Presentation on theme: "Evaluation of Laboratory Data in Nutrition Assessment"— Presentation transcript:
1 Evaluation of Laboratory Data in Nutrition Assessment Cinda S. Chima, MS, RD
2 Laboratory Data and the NCP Used in nutrition assessment (a clinical sign supporting nutrition diagnosis)Used in Monitoring and Evaluation of the patient response to nutritional intervention
3 Specimen TypesSerum: the fluid from blood after blood cells and clot removedPlasma: fluid from blood centrifuged with anticoagulantsErythrocytes: red blood cellsLeukocytes: white blood cellsOther tissues: scrapings and biopsy samplesUrine: random samples or timed collectionsFeces: random samples or timed collectionsLess common: saliva, nails, hair, sweat
4 Interpretation of Routine Medical Laboratory Tests Clinical Chemistry PanelsBasic metabolic panelComprehensive metabolic panelComplete blood countUrinalysisHydration status
5 Clinical Chemistry Panels: Basic Metabolic Panel (BMP) Also called Chem 7IncludesElectrolytes: Na+, K+, Cl-, HCO3 or total CO2GlucoseCreatinineBUN
7 Clinical Chemistry Panels: Comprehensive Metabolic Panel IncludesBMP except CO2AlbuminSerum enzymes (alkaline phosphatase, AST [SGOT], ALT [SGPT]Total bilirubinTotal calciumPhosphorus, total cholesterol and triglycerides often ordered with the CMP
8 Clinical Chemistry Panels: Complete Blood Count (CBC) Red blood cellsHemoglobin concentrationHematocritMean 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
10 Types of AssaysStatic assays: measures the actual level of the nutrient in the specimen (serum iron, white blood cell ascorbic acid)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)
12 Assessment of Hydration Status Dehydration: a state of negative fluid balance caused by decreased intake, increased losses, or fluid shiftsOverhydration or edema: increase in extracellular fluid volume; fluid shifts from extracellular compartment to interstitial tissuesCaused by increase in capillary hydrostatic pressure or permeabilityDecrease in colloid osmotic pressurePhysical inactivityUse laboratory and clinical data to evaluate pt
13 Hypovolemia Isotonic fluid loss from the extracellular space caused by Fluid loss (bleeding, fistulas, nasogastric drainage, excessive diuresis, vomiting and diarrhea)Reduced fluid intakeThird space fluid shift, when fluid moves out of the intravascular space but not into intracellular space (abdominal cavity, pleural cavity, pericardial sac) caused by increased permeability of the capillary membrane or decrease on plasma colloid osmotic pressure
14 Symptoms of Hypovolemia Orthostatic Hypotension (caused by change in position)Central venous and pulmonary pressures Increased heart rateRapid weight lossDecreased urinary outputPatient cool, clammyDecreased cardiac outputAsk the medical team!!
15 Treatment of Hypovolemia Replace lost fluids with fluids of similar concentrationRestores blood volume and blood pressureUsually isotonic fluid like normal saline or lactated Ringer’s solution given IV
16 HypervolemiaExcess of isotonic fluid (water and sodium) in the extracellular compartmentOsmolality is usually not affected since fluid and solutes are gained in equal proportionElderly and those with renal and cardiac failure are at risk
17 Causes of Hypervolemia Results from retention or excessive intake of fluid or sodium or shift in fluid from interstitial space into the intravascular spaceFluid retention: renal failure, CHF, cirrhosis of the liver, corticosteroid therapy, hyperaldosteronismExcessive intake: IV replacement tx using normal saline or Lactated Ringer’s, blood or plasma replacement, excessive salt intake
18 Causes of Hypervolemia Fluid shifts into vasculature caused by remobilization of fluids after burn tx, administration of hypertonic fluids, use of colloid oncotic fluids such as albumin
19 Symptoms of Hypervolemia No single diagnostic test, so signs and symptoms are keyCardiac output increasesPulse rapid and boundingBP, CVP, PAP and pulmonary artery wedge pressure riseAs the heart fails, BP and cardiac output dropDistended veins in hands and neck
20 Symptoms of Hypervolemia Anasarca: severe, generalized edemaPitting edema: leaves depression in skin when touchedPulmonary edema: crackles on auscultationPatient SOB and tachypneicLabs: low hematocrit, normal serum sodium, lower K+ and BUN (or if high, may mean renal failure)ABG: low O2 level, PaCO2 may be low, causing drop in pH and respiratory alkalosis
21 Treatment of Hypervolemia Restriction of sodium and fluid intakeDiuretics to promote fluid loss; morphine and nitroglycerine to relieve air hunger and dilate blood vessels; digoxin to strengthen heartHemodialysis or CAVH
22 Dehydration Excessive loss of free water Loss of fluids causes an increase in the concentration of solutes in the blood (increased osmolality)Water shifts out of the cells into the bloodCauses: prolonged fever, watery diarrhea, failure to respond to thirst, highly concentrated feedings, including TF
23 Symptoms of Dehydration ThirstFeverDry skin and mucus membranes, poor skin turgor, sunken eyeballsDecreased urine outputIncreased heart rate with falling blood pressureElevated serum osmolality; elevated serum sodium; high urine specific gravity
24 Treatment of Dehydration Use hypotonic IV solutions such as D5WOffer oral fluidsRehydrate gradually
25 Laboratory Values and Hydration: BUN Lab TestHypo-volemiaHyper-volemiaOther factors influencing resultBUNNormal: mg/dlIncreasesDecreasesLow: inadequate dietary protein, severe liver failureHigh: prerenal failure; excessive protein intake, GI bleeding, catabolic state; glucocorticoid therapyCreatinine will also rise in severe hypovolemiaAdapted from Charney and Malone. ADA Pocket Guide to Nutrition Assessment, 2004.
26 Laboratory Values and Hydration Status: BUN:Creatinine Ratio Lab TestHypo-volemiaHyper-volemiaOther factors influencing resultBUN: creatinine ratioNormal: 10-15:1IncreasesDecreasesLow: inadequate dietary protein, severe liver failureHigh: prerenal failure; excessive protein intake, GI bleeding, catabolic state; glucocorticoid therapyAdapted from Charney and Malone. ADA Pocket Guide to Nutrition Assessment, 2004.
27 Laboratory Values and Hydration: HCT Lab TestHypo-volemiaHyper-volemiaOther factors influencing resultHemato-critNormal:Male:42-52%Female: 37-47%IncreasesDecreasesLow: anemia, hemorrhage with subsequent hemodilution (occurring after approximately hours)High: chronic hypoxia (chronic pulmonary disease, living at high altitude, heavy smoking, recent transfusion)Adapted from Charney and Malone. ADA Pocket Guide to Nutrition Assessment, 2004.
28 Laboratory Values and Hydration: Alb, Na+ Lab TestHypo-volemiaHyper-volemiaOther factors influencing resultSerum albuminLow: malnutrition; acute phase response, liver failureHigh: rare except in hemoconcentrationSerum sodiumTypical-ly can be normal or , normal or Serum sodium generally reflects fluid status and not sodium balanceAdapted from Charney and Malone. ADA Pocket Guide to Nutrition Assessment, 2004.
29 Laboratory Values and Hydration Status Lab TestnormalHypo-volemiaHyper-volemiaOther factors influencing resultSerum osmolality( mosm/kg)Typically but can be normal or Typically but can be normal or Urine sp. GravityUrine osmolality ( mosm/kg)Low: diuresis, hyponatremia, sickle cell anemiaHigh: SIADH, azotemia,Adapted from Charney and Malone. ADA Pocket Guide to Nutrition Assessment, 2004.
30 Laboratory Values and Hydration Status Lab TestHypo-volemiaHyper-volemiaOther factors influencing resultSerum albuminLow: malnutrition; acute phase response, liver failureHigh: rare except in hemoconcentrationSerum sodiumTypically can be normal or , normal or Adapted from Charney and Malone. ADA Pocket Guide to Nutrition Assessment, 2004.
31 Hypokalemia (K+< 3.5 mEq/L) ↑ renal losses (diuresis)↑ GI losses (diarrhea, vomiting, fistula)K+ wasting meds (thiazide and loop diuretics, etc)Shift into cells (anabolism, refeeding, correction of glucosuria or DKA)Inadequate intake
32 Hyperkalemia (K+>5.0 mEq/L) Decreased renal excretion as in acute or chronic renal failureMedications, e.g. potassium sparing diuretics, beta blockers, ACE inhibitorsShift out of cells (acidosis, tissue necrosis, GI hemorrhage, hemolysis)
33 Serum CalciumNormal serum mg/dL (includes ionized calcium and calcium bound to protein, primarily albumin, and ions)Ionized calcium: mg/dLNormal levels maintained by hormonal regulation using skeletal reservesIonized calcium is more accurate, especially in pt with hypoalbuminemia; evaluate before repleting Ca+Charney and Malone, 2004, p. 89
34 Hypocalcemia (serum calcium <9.0 mg/dL; ionized Ca+ <4.5 mg/dL) HypoalbuminemiaHypoparathyroidismHypomagnesemiaRenal failure, renal tubular necrosisVitamin D deficiency or impaired metabolism
35 Hypercalcemia (serum calcium >10. 5 mg/dL; ionized Ca+ >5 Hypercalcemia (serum calcium >10.5 mg/dL; ionized Ca+ >5.6 mg/dL)HyperparathyroidismSome malignancies, especially breast, lung, kidney; multiple myeloma, leukemia, lymphomaMedications: thiazide diuretics, lithium, vitamin A toxicityImmobilizationHyperthyroidismCharney and Malone, 2004, p. 91
36 Serum Phosphorus (normal 3.0-4.5 mg/dL) Serum phos a poor reflection of body stores because <1% is in ECFBones serve as a reservoir
37 Hypophosphatemia (<3.0 mg/dL) Impaired absorption (diarrhea, Vitamin D deficiency, impaired metabolism)Medications: phosphate binding antacids, sucralfate, insulin, steroids)Alcoholism, especially during withdrawalIntracellular shifts in alkalosis, anabolism, neoplasmsRefeeding syndromeIncreased losses: hyperparathyroidism, renal tubular defects, DKA recovery, hypomagnesemia, diuretic phase of ATNCharney and Malone, 2004, p. 93
38 Hyperphosphatemia (>4.5 mg/dL) Decreased renal excretion: acute or chronic renal failure (GFR<20-25 mL/min); hypoparathyroidismIncreased cellular release: tissue necrosis, tumor lysis syndromeIncreased exogenous phosphorus load or absorption, phosphorus containing laxatives or enemas, vitamin D excessAcidosis
39 Hypomagnesemia <1.3 mEq/L (normal 1.3-2.1 mEq/L) Decreased absorption: prolonged diarrhea, intestinal or biliary fistula, intestinal resection or bypass, steatorrhea, ulcerative colitis; upper GI fluid loss, gastric suctioning, vomitingRenal losses: osmotic diuresis, DM with glucosuria, correction of DKA, renal disease with magnesium wasting, hypophosphatemia, hypercalcemia, hyperthyroidismAlcoholismInadequate intake: malnutritionMedicationsIntracellular shift: acute pancreatitisRefeeding syndrome
40 Hypermagnesemia (>2.1 mEq/L) Acute or chronic renal failure
41 Assessment for Protein-Calorie Malnutrition Hormonal and cell-mediated response to stressNegative acute-phase respondentsPositive acute-phase respondentsNitrogen balance
42 Assessment for Protein-Calorie Malnutrition–cont’d Hepatic transport proteinsAlbuminTransferrinPrealbuminRetinol-binding proteinC-reactive proteinCreatinineImmunocompetence
43 Hormonal and Cell-Mediated Response to Inflammatory Stress Acute illness or trauma causes inflammatory stressCytokines (interleukin-1, interleukin-6 and tumor necrosis factor) reorient hepatic synthesis of plasma proteinsAlthough protein-energy malnutrition can occur simultaneously, interpretation of plasma proteins is problematic
44 Hormonal and Cell-Mediated Response to Inflammatory Stress Negative acute-phase respondents (albumin, transthyretin or prealbumin, transferrin, retinol-binding protein) decreasePositive acute-phase reactants (C-reactive protein, orosomucoid, fibrinogen) increaseThe change in these proteins is proportional to the physiological insult
45 Nitrogen Balance Studies Oldest biochemical technique for assessment protein statusBased on the fact that 16% of protein is nitrogenNitrogen intake is compared to nitrogen output, adjusted for insensible losses (skin, hair loss, sweat)
46 Nitrogen Balance Studies Nitrogen balance in healthy adults is 0Nitrogen balance is positive in growing children, pregnant women, adults gaining weight or recovering from illness or injuryNitrogen balance is negative during starvation, catabolism, PEM
48 Nitrogen Balance Challenges Urea nitrogen is highly variable as a percent of total nitrogen excretedIt is nearly impossible to capture an accurate nitrogen intake for patients taking food poMost useful in evaluating the appropriateness of defined feedings, e.g. enteral and parenteral feedings
49 Visceral Proteins: Serum Albumin Reference range: g/dlAbundant in serum, stable (half-life 3 weeks)Preserved in the presence of starvation (marasmus)Negative acute phase reactant (declines with the inflammatory process)Large extravascular pool (leaves and returns to the circulation, making levels difficult to interpret)Therefore, albumin is a mediocre indicator of nutritional status, but a very good predictor of morbidity and mortality
50 Visceral Proteins: Plasma Transferrin Reference range: mg/dlHalf-life: 1 weekNegative acute phase respondentIncreases when iron stores are depleted so affected by iron status as well as protein-energy statusResponds too slowly to be useful in an acute setting
51 Visceral Proteins: Transthyretin (Prealbumin) Reference range: mg/dlHalf-life: 2 daysNegative acute-phase reactantZinc deficiency reduces levelsDue to short half-life, it is useful in monitoring improvements in protein-energy status if baseline value is obtained near the nadir as inflammatory response wanes
52 Visceral Proteins: Retinol-Binding Protein Reference range: mg/dlHalf-life: 12 hoursNegative acute-phase proteinUnreliable when vitamin A (retinol) status is compromisedElevated in the presence of renal failure, regardless of PEM status
53 Visceral Proteins: C-Reactive Protein Positive acute-phase reactantIncreases within 4-6 hours of injury or illnessCan be used to monitor the progress of the stress reaction so aggressive nutrition support can be implemented when reaction is subsidingMildly elevated CRP may be a marker for increased risk for cardiovascular disease
55 Urinary Creatinine Formed from creatine, produced in muscle tissue The body’s muscle protein pool is directly proportional to creatinine excretionSkeletal muscle mass (kg) = 4.1 = 18.9 x 24-hour creatinine excretion (g/day)Confounded by meat in dietRequires 24-hour urine collection, which is difficult
56 Markers of Malabsorption Fecal fatFat-soluble vitaminsVitamin D
57 Lipid Indices of Cardiovascular Risk Total cholesterolLDLHDL: HDL2a, HDL2b, HDL2c, HDL3a, HDLdbIDLVLDLLp(a)
58 Nutrition Diagnoses and Laboratory Indices Nutrition-related labs can be used either as diagnostic labels or a clinical sign
59 Examples of Nutrition Diagnostic Statements Related to Lab Values Altered nutrition-related lab values (NC-2.2) related to excessive intake of saturated fat and cholesterol and genetic factors as evidenced by diet history and client history.Inappropriate intake of food fats (saturated fat and cholesterol) (NI-5.6.3) related to frequent use of baked goods and fried foods as evidenced by diet history and elevated LDL and TC
60 Examples of Nutrition Diagnostic Statements Related to Lab Values Excessive carbohydrate intake related to evening visits to Coldstone Creamery as evidenced by HS blood glucose and diet history