to the intake of water that cannot be excreted (too much water or overhydration) hypernatremia is primarily due to the loss of water that has not been replaced hypovolemia represents the loss of sodium and water edema is primarily due to sodium and water retention

Hydration Status Dehydration is defined as a reduction in TBW below the normal level without a proportional reduction in sodium and potassium, resulting in a rise in the plasma sodium concentration Hyponatremia (too much water) Hypernatremia (too little water) Hypovolemia (too little sodium, the main extracellular solute) Edema (too much sodium with associated water retention)

Hypovolemia In a variety of clinical disorders, fluid losses reduce extracellular fluid volume, potentially compromising tissue perfusion Volume depletion results from loss of sodium and water from the following anatomic sites: Gastrointestinal losses, including vomiting, diarrhea, bleeding, and external drainage Renal losses, including the effects of diuretics, osmotic diuresis, salt-wasting nephropathies, and hypoaldosteronism Skin losses, including sweat, burns, and other dermatological conditions Third-space sequestration, including intestinal obstruction, crush injury, fracture, and acute pancreatitis

Edema (hypervolemia) Edema is defined as a palpable swelling produced by expansion of the interstitial fluid volume. A variety of clinical conditions are associated with the development of edema heart failure Cirrhosis nephrotic syndrome

Edema An increase in interstitial fluid volume that could lead to edema does not occur in normal subjects because of the tight balance of hemodynamic forces along the capillary wall and the function of the lymphatic vessels. For generalized edema to occur, two factors must be present: An alteration in capillary hemodynamics that favors the movement of fluid from the vascular space into the interstitium The retention of dietary or intravenously administered sodium and water by the kidneys ●The initial movement of fluid from the vascular space into the interstitium reduces the plasma volume, and consequently reduces tissue perfusion. ●In response to these changes, the kidney retains sodium and water. ●Some of this fluid stays in the vascular space, returning the plasma volume toward normal. However, the alteration in capillary hemodynamics results in most of the retained fluid entering the interstitium and eventually becoming apparent as edema

Laboratory Values and Hydration: BUN
Lab Test Hypo-volemia Hyper-volemia Other factors influencing result BUN Normal: mg/dl Increases Decreases Low: inadequate dietary protein, severe liver failure High: pre-renal failure; excessive protein intake, GI bleeding, catabolic state; glucocorticoid therapy Creatinine will also rise in severe hypovolemia Adapted from Charney and Malone. ADA Pocket Guide to Nutrition Assessment, 2004.

Laboratory Values and Hydration Status
Lab Test Hypo-volemia Hyper-volemia Other factors influencing result Serum albumin   Low: acute phase response, liver failure Serum sodium Can be high, normal, or low , normal or  Serum sodium generally reflects fluid status and not sodium balance The plasma sodium concentration in hypovolemic patients may be normal, low (most often due to hypovolemia-induced release of ADH, which limits urinary water excretion), or high (if water intake is impaired). The effect on the plasma sodium concentration depends upon both the composition of the fluid that is lost and fluid intake Adapted from Charney and Malone. ADA Pocket Guide to Nutrition Assessment, 2004.

Serum Proteins as Markers of Nutritional Status
Albumin, prealbumin, transferrin, and retinol binding protein synthesized in the liver and integrate protein synthesis and degradation over longer periods of time Traditionally used as part of the nutritional assessment, even part of our malnutrition diagnostic criteria (prealbumin) These levels are not indicative of patient’s protein status and thus are not appropriate to use to as an indicator of nutritional status Compared to say nitrogen balance studies

Many factors affect serum albumin levels
more than 50% is located extravascularly (outside of the blood vessels) Majority of the body’s albumin is distributed between the vascular and interstitial spaces protein intake has very little effect on total albumin on a daily basis Very little of the body’s albumin pool is comprised of newly synthesized albumin Hydration status being a major factor Many factors affect serum albumin levels Albumin is a serum protein with a relatively large body pool size, and ~5% of which is synthesized in the liver daily. Many factors affect serum albumin levels. Serum proteins are affected by capillary permability, drugs, impaired liver function, and inflammation among other factors. Hydration status is a major factor with albumin

Albumin: Negative Acute Phase Protein
Increased in: Decreased in: Dehydration Fluid overload/ascites Marasmus Hepatic failure Blood transfusions CHF Exogenous albumin Protein losing states Nephrotic syndrome Inflammation/infection/metabolic stress Burns/trauma/post-op Kwashiokor Cancer Corticosteroid use Redistribution of albumin between the extravascular and intravascular space occurs frequently. This is affected by infusion of large amounts of fluid These are negative acute phase proteins, levels will be decreased during the acute phase response Albumin has a long half life = days

Prealbumin Like albuminvisceral protein and a negative acute phase reactant Initially thought to be a better marker of nutritional status compared to albumin due to shorter half-life More indicative of current nutritional status? Levels are often normal in chronically malnourished patients, including in the setting of anorexia nervosa Levels are often decreased in well-nourished persons who have undergone a recent stress or trauma (s/p surgery) PAB half life is 2-3 days vs days. So it was thought that it would change more rapidly in response to changes in nutritional status (more indicative of current nutritional status)

Factors Affecting Prealbumin
Increased in: Renal failure (degraded by the kidney) Corticosteroid use Oral Contraceptives Decreased in: Post-operative Liver disease Infection/Stress/inflammation What positive acute phase reactant might be checked in conjunction with PAB? Dialysis Significant hyperglycemia Zinc deficiency Prealbumin drops when inflammation present, does not improve with aggressive nutrition support Serum prealbumin levels decrease in the setting of zinc deficiency – zinc is required for the hepatic synthesis and secretion or prealbumin

Studies There have been many randomized, interventional and prospective studies that have demonstrated a poor relationship between serum protein levels and nutritional status Decreased protein energy intake has not been consistent with decreased serum protein, same is true for increase protein-energy intake Patients with anorexia nervosa, in whom malnutrition is indisputable, have normal levels of serum proteins Well nourished individuals s/p stress/trauma/infection will often have low levels of serum protein

Take-home message Serum protein markers are not specific or sensitive indicators of nutritional status Greatly influenced by the inflammatory response Levels are often maintained in a chronic malnourished state, and decreased in well-nourished individuals who have experienced a recent stress or trauma

Vitamin D 25HD (25-Hydroxyvitamin D) The best laboratory indicator of vitamin D Vitamin D deficiency: < 20 ng/mL Vitamin D insufficiency: < 30 ng/mL Vitamin D toxicity: > 150 ng/mL Optimal serum 25 HD levels: 30 – 80 ng/mL I bring up vitamin D because we hear a lot in the news and in articles about vitamin D, and doctors check vitamin D levels A LOT.

What is fueling this demand for vitamin D testing?
Vitamin D deficiency is a worldwide epidemic! Most recent NHANES analyzed data only 23% of US adolescents and adults had serum levels >30ng/mL The mean concentration of vitamin D across the world is ~20ng/dl deficient More variation within countries than between countries Persistent headlines linking a multitude of benefits with adequate vitamin D More variation within countries than between countries is interesting because this variation cannot just be explained on just geography for instance. Likely a genetic component goes back to precision medicine and that as individuals it is likely a much more complex issue with regard to what controls each of our vitamin D status, but also what controls our bodies response to supplementation? Looker AC, Johnson CL, Lacher DA, et al. Vitamin D status: United States 2001–2006. NCHS data brief, no 59. Hyattsville, MD: National Center for Health Statistics Bouillon R. Lancet. 2010 Jul 17;376(9736): doi: /S (10) Epub 2010 Jun 10

Research behind the health claims
Strong research showing consistent benefits of vitamin D supplementation is lacking Vitamin D as an exposure – is difficult to control (comparing groups becomes difficult) Many studies are observational in design Does high dose vitamin D make people healthier – or do healthier people do the sorts of things that raise their vitamin D?

What’s in a level? What came first – disease or deficiency
A big study from 2009 at a medical center in Utah found that heart failure was 90% more common in those with lowest vitamin D levels vs. the highest, previous heart attack was 81 percent more likely, and a stroke was 51% more likely. Are they experiencing these things because of low vitamin D, or is there vitamin D low because of these conditions? Not able to get outside and exercise, not eating well Also obesity – excess fat absorbs and holds on to vitamin D so it is not used as efficiently in the body. So in this case, is low vitamin D a marker of obesity? Is vitamin D just a marker for poor health? Do these conditions improve or risk lower with supplementation of vitamin or adequate sun exposure? That’s what we don’t know, we don’t have good studies to show this temporality. There is a large clinical trial looking at over 20,000 people The VITamin D and OmegA-3 TriaL (VITAL) aims to find out if taking 2,000 international units (IU) of vitamin D or fish oil tablets reduces the risk of cancer, heart disease, and stroke in people who don’t currently have these illnesses. This is expected to have results in 2017

Consensus is…..there is no consensus
Adults who do not have regular effective sun exposure year round should consume at least 600 to 800 international units (units) of vitamin D3 (cholecalciferol) daily High risk groups may require more

IOM Conclusion “Scientific evidence indicates that calcium and vitamin D play key roles in bone health. The current evidence, however, does not support other benefits for vitamin D or calcium intake. More targeted research should continue. Higher levels have not been shown to confer greater benefits, and in fact, they have been linked to other health problems, challenging the concept that ‘more is better’.” The evidence supporting a benefit of vitamin D on extraskeletal outcomes was inconsistent, inconclusive as to causality, and insufficient, and therefore could not serve as a basis for dietary reference intake development Dietary Reference Intakes for Calcium and Vitamin D. Institute of Medicine Report Brief. November 2010. Dawson-Hughes, B. Vitamin D deficiency in adults: Definition, clinical manifestations, and treatment. UpToDate. May 02, 2016.

Vitamin D The IOM concluded that a serum 25(OH)D concentration of 20 ng/mL (50 nmol/L) is sufficient for most individuals Most people have adequate amounts of vitamin D in the blood supplied by their diets and natural sources like the sun, for most people taking extra calcium and vitamin D is not warranted What does this mean for health practitioners who don’t deal with most people? Dietary Reference Intakes for Calcium and Vitamin D. Institute of Medicine Report Brief. November 2010.

Is this precision medicine?
Vitamin D deficiency: < 20 ng/mL Vitamin D insufficiency: < 30 ng/mL Vitamin D toxicity: > 150 ng/mL Optimal serum 25 HD levels: 30 – 80 ng/mL It is believed that each of us has a genetic disposition to maintain a certain level of vitamin D – no number is perfect for everyone Sandra Bouma RD, MS S:\Shared\Restricted\Nutrition Services Clinical\Resources and References\Treating Vitamin D insufficiency - both.doc 5/10/2016

Consult the Dietitian! Combining lab value data and a comprehensive nutrition assessment can help guide appropriate next steps Need to take into account sun exposure Sunscreen use Dietary intake of foods rich in vitamin D or fortified with vitamin D Cold water fish intake Fortified dairy and other Replace then maintain May not need as much as we think

Dietary Sources of Vitamin D
Nutrient Profile Cow’s Milk Soy Milk (Original) Soy Milk (vanilla) Almond Milk Almond Milk (vanilla) Almond Milk (chocolate) Rice Milk Rice Milk (vanilla) Coconut Milk Oat Milk Hemp Milk Calories per 8 oz 150 110 100 60 80 120 130 70 Protein (grams) per 8 oz 8 6 1 4 3 Fat (grams) per 8 oz 4.5 3.5 2.5 5 Calcium (mg) per 8 oz 300 450 350 Vitamin D (IU) per 8 oz ~

Other Considerations: screening
Skin pigmentation  (97% of African Americans in the US are considered deficient) Obese Hospitalized or Institutionalized persons Limited effective sun exposure due to protective clothing or consistent use of sun screens Osteoporosis Malabsorptive condition Such as including inflammatory bowel disease and celiac disease

Take Home Message What does it really mean to be “deficient” or “insufficient” with regard to vitamin D status? Do we know? Is it different for everyone? Proceed with caution and look at the entire clinical picture

Energy Expenditure: Predictive Equations
Objectives: Compare/contrast predictive equations used to calculate energy requirements Discuss the strengths and limitations of various predictive equations used in clinical practice Describe the role of indirect calorimetry (IC) in assessing energy expenditure

Review of Terminology Basal metabolic rate (BMR)
Resting metabolic rate (RMR) Resting energy expenditure (REE) Estimated energy expenditure (EEE) Total energy expenditure (TEE)

Predictive Equations So many choices….

Harris-Benedict Equation
Basal energy expenditure Men: BEE= (W) + 5(H) – 6.75(A) Women: BEE = (W)+1.85(H)–4.68(A) Activity factors Stress/injury factors W=weight in kg; H=height in cm; A=age in years Based on regression analyses from IC measured in young/healthy volunteers who were not obese Does not account for generational differences in body composition Uses adjusted versus actual weight The more commonly used Harris Benedict equation has a tendency to overestimate energy expenditure, especially in obese individuals

Mifflin-St. Jeor Equation
Resting metabolic rate Men: RMR = 10(W) (H) – 5(A) + 5 Women: RMR = 10(W) (H) – 5(A) -161 Activity factors Stress/injury factors TEE = REE x AF (study or population-specific activity factor) W=actual weight in kg; H=height in cm; A=age in years The more commonly used Harris Benedict equation has a tendency to overestimate energy expenditure, especially in obese individuals the Mifflin-St. Jeor equation using actual weight is the most accurate for estimating RMR for overweight and obese individuals.

Normal activities of daily living (ADLs): 1.5 Skeletal trauma: 1.1–1.6
Activity factors Injury factors Comatose: 1.1 Surgery: Confined to bed: 1.2 Minor: 1.0–1.2 Out of bed: 1.3 Major: 1.1–1.3 Normal activities of daily living (ADLs): 1.5 Skeletal trauma: 1.1–1.6 Head trauma: 1.6–1.8 Infection: Mild: 1.0–1.2 Moderate: 1.2–1.4 Severe: 1.4–1.8 Burns (% body surface area [BSA]): <20% BSA: 1.2–1.5 20%–40% BSA: 1.5–1.8 >40% BSA: 1.8–2.0

Simplistic Weight-Based Equations
11-14 kcal/kg (obesity) 15-18 kcal/kg (obese/overweight) 22-25 kcal/kg (normal, healthy weight) 25-30 kcal/kg (underweight, or have increased needs) 30-35 kcal/kg (underweight, higher degree of increased needs, hematologic malignancy) 40+ kcal/kg (increased needs, weight gain)

Critical Illness—Non-obese: Swinamer equation
Resting energy expenditure REE = 945(BSA) – 6.4(Age) + 108(Tmax) + 24(RR) (VT)– 4349 BSA=body surface area in m2; A=age in years; Tmax=degrees Celsius; RR=respiratory rate in breaths/min; VT=tidal volume in liters

Critical Illness— obese and Non-obese: Penn State Equation
Resting metabolic rate 2003a (non-obese) RMR = BMR(0.85) + VE(33) + Tmax(175) – 6433 2003b (obese) RMR = BMR(0.96) + VE(31) + Tmax(167) – 6212 BMR calculated using the HBE or MSJ equation; VE=minute ventilation in liters per minute; Tmax=degrees Celsius

Critical Illness— Mechanically Ventilated, Obese: Ireton-Jones Equation (1992)
Estimated energy expenditure Ventilator-dependent patients: EEE = (W) – 10(A) + 281(S) + 292(T) + 851(B) Obese patients: EEE = (S) + 9(Q=W) – 12(A) + 400(V) A=age in years; W=actual weight in kg; V=ventilated (0=absent, 1=present); S=sex (0=female, 1=male); T=trauma (0=absent, 1=present)

Indirect Calorimetry IC measures the volume of inspired oxygen and expired carbon dioxide to determine VO2 and VCO2 to calculate resting energy expenditure (REE) and respiratory quotient (RQ). “Gold Standard” “First Choice” “Predictive methods of EE are often inaccurate because EE of hospitalized obese patients is highly variable.” This is related to: “varying proportion of metabolically active tissue, down-regulation of EE by hypocaloric feeding, varying influence of acute illness, presence of chronic disease that influences EE.”

Indications for IC Inability to accurately estimate energy requirements Inadequate clinical response to nutrition therapy

Inability to Accurately Estimate Energy Requirements
Trauma SIRS/fever MODS ARDS COPD Paralysis Altered body composition: Underweight Obesity Alterations in fluid balance Wounds Paralytics Sedation

Inadequate Clinical Response to Nutrition Therapy
Malnutrition despite “adequate” nutrition support Poor wound healing Failure to wean from mechanical ventilation Underfeeding vs. overfeeding

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Nutrition Assessment: Role of Laboratory Data

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