Sodium (Na+) Normal Values: Adult < 65: 135 147 mEq/L Adult 65: 132 142 mEq/L

q/L Most abundant cation in electrolyte fluid and the chief base of the blood. Concentration controlled by kidneys And CNS through endocrine system. Hyponatremia Usually reflects a relative excess of Body H2), NOT a low total body Na+. Conditions promoting hyponatremia: a. Severe Burns b. Severe Diarrhea c. Vomiting d. Excess IV Fluid e. Addisons Disease f. Severe Nephritis g. Diabetic Acidosis h. Drugs i. Edema

Hypernatremia Uncommon Conditions promoting hypernatremia: a. Dehydration b. Coma c. Diabetes insipidus d. Cushings Disease e. Insufficient H2O Intake Potassium (K+) Normal Values 3.5 5.0 mEq/L (Avg. 4.0 4.7 mEq/L) Principal cation of intracellular fluid and primary buffer within cells themselves. Concentration greatly affected by adrenal hormones. Hypokalemia More commonly associated with deficiency, rather than normality. Falling trend (0.1 0.2 mEq/L/Day) indicates a developing potassium deficiency. Most common cause of K+ deficiency: GI Loss Most common cause of K+ depletion: Diuresis Without adequate K+ supplementation

Conditions promoting hypokalemia: a. Diarrhea b. Pyloric Obstruction c. Starvation d. Malabsorption e. Severe Vomiting f. Severe Burns g. Primary Aldosteronism h. Excessive Licorice Ingestion i. Renal Tubular Acidosis j. Diuretic Administration k. Other Drugs l. Familial Periodic Paralysis m. Liver Dis. with Ascites n. Chronic Stress o. Crash Dieting p. Chronic Fever Hyperkalemia: Conditions promoting hyperkalemia: a. Inadequate Excretion (i.e.Renal Failure) b. Cell Damage (burns, accidents, surgery Damaged cells release K+ into blood) c. Acidosis (drives K+ out of cells) Increased levels associated with: a. Addisons Dis. b. Acute Renal Failure 1)Anuria 2) Oliguria c. Selective Hypoaldosteronism d. Internal Hemorrhage

e. Uncontrolled Diabetes f. Acidosis Chloride (Cl-) Normal Values: 95 105 mEq/L Chloride is an anion existing predominantly in extracellular spaces. It exists primarily in combinations such as NaCl and HCl. Concentration controlled primarily by the kidney. 1) When the serum level is much below 100 mEq/L, urinary excretion falls to a very low level. 2) The reason for decreased Cl- levels in acute infection is not clear. 3) Chloride measurement is of limited value in renal disease because plasma chloride can be maintained near normal limits even with a considerable degree of renal failure. Decreased chloride occurs in: a. Severe Vomiting b. Severe Diarrhea c. Ulcerative Colitis d. Pyloric Obstruction e. Severe Burns f. Heat Exhaustion g. Diabetic Acidosis h. Addisons Disease i. Fever

j. Acute Infection (e.g. pneumonia) k. Use of diuretic agents Increased chloride occurs in a. Dehydration b. Cushings Syndrome c. Hyperventilation d. Eclampsia e. Anemia f. Cardiac Decompensation g. Some Kidney Disorders Carbon Dioxide (CO2) Normal Values: 22 28 mEq/L In plasma, > 95% of Total C O2 content is contributed by bicarbonate (HCO3), which is regulated by the kidneys. Increased CO2 content occurs in: a. Severe Vomiting b. Emphysema c. Aldosteronism d. Use of diuretics Decreased CO2 content levels occur in: a. Severe Diarrhea b. Starvation c. Acute Renal Failure d. Salicylate Toxicity e. Diabetic Acidosis f. Use of Thiazide Diuretics

Anion Gap Normal Values: 10 15 mEq/L The difference between anions and cations (Na + K) (Cl +CO2) Note: In Diabetic Ketoacidosis, the supply of ketoacids exceeds the demands of the cell. Blood plasma acids rise. Blood plasma HCO3 decreases because it is used to neutralize these Acids. Blood Urea Nitrogen (BUN) Normal Values: 8 20 mg/dL Explanation of Test: Urea is formed in the liver, constituting the major nonprotein nitrogenous end-products of protein catabolism. The urea is then carried to the kidneys by the blood for excretion in the urine. Increased BUN (aka Azotemia) Prerenal causes: decreased renal perfusion, dehydration, blood loss, shock, severe heart failure, increased protein breakdown, or antianabolism (urea appearance), GI Bleeds, crush injuries, burns, fever, corticosteroids, tetracycline, excessive amino acid or protein intake.

Intrarenal (intrinsic) causes: acute renal failure, nephrotoxic drugs, severe hypertension, glomerulonephritis, tubular necrosis, chronic renal dysfunction, pyelonephritis, diabetes, renal tubular disease, amyloidosis, arteriosclerosis, collagen vascular disease. Postrenal causes: obstruction of ureter, bladder neck, or urethra. Decreased BUN: Liver failure, malnutrition, overhydration. Creatinine (Cr) Normal Values: Females: 0.6 1 mg/dL Males: 0.8 1.7 mg/dL Values are method-dependent. Creatinine is a byproduct in the breakdown of muscle creatine phosphate, resulting from energy metabolism. It is produced at a constant rate, depending on muscle mass. It is removed from the body by the kidneys. Production is constant, as long as muscle mass remains constant. Disorder of kidney function reduces excretion of creatinine, elevating blood levels.

Increased Creatinine levels occur in: a. Impaired excretion 1) Impaired renal function (e.g. by nephrotoxic agents) 2) Obstruction of Urinary Tract b. Increased production 1) Muscle Disease (e.g.Acromegaly, Gigantism) 2) Excess catabolism 3) Excess exercise 4) Fever 5) Hyperthyroidism Decreased Creatinine levels occur in: a. Cachexia b. Decreased activity Serum BUN/Serum Creatinine Ratios Ratios of BUN to Scr of >20 suggest a prerenal cause of Azotemia. Ratios of BUN to Scr of 10 20 suggest intrinsic renal damage. Creatinine Clearance - Normal Values Females: 110 mL/min/1.73 m2 Males: 125 mL/min/1.73 m2 BSA (m2) = [(kg wt)0.425 x (cm ht)0.725 x 71.84] / 10, 000 BSA (m2) = 0.061 (kg wt)0.805 CrCl (mL/min) x 1.73 /BSA = CrCl (mL/min/1.73 m2)

CrCl (mL/min) = [(140 - age) (kg wt)] / 72 x Scr if female, multiply by 0.85 CrCl (mL/min/1.73 m2) = [98 0.8 (age20)] / Scr If female, multiply by 0.90 Actual Creatinine Clearance Creatinine Clearance = Ucr x V / Scr

Ucr = Conc. Of creatinine in urine (mg/dL) V = Volume of urine/time period (mL/min) Scr = Conc. of creatinine in serum (mg/dL)

Glucose Normal Values Fasting Serum: 70 100 mg/dL [FBS] Fasting Whole Blood: 60 100 mg/dL Explanation of Test Purpose is to detect any disorder of glucose metabolism, mainly diabetes. Glucose is formed from digestion of carbohydrates and conversion of glycogen by the liver. Two hormones (Glucagon and Insulin) directly regulate blood glucose. Glucagon accelerates breakdown of glycogen in the liver, raising blood glucose levels. Insulin increases call membrane permeability to glucose, transporting glucose into cells for metabolism, and further stimulates formation of glycogen and reduces serum blood glucose levels. Other hormones with roles in glucose metabolism: ACTH,

epinephrine, adrenocorticosteroids, thyroxine. Elevated blood sugar (hyperglycemia) 1. Diabetes Values over 140 mg/dL on repeat testing may indicate diabetes mellitus. FBS rarely exceeds 120mg/dL, except in diabetes. 2. Other possible causes: a. Insulin overdose b. Acute stress c. Pheochromocytoma d. Pituitary Adenoma e. Hyperthyroidism f. Adenoma of Pancreas g. Pancreatitis h. Brain trauma i. Chronic liver disease j. Chronic Illness k. Chronic Malnutrition l. Potassium deficiency m. Prolonged Physical Inactivity Decreased Blood Sugar (hypoglycemia) a. Insulin overdose b. Addisons Dis. c. Bacterial Sepsis d. Islet Cell Carcinoma f. Hypothyroidism e. Hepatic necrosis g. Psychogenic causes h. Glycogen storage dis.

Calcium (Ca++) Normal Values: Total: 9 11 mg/dL Ionized: 3.9 4.5 mg/dL The test measures concentration of total calcium in the blood, and is used to measure parathyroid function, calcium metabolism, and in evaluation of malignancies. Factors Influencing Calcium Levels A. Parathyroid Hormone 1. Blood calcium is regulated by parathyroid hormone, by a direct effect on bone to release calcium into the blood. 2. Parathyroid hormone also acts on the intestines (increasing absorption of calcium) and on the kidneys (causing calcium reabsorption by the proximal tubules). B. Calcitonin: Hormone lowers blood calcium levels by increasing calcium clearance by the kidneys. C. Vitamin D: Stimulates intestinal absorption of calcium. D. Estrogens and Androgens 1. Estrogens increase calcium deposits in bones. (Used for treatment of postmenopausal osteoporosis) 2. Androgens produce hyperfunction of adrenal cortex and thyroid, resulting

in hypocalcemia and bone decalcification. E. Carbohydrates and Lactose 1.Carbohydrates increase intestinal absorption of calcium. 2. Adding lactose to the diet increases absorption and retention of calcium. Normal Levels of Total Calcium combined with other findings: 1. Normal calcium levels with overall normal findings in other tests indicate there are no problems with calcium metabolism. 2. Normal calcium and abnormal phosphate indicate impaired calcium absorption due to alteration of parathyroid hormone activity or secretion. In rickets, the calcium level may be normal or slightly lowered, and the phosphorus level is depressed.

3. Normal calcium and elevated BUN indicates: a. Possible secondary hypoparathyroidism. Initially, a lowered serum calcium results from uremia and acidosis. The lower calcium level stimulates the parathyroid to release parathyroid hormone, acting on bone to release more calcium. b. Possible primary hyperparathyroidism. Excessive amounts of parathyroid hormone cause elevation in calcium levels, but secondary kidney disease would cause retention of phosphate and concomitant lower calcium. 4. Normal calcium and decreased albumin. Indicative of hypercalcemia, since there is a decrease in albumin because of 50% of serum calcium being protein-bound.

B. Hypercalcemia Associated with many disorders, but the greatest clinical importance is association with cancer, including multiple myeloma, parathyroid tumors, nonendocrine tumors producing a parathyroid-like substance, and cancers metastasizing to bone. Increased calcium levels are caused by or associated with: 1. Hyperparathyroidism due to: a. Parathyroid adenoma b. Hyperplasia of parathyroid glands 2. Cancer a. Metastatic cancers involving bone [Cancers of lung, breast, thyroid, kidney and testes may metastasize to bone.] b. Hodgkins Disease and other lymphomas c. Multiple Myeloma in which extensive bone destruction occurs. d. Lung and renal cancers may produce parathyroid hormone, resulting in symptoms of hypercalcemia. e. Sarcoidosis due to increased IgG or IgA. f. Leukemia 3. Addisons Disease 4. Hyperthyroidism

5. Pagets Disease of Bone (also accompanied by high levels of alkaline phosphatase) 6. Prolonged immobilization 7. Bone fractures combined with bedrest 8. Excessive intake of Vitamin D 9. Prolonged use of diuretics, esp. thiazides 10. Respiratory acidosis 11. Milk-Alkali Syndrome (History of peptic ulcer disease could prompt excessive intake of milk and antacids. C. Hypocalcemia Commonly caused by or associated with: 1. Pseudohypocalcemia: Here, what looks like hypocalcemia really reflects reduced albumin (revealed by serum electropheresis). The reduced protein is responsible for the low calcium, since 50% of calcium is protein-bound. Ca Correction: obs. Ca + 0.8 (Optimal albumin Observed albumin) 2. Hypoparathyroidism May be due to accidental removal of parathyroid glands during thyroidectomy, irradiation, hypomagnesemia, GI disorders, and renal wasting.

3. Hyperphosphatemia Due to renal failure, laxatives, cytotoxic drugs. 4. Malabsorption Due to sprue, celiac disease, pancreatic dysfunction. [Fatty acids combine with calcium and are precipitated and excreted in the feces.] 5. Acute Pancreatitis 6. Alkalosis [Calcium ions become bound to protein.] 7. Osteomalacia 8. Diarrhea 9. Rickets D. Increased Ionized Calcium 1. Primary hyperparathyroidism 2. Ectopic parathyroid hormoneproducing tumor 3. Excessive intake of Vitamin D 4. Various malignancies E. Decreased Ionized Calcium Primary hypoparathyroidism is associated with low ionized calcium level and low total calcium level.

Magnesium (Mg++) Normal Values 1.8 3 mg/dL or 1.6 2.4 mEq/L Magnesium is required for use of adenosine triphosphate (ATP) as a source of energy. It is necessary for the action of numerous enzyme systems including: 1. Carbohydrate metabolism 2. Protein synthesis 3. Nucleic acid synthesis 4. Contraction of muscular tissues Normally, 95% of magnesium filtered through the glomerulus is reabsorbed in the tubule. When kidney function decreases, greater amounts of magnesium are retained, raising serum levels. The bulk of total body magnesium is concentrated in bone, cartilage and within the cells themselves. Decreased Mg levels are associated with: a. Chronic diarrhea b. Post hemodialysis c. Chronic renal disease d. Hepatic cirrhosis e. Chronic Pancreatitis f. Use of diuretics g. Aldosteronism h. Ulcerative colitis i. Hyperaldosteronism j. Toxemia of Pregnancy k. Hyperthyroidism/hypoparathyroidism l. Excessive lactation

m. Cirrhosis of liver n. Malabsorption syndromes o. Chronic alcoholism p. Prolonged gastric drainage In magnesium deficiency states, urinary magnesium rises before serum levels. Increased Mg levels are associated with: a. Renal failure/reduction b. Hypothyroidism c. Addisons disease d. Post Adrenalectomy e. Diabetic Ketoacidosis f. Controlled diabetes in older patients g. Use of Mg-containing antacids h. Dehydration i. Use of thiazides j. Use of ethacrinic acid (before treatment) Phosphate (PO4) Normal Values Adults: 2.5 4.8 mg/dL Children: 3.5 5.8 mg/dL Approximately 85% of total body phosphorus content is combined with calcium in bone. The remainder is located within cells. Most phosphorus in the blood exists as phosphates or esters.

Hypophosphatemia a. Hyperparathyroidism b. Rickets or Osteomalacia c. Diabetic coma because of increased carbohydrate metabolism d. Hyperinsulinemia e. Continuous administration of IV glucose in a nondiabetic patient. Hyperphosphatemia : Most common causes of elevated blood phosphate levels Are found in associated kidney dysfunction and uremia. a. Renal insufficiency and severe nephritis b. Hypoparathyroidism c .Hypocalcemia d. Excessive alkali intake e. Excessive Vitamin D intake f. Fractures in the healing stage g .Bone tumors h Addisons Dis. i. Acromegaly Albumin (Alb) Normal Values 3.5 5.5 g% Albumin is a protein formed in the liver, that helps maintain normal distribution of water in the body, as well as transport in the blood such constituents as ions, pigments, bilirubin, hormones, fatty acids, enzymes, and certain drugs.

Approximately 52 60 % of total protein is albumin, the rest being globulin, which functions in antibody formation, and other plasma protein (fibrinogen and prothrombin) functioning in coagulation. Hypoalbuminemia associated with edema and decreased transport function such as hypocalcemia. Causes of decreased albumin levels: a. Inadequate iron intake b. Severe liver disease c. Malabsorption d. Diarrhea e. Eclampsia f. Nephrosis g. Exfoliative dermatitis h. Third-Degree Burns i. Starvation j. Excessive administration of IV glucose in water

Clinical Pharmacokinetics Volume of Distribution (Vd) Vd = Dose / Cpo Factors that control Vd: 1. Lipid vs. Water Solubility of Drug 2. Plasma Volume 3. Binding to Tissue Sites 4. Plasma Protein Volume Factors that alter Vd: 1. Obesity (Total Body Weight vs. Ideal Body Weight) 2. Changes in Binding Affinity to Plasma or Tissue Sites 3. Disease States (renal failure, Ascites, dehydration, surgery) 4. Drug interactions (e.g. beta-lactam antibiotics can bind and inactivate aminoglycosides.) Loading Dose: Vd x Cp desired FxS Elimination Cp2 = Cp1(e-ket) Ke = ln (Cp1/Cp2) t

Ke = 0.693 = Cl t Vd Clearance (Cl) Cl = Vd x Ke Cl in L/hr, Vd in L, and Ke in Hr -1 Legend Ro = Infusion Rate = Dose/t Ctr = Actual tough at time of sampling Cpk = Actual peak at time of sampling Cextr pk = Peak back extrapolated to the end of the infusion o Cp = Peak time back extrapolated to time Zero T = Time between Cpk and Ctr T = Post infusion time (i.e. hrs after Infusion until time of sampling) t = Infusion time = Dosing interval t = Time between Cp1 and Cp2

Aminoglycosides Therapeutic Range: gent/tobra Peak (mcg/mL) UTI/Synergy 4 6 Bacteremia 57 Pneumo/Sepsis7 9 Osteomyelitis 8 10 Trough (mcg/mL)0.5 2.0

amikacin 18 20 20 24 25 28 28 30 5 10

Exact desired peak and trough concentrations will be determined by site and severity of infection, causative organisms, and their minimum inhibitory concentrations (MIC), immunocompetence of the patient, intent of therapy, etc. Time of Sampling 1) Peak will be drawn 30 minutes after completion of a 30-minute infusion 2) Trough will be drawn immediately prior to dose. 3) Levels will be drawn at steady state (i.e. after 4 to 5 estimated half-lives. 4) Estimate Vd Vd = 0.25 L/Kg Average Vd = 0.20 L/Kg if Dehydrated Vd = 0.30 L/Kg if Volume Overloaded (CHF, Ascites, etc.)

5) Estimate Ke Ke = 0.00293 x CrCl + 0.0186 [CrCl in mL/min] Ke = Cl / Vd [Cl in L/hr] 6) Estimate t t = 0.693 / Ke 7) Calculate for desired Peak and Trough = ln (Cpk / Ctr) + t + T Ke 8) Calculate Loading Dose LD = Vd x Csspk or 1.5 to 2 mg/Kg or Csspk x Vd x Ko x t (1 e-ket) (e-ke) 9) Calculate Maintenance Dose Dose = Csspk x Vd x Ke x t (1- e-ke) 1-e-ket) (e-keT) 10) Estimate Trough Csstr = Csspk (e-ke) Dosage Adjustment Aminoglycosides 1) Verify administration and sampling times.

2) Verify actual Ke Ke = ln (Cpk / Ctr) T Use this Ke for all of the equations below. 3) Calculate actual t t = 0.693 / Ke 4) Calculate Vd Avg Vd for AG = 025 L/Kg (0.1 to 0.5 L / Kg) Vd = Dose / t (1 e-ket) (e-ke) Csspk x Ke (1-e-ke) 5) Calculate new =[ { ln (Cpkdesired / Ctrdesired)} / Ke ] +t+T Use this in the following equations. 6) Calculate new dosing regimen Dose = [ Csspkdesired x Vd x Ke x t(1-eke )] / (1 e-ket) (e-keT) 7) Determine peak C extr pk = Dose / t (1 eket) Vd x ke (1 e-ke) 8) Calculate trough of new dosing regimen Csstr = Csspk x e-keT 9) Document recommendations, calculated pharmacokinetic parameters, and

monitoring parameters in progress notes of the chart. Vancomycin Therapeutic Levels Peak: 20 40 mcg/mL Trough: 5 10 mcg/mL Time to Sample 1) The peak should be at least one hour after the end of a 1 - to 2 - hour infusion. 2) The trough should be drawn immediately prior to a dose. 3) Proper documentation of times is essential for accurate calculation of pharmacokinetic parameters. Recommended Frequency of Sampling 1) Routine use in uncomplicated patients Initial Peak & Trough Serum creatinine 3 times per week Trough levels every 7 days in extended therapy 2) Use in patients with changing renal function, risk factors for toxicity, or unusually high MICs: Initial Peak & Trough Serum creatinine daily Repeat Peak & Trough weekly (more frequently if dictated by clinical condition)

Initial Dosing 1) Select desired peak & trough blood levels. 2) Estimate creatinine clearance using Cockroft-Gault, use Ideal Body Weight. 3) Estimate Vd Vd = 0.7 L / Kg (Use Ideal Body Weight) 4) Estimate clearance Cl = o.65 x CrCl (in L / hr) 5) Estimate Ke Ke = Cl / Vd 6) Calculate t t = 0.693 / Ke 7) Calculate for desired peak and trough = ln (Cpk / Ctr) + t + T Ke 8) Calculate loading dose LD = Vd x Csspk or 15 mg/Kg or Csspk x Vd x Ke x t (1 e-let) ( e-keT) 9) Calculate maintenance dose MD = 15 mg/Kg every (calculated above) or Dose = Csspk x Vd x Ke x t (1-e-keT) (1 e-ket) ( e-keT) 10) Estimate trough Csstr = Csspk (e-ke)

Dosage Adjustment Use same equations as for AGs 1) Verify administration and sampling times 2) Calculate Ke 3) Calculate Vd Normal = 0.7 L / Kg (range 0.4 L / Kg to 0.9 L / Kg) 4) Use equations 4-8 for AGs as well. Energy Requirement Equations Basal Energy Expenditure (BEE) Harris-Benedict Men: 66 + (13.7 x W) + (5.0 x H) (6.8 x A) Women: 655 + (9.6 x W) + (1.7 x H) (4.7 x A) W (Kg) H (cm) A(years) STRESS FACTORS (% of BEE to provide daily calorie needs) Starvation 0.85 1.0 Normal / Non-Stressed 1.2 1.3 S/P elective surgery w/o complications 1.25 1.35 Mod stress from chronic illness 1.35 1.5 Sev stress from acute illness, severe infection, trauma, or ventilation 1.5 Burns > 20% of total BSA 2 or >

EST. DAILY PROTEIN REQUIREMENTS

Normal / Non-Stressed 0.8 g/Kg Oncology/Stressed/Surgical 1 1.5 g/Kg Sev stress/burns/mult trauma 1.5 2.5 g/Kg Bone marrow transplant 2 g/Kg* Renal failure (no dialysis) 0.6 0.8 g/Kg Renal failure (w dialysis) 1.2 1.5 g/Kg** Hepatic encephalopathy 0.4 g/Kg * unless in renal failure ** depends on BUN/Scr NITROGEN BALANCE (+2 to +5 is goal) N2 Balance = (N2 in) (N2 out) N2 in = Protein intake (g) / 6.25* N2 out = 24 hour urine urea Ns (UUN) + 4** * 6.25 g protein provides 1 g Nitrogen (standard oral diet) ** where 4 = insensible N2 losses (stool, sweat, hair, etc.)

Electrolyte Maintenance Sodium Chloride 1-2-3 mEq/Kg/day Acetate Phosphate Potassium Chloride 0.5-1-2 mEq/Kg/day Acetate Phosphate 12-15 Mol/1000kcal Calcium Gluconate 5 mEq/L Magnesium Sulfate 8-24 mEq/day 12-16 mEq/day BOLD indicates most appropriate DAILY FLUID REQUIREMENTS Based on weight First 10 Kg 100 mL/Kg Second 10 Kg 50 mL/Kg All Kg > 20 Kg 20 mL/Kg OR 30-35 mL/Kg (25 mL/Kg for elderly patient)

LIPID CALORIES 10% fat 20% fat Daily Dose 50 kcal/day 1000 kcal/day Every 275 kcal/day 500 kcal/day Other Day Mon/Thur ONLY 157 kcal/day 286 kcal/day

Dextrose Calories = 3.4 kcal/g Protein Calories = 4 kcal/g BLOOD GASES pH / PCOs / HCO3 / %O2 Blood Gas Disorders pH HCO3 pCO2 Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis Metabolic Alkalosis

FLUID COMPOSITIONS (mEq/L) Na K Cl HCO3- L/day Diarrhea 50 35 40 45 varies Ileostomy 140 20 100 25 0.5 - 2.0 Gastric 80 10 100 -2.0 Bile 145 5 100 40 1.5 Pancreatic 140 5 75 85 0.75-1.0 Fluid and Electroylte Abnormalities in TPN Management [PF = Predisposing Factors] [MGT = Management] Hypovolemia PF-GI losses, osmotic diuresis; MGT- increased fluid intake Hypervolemia PFrenal failure, excess fluid intake; MGT-decreased fluid intake Hyponatremia PF-GI losses, fluid overload, diuretics; MGT-varies with cause Hypernatremia PF-dehydration; MGTincrease fluid intake Hypokalemia PF-GI losses, diuretics, anabolism; MGT-increase K+ intake Hyperkalemia PF-renal failure; MGTdecrease K+ intake Hypophosphatemia PF-phosphate binding antacids, anabolism, PO4-free dialysis; MGT-D/C PO4 binders, increase phosphate intake Hyperphosphatemia PF-renal failure; MGT-decrease phosphate intake

Hypomagnesemia PF-diarrhea, malabsorption, anabolism; MGT-increase Mg++ intake Hypermagnesemia PF-renal failure; MGTdecrease Mg++ intake Hypercalcemia PF-cancer, hyperparathyroidism; MGT-decrease Ca++ in TPN, cautious volume expansion, drug treatment Hypocalcemia PF-hypoalbuminemia, chronic renal failure; MGT-increase Ca++ intake in CRF only Metabolic Acidosis PF-diarrhea, high output fistula, renal failure, excess amino acid intake; MGT-decrease Cl- in TPN, increase acetate in TPN Metabolic Alkalosis PF-gastric losses; MGT-increase Cl- in TPN, decrease acetate in TPN