Case-19-21 Chronic Kidney Disease (CKD) Treated With Dialysis – Medical Nutrition Therapy: A Case-Study Approach : Book Guide

This Document Contains Cases 19 to 21 Case 19 – Chronic Kidney Disease (CKD) Treated with Dialysis I. Understanding the Disease and Pathophysiology 1. Describe the basic physiological functions of the kidneys. The kidneys maintain homeostatic balance in the body through 3 basic functions: • Filtration: Continuous filtration of blood removes waste products and fluid. • Electrolyte/pH balance: the kidney plays a crucial role in regulating the blood levels of electrolytes and maintaining physiological pH (via regulating H+ and HCO3- reabsorption/excretion) • Blood pressure control ○ Specialized cells (of the glomerulus) in the kidneys secrete renin to form angiotensin I ○ Angiotensin I is converted to angiotensin II, a powerful vasoconstrictor ○ Angiotensin II also stimulates production of aldosterone and control of blood pressure • Hormone production ○ Kidneys produce erythropoietin, a hormone responsible for red blood cell production in bone marrow ○ Active form of vitamin D is also produced by the kidneys, allowing calcium to be absorbed 2. List the diseases/conditions that most commonly lead to chronic kidney disease (CKD)? Explain the role of diabetes in the development of CKD. • Primary diseases that lead to CKD are: ○ Diabetes (45% of patients) ○ Hypertension (27%) ○ Glomerulonephritis (13%) ○ Hereditary cystic and congenital renal disease (4%) ○ Interstitial nephritis and pyelonephritis • In diabetic nephropathy, the earliest detectable change is a thickening in the glomerulus probably caused by hyperglycemia and a change in the basement membrane. • At this stage, the kidney may start allowing more protein (albumin) than normal to be excreted in the urine. • As nephropathy progresses, increasing numbers of glomeruli are destroyed and increasing amounts of albumin are excreted. • As the number of functioning nephrons declines, each remaining nephron must clear an increasing solute load. • Eventually, the limit to the amount of solute that can be cleared is achieved and the concentration in body fluids increases, leading to azotemia and uremia. • Because progression is slow (microalbuminuria can last up to 5-10 years before other symptoms develop), the body can partially adapt to the changes. • As diabetic nephropathy progresses, increasing numbers of glomeruli are destroyed. • At this stage, the amount of albumin being excreted in the urine increases, and can be detected by a urinalysis. • In addition to the damage to the glomerulus, the increased blood pressure that can be a result of diabetes can further exacerbate kidney damage 3. Outline the stages of CKD, including the distinguishing signs and symptoms. The general course of progress kidney failure is now divided into five stages. Stage Description GFR (mL/min/1.73 m2) -- At increased risk ≥60 (with CKD risk factors) 1 Kidney damage with normal or increased GFR ≥90 2 Kidney damage with mild decrease in GFR 60-89 3 Moderate decrease in GFR 30-59 4 Severe decrease in GFR 15-29 5 Kidney failure <15 (or dialysis) • CKD is defined as either kidney damage or GFR 35 kcal/kg (using adjusted body weight) for individuals under the age of 60: 70.75  35 = 2476 kcal. This should include the kcal provided by dialysate. ABW: 70.75 kg; 2476 - Will need to adjust to accommodate kcal form dialysate. SBW: 61 kg; 2135 kcal- Will need to adjust to accommodate kcal form dialysate. Using K/DOQI guidelines, 1.2-1.3 g protein/kg (using adjusted body weight): 70.75  1.2-1.3 = 85-92 grams with 50% HBV. 85-92 g protein (ABW); 73-79 g protein (SBW) 10. List all medications that Mrs. Caldwell is receiving. Determine the action of each medication and identify any drug–nutrient interactions that you should monitor for. Medication Indications/Mechanism Nutritional Concerns Catapres Antihypertensive -- α-2 adrenergic agonist N/V, dry mouth, constipation, avoid alcohol Procardia Calcium channel blocker -- vasodilator Nausea, vomiting, diarrhea or constipation; avoid alcohol, licorice, and grapefruit; take with a low-fat meal Carvedilol Beta blocker -- reduce cardiac output Fluid retention, hyperglycemia; take with food Lasix Diuretic—prevent fluid retention/can be used to treat hypertension Hypokalemia, increased thirst Prednisone Immunosuppressant—prevent rejection of transplant Increased appetite, osteoporosis, hyperglycemia, fluid retention, poor wound healing Gengraf Immunosuppressant; prevent rejection of transplant Nausea, vomiting, upper abdominal pain, itching, loss of appetite, dark urine, clay-colored stools, jaundice, hyperkalemia CellCept Immunosuppressant; prevent rejection of transplant GI bleeding, N/V, abdominal pain, dyspepsia, peripheral edema, hypophosphatemia, hypercholesterolemia, hyperglycemia; do not take Ca, Mg, Fe, or Al supplements within 2 hours of taking; take on empty stomach Fish oil Anti-inflammatory Increased risk of bleeding Prinivil Antihypertensive (angiotensin-converting enzyme [ACE] inhibitor) Hyperkalemia; herbs may attenuate effects (e.g. cayenne, ginger, ginseng, licorice, etc.) Sodium bicarbonate Normalize blood pH • High in sodium • Take Fe supplement separately, 1 hr before or 2 hr after drug • Increased thirst • Increased weight (edema) Renal caps Replace vitamins lost in dialysis • GI irritation • N/V • Take after dialysis Renvela Phosphate binder used in CKD • Low-phosphorus diet • Nausea • Dyspepsia • Diarrhea • Constipation • Flatulence • Severe decrease in GI motility • Low serum phosphorus, calcium Calcitriol Vitamin D • Nausea, vomiting, stomach pain, constipation • Loss of appetite • Dry mouth, increased thirst • Metallic taste 11. Mrs. Caldwell’s laboratory values that you discussed previously in this case indicate she has anemia. Why do renal patients suffer from anemia? How is this typically treated in dialysis patients? The loss of the kidney’s ability to synthesize erythropoietin decreases red blood cell production. The K/DOQI anemia guidelines recommend administration of rHuEPO. Additionally, oral and intravenous iron supplementation can be prescribed. 12. What factors in Mrs. Caldwell’s history may affect her ability to eat? What are the most likely causes of these symptoms? Is it realistic to expect that they will change? Mrs. Caldwell states that she has noticed her appetite has not been as good lately. She describes mild nausea but no vomiting. She relates that food has a bad taste. Most of these symptoms are most likely related to her increasing uremia. Symptoms should certainly improve as Mrs. Caldwell begins dialysis again and her BUN and creatinine levels diminish. 13. Evaluate Mrs. Caldwell’s diet history and 24-hour recall. Is her usual diet consistent with her inpatient diet order? AM: Egg McMuffin™, 6 oz orange juice, coffee Lunch: Cheeseburger, fries, apple pie, and 12 oz Coke Dinner: Roast beef au jus; 3 small oven-browned potatoes, 1/4 c broccoli, iced tea, roll with butter kcal: 2270 kcal 95 g protein 3004 mg sodium 565 mg calcium 3798 mg potassium 1244 mg phosphorous This is higher than her prescribed energy needs and high in phosphorous and potassium. IV. Nutrition Diagnosis 14. Identify the pertinent nutrition problems and the corresponding nutrition diagnoses. Altered nutrition-related laboratory values Undesirable food choices Excessive mineral intake (phosphorous/potassium) Predicted suboptimal nutrient intake 15. Write a PES statement for each high-priority nutrition problem. • Altered nutrition-related laboratory values related to chronic kidney disease as evidenced by increasing BUN, Cr, PO4. • Excessive mineral intake related to consumption of high-phosphorous and high-potassium foods as evidenced by serum PO4 level and intake of >1200 mg, intake of ~3900 mg of K, excessive consumption of meats, and usual consumption of orange juice, potatoes, and broccoli (high-K foods). • Predicted suboptimal nutrient intake related to nausea, metallic taste, and edema as evidenced by patient interview. V. Nutrition Intervention 16. Determine the amount of energy that Mrs. Caldwell’s PD prescription will provide each day. How will this affect your nutrition recommendations? CCPD daily. Ca 2.50; Mg 0.5, Dextrose 2.5%. Total fills (or exchanges) 3 (3 fills/cycle @2500 mL). Total fill volume/24 hours: 7500 mL. Estimating intake using a percentage of grams absorbed: (Grams infused/day of monohydrous glucose)  3.4 kcal = available kilocalories Multiply available kilocalories by: 60-70% absorption for CAPD 7.5 L of 2.5%; 10  25 g/L = 187.5 g 187.5 g  3.4 kcal/g  0.6-0.7 = 382.5-446.25 kcal from CAPD 17. Using the KDOQI adult guidelines for peritoneal dialysis patients, determine Mrs. Caldwell’s nutrition prescription for outpatient use. (Include energy, protein, phosphorus, calcium, potassium, sodium, and fluid.) Nutrition Therapy for PD Mrs. Caldwell 35 kcal/kg adjusted body weight or SBW ABW: 70.75 kg 2476 (- 510 kcal from dialysate) = 1950-2000 kcal SBW: 61 kg 2135 kcal (- 510 kcal from dialysate) = 1625-1650 kcal 1.2-1.3 g protein/kg adjusted body weight or SBW 85-92 g 73-79 g 2-4 g K (adjust by serum levels) 2-4 g K (adjust by serum levels) 800-1000 mg phosphorus 800-1000 mg phosphorus 2-3 g Na 2-3 g Na Fluid – not restricted (maintain balance) Fluid – not restricted (maintain balance) 18. Using the identified nutrition problems (and with the understanding that Mrs. Caldwell has received a significant amount of nutrition education in the past), what would you determine to be the most important topics for nutrition education when she returns to the PD clinic? Review of basic guidelines for phosphorous and potassium restriction (discussing high- and low-forms of food); encouragement of adequate kilocalories and protein with suggestions to maximize PO intake in face of her current symptoms of nausea and dysgeusia. VI. Nutrition Monitoring and Evaluation 19. List factors that you would monitor to assess Mrs. Caldwell’s nutritional status when she returns to the PD clinic. Serum albumin Monthly nPNA Every 4 months % Usual dry weight (post dialysis or post-drain) Monthly % Standard body weight Every 4 months Subjective global assessment Biannually Diet interview/diary Biannually Anthropometrics, DEXA, prealbumin, creatinine index, creatinine, urea nitrogen, cholesterol, RBC/Hct/Hgb, serum electrolytes (Ca, P, K, Na) As needed Additional evaluations: --knowledge and adherence to her prescribed diet -- progress towards behavioral/lifestyle/clinical goals/changes Adapted from: NKF KDOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis. 2000;35(6)suppl 2:S1-S140. Case 21 – Acute Kidney Injury (AKI) I. Understanding the Disease and Pathophysiology 1. Define Mr. Maddox’s diagnosis of acute kidney injury. • AKI patients are likely to produce 75 years • CKD • cardiac failure • liver disease • diabetes • nephrotoxic medications • sepsis • hypovolemia 3. Explain the major causes of prerenal, postrenal, and intrarenal/intrinsic AKI. Identify the staging for AKI. What do you suspect is the major etiology of Mr. Maddox’s AKI? Typically, AKI is characterized by a rapid decline in kidney function with an acute elevation of serum creatinine at baseline. There are three types of causes for the kidney dysfunction: • Prerenal: ○ An underlying condition deprives the kidneys of necessary blood flow and decreases the GFR. ○ Due to: volume depletion (e.g. via the GI tract or extensive wounds), hypotension/shock, CHF, renal vasoconstriction from medications or hepatorenal issues, and renal artery occlusion from an embolism or thrombosis. ○ If blood flow is not restored, necrosis of the cells will occur. • Intrarenal/Intrinsic: ○ Occurs when parts of the kidneys such as the tubule, the interstitium, the glomerulus, or the vasculature are damaged (true kidney problem). ○ Underlying conditions that can lead to kidney damage include hypertension, interstitial inflammation from an infection or disease (e.g. lupus, Goodpasture syndrome, acute glomerulonephritis), acute tubular necrosis, acute interstitial nephritis, nephrotoxicity, or intrarenal obstruction. • Postrenal: Results when crystals, protein deposits, blood clots, or malignant tumor infiltration obstruct urine flow. • There are typically 4 stages involved with AKI: ○ Initiation: when GFR declines ○ Extension: when ischemia and inflammatory damage occur ○ Maintenance: when GFR is at its lowest level ○ Recovery: when epithelial cells regenerate Mr. Maddox is most likely experiencing AKI due to a deprivation of blood (oxygenation) during recovery from surgery as it was noted that he had a sudden drop of blood pressure. The infection following his CABG  3, which may have lead to inflammation and therefore kidney damage, may also have been a contributing factor. 4. Explain the major nutrient/metabolic changes (glucose, lipid, protein, and energy expenditure) that may occur during AKI and that would potentially affect your nutrition recommendations. • Major nutrient and metabolic changes that can occur during an AKI include a rapid decrease in urine output, which can lead to acidosis, electrolyte imbalances (hyperkalemia, hyperphosphatemia), fluid disturbances, impaired glucose utilization, protein catabolism, and accumulation of metabolic waste products. • Energy: 25-35 kcal/kg based on the stress and normal nutrition status of the patient before the injury (if the patient was malnourished beforehand, he would have higher energy needs than this) • Impaired glucose utilization and protein catabolism from uremia Protein needs range from 0.8 to 2.0 g/kg/d • non-catabolic, not dialyzed: 0.8-1.0 g/kg/d • on renal replacement therapy: 1.0-1.5 g/kg/d • hypercatabolic, receiving CRRT: up to 2.0 g/kg/d Hyperglycemia may arise due to calories from CRRT and response to metabolic stress • Insulin may be needed due to insulin resistance resulting from AKI • Serum TG should be within normal range if started on enteral or parenteral nutrition because a high TG value may indicate a reduced hepatic capacity for removal of long-chain and medium-chain fatty acids; if TG are high at first, these levels will need to be monitored closely for tolerance. 5. What laboratory values or other tests support Mr. Maddox’s diagnosis of AKI? List all abnormal values and explain the likely cause for each abnormal value. • High K due to tissue destruction, shock, acidosis, dehydration, and inadequate kidney function • High BUN due to hypercatabolism and the acute assault to his kidneys • High Cr due to AKI. Creatinine is a breakdown product of creatine (a part of muscle) that can be produced as a result of the acute assault to the kidney; there is also a lot of nitrogenous waste accumulation currently. • Low GFR (8 mL/min./1.73 m2): the most common measurement of kidney function, which is reflected in clearance tests. This measures the rate at which substances are cleared from the plasma by the glomeruli; normal GFR is 135-200 liters/day, of which 98-99% is reabsorbed with urine output. This is low most likely due to the low renal blood supply or damage from the infection causing the kidney dysfunction. • High glucose due to the patient’s history of diabetes, as well as the acute infection and recent events (MI, surgery) that cause systemic stress and decreased glucose utilization (insulin resistance due to AKI). • High phosphorus is common with insufficient kidney function because the kidneys cannot filter this electrolyte as efficiently. Thus, phosphate and potassium are the most common electrolyte imbalances. These electrolyte imbalances are probably not due to excessive protein intake based on the low protein value and documented low PO intake. • Low protein could be due to excessive fluid (present edema) and protein losses due to kidney dysfunction • Low albumin due to fluid overload (present edema), the inflammatory response from the infection and protein losses due to kidney dysfunction • Low prealbumin due to fluid overload (present edema), the inflammatory response from the infection and protein losses due to kidney dysfunction • Low RBC count due to blood loss from recent surgery • Low hemoglobin/mean cell hemoglobin/mean cell hemoglobin content due to fluid overload (present edema), blood loss from recent surgery • Low hematocrit due to a possible underlying anemias, blood loss (from surgery) • High RBC distribution due to underlying anemia 6. Mr. Maddox will be started on continuous renal replacement therapy (CRRT). Describe the basic mechanisms of this therapy. • CRRT is a type of dialysis, or a renal replacement procedure that removes excessive and toxic by-products of metabolism from the blood, thus replacing the filtering function of healthy kidneys. CRRT is generally the mode of treatment for AKI because it will provide dialysis over a continuous period of time that will allow for a significant amount of fluid (1-2 L) to be removed. • It is meant to slowly remove fluids and solutes while correcting the electrolyte and metabolic abnormalities associated with AKI. • Two types of CRRT: ○ Arteriovenous renal replacement therapies: continuous dialysis/hemofiltration by cannulation of an artery or vein; the patient’s blood pressure is used to pump blood through the dialysis filter. ○ Venovenous renal replacement therapies involve continuous dialysis/hemofiltration by a venovenous circuit and a pump to assist blood flow through the dialysis circuit. • Venovenous renal replacement is usually used in the critical patient as the patient’s blood pressure is usually unstable. 7. Explain how nutrition therapy recommendations for an AKI patient may differ if he is receiving CRRT versus not receiving any dialysis treatment. • Higher protein needs; CRRT can remove amino acids and proteins, so a minimum protein intake of 1.5 g/kg/day is recommended (up to 2.0 g/kg/day if hypercatabolic). • There does not need to be a fluid restriction with CRRT as it removes 1-2 L per day; with no dialysis, it is urine output plus 500 mL (very minimal to avoid fluid accumulation). • Vitamin replacement may be necessary because of the loss of water-soluble vitamins with CRRT. • If the patient was not receiving any dialysis, he would not tolerate fluid or protein as these would contribute to the major complications of AKI. II. Understanding the Nutrition Therapy 8. Mr. Maddox has not eaten since his surgery. He was started on clear liquids several days ago but has taken in very little. Using the ASPEN guidelines, justify his requirement for nutrition support. • Mr. Maddox is a candidate for enteral nutrition support because he has had inadequate PO intake greater than 7 days and it is expected that this will continue. Also, it is important that he meets his nutritional needs at this time because he is s/p major surgery and is in a hypermetabolic state during sepsis and organ failure. Because he has no major injury to his GI tract, it is safe to administer the enteral feeding through an NG tube to the stomach for short-term use (<30 days). • He is currently hemodynamically stable after experiencing hypotension immediately post-op. • Nutrition support can be beneficial for this patient because it can preserve gut function, support immune function, and decrease episodes of bactremia and infection. ○ Macronutrient, total fluid, electrolyte, and mineral content should to be considered. ○ Formulas that are concentrated with minimal fluid load are desired. ○ Flushes may not be tolerated well and must be monitored with fluid status. ○ With CRRT, a standard, high-protein formula would be best. • Once Mr. Maddox meets 60% of his needs through oral intake, weaning from EN can ensue. III. Nutrition Assessment 9. Assess Mr. Maddox’s height, weight, and BMI. What factors from his medical record will affect your interpretation of his weight? Height: 6’2” (74”), 1.88 m Current weight: 225#/102.2 kg Admission weight: 208#/94.5 kg Admission BMI: 26.8 kg/m2 (overweight) Ideal body weight: 190 lbs (86.3 kg ) or 171-209 per Hamwi equation +/- 10% The patient’s admission weight most likely reflects his true weight, due to his AKI that occurred during his hospital stay. During an AKI, the patient is unable to excrete excess fluid and thus begins to retain it, which can cause a falsely high weight (fluid overload). His “dry weight” is most likely close to his admission weight. This is consistent with his medical record because of his documented 3+ pitting edema, +5,295 mL I/O since admission, and his poor urine output despite being on Lasix. He has also had a 17# weight gain since admission despite poor PO intake. 10. While conducting a nutrition-focused physical examination, the RD discovers that Mr. Maddox exhibits evidence of temporal wasting and loss of preorbital fat pads, as well as some evidence of triceps fat loss. How might this impact the nutrition recommendations the RD will make? Describe the etiology of the protein-energy wasting that may occur with AKI. • The temporal wasting is evidence of muscle-wasting • Losses in the preorbital pads and triceps suggests subcutaneous fat loss. • These pieces of evidence should indicate acute malnutrition and the RD should adjust his/her energy/protein recommendations: ○ Energy: 30-35 kcal/kg ○ Protein: 2.0 g/kg • The etiology of protein-energy malnutrition from AKI is related to the metabolic derangements that occur from it (and from the underlying catabolic illness/precipitating factor) and results in the degradation of proteins and amino acids. Additionally, fuel substrates may not be utilized efficiently due to the presence of cortisol and epinephrine. Together, these will result in an increase in lipolysis, lower the uptake of glucose by peripheral tissues, and result in protein sparing. This overactive use of the Cori cycle is an inefficient utilization of energy substrates. 11. Determine Mr. Maddox’s energy and protein requirements. Explain the rationale for the method you used to calculate these requirements. • Estimated energy needs: 30-35 kcal/kg IBW/day = 2590-3023 kcal/day or 2600-3000 kcal/day • Estimated protein needs: 1.8-2.0 g protein/kg IBW/day = 155-173 g protein/day These estimations were based on ideal body weight because of the fluctuation of weight this patient has experienced since admission. Additionally, would want to avoid the risks of overfeeding the patient (hyperglycemia, increased CO2) while he is in critical condition. These ranges were selected based on the previous estimations for a patient with AKI who is going to be on CRRT. IV. Nutrition Diagnosis 12. Identify the pertinent nutrition problems and the corresponding nutrition diagnoses. Elevated P and K – altered nutrition-related laboratory value Inadequate PO intake – predicted suboptimal nutrient intake Inadequate PO intake -- Inadequate protein intake Hypercatabolic state -- Increased nutrient needs 13. Write two PES statement for each high-priority nutrition problem. Altered nutrition-related laboratory value – potassium and phosphorous related to AKI as evidenced by serum K 5.7 mEq/L and serum PO4 5.3 mg/dL. Malnutrition related to critical illness/hypercatabolism as evidenced by inadequate energy intake for previous 7 days, preorbital and tricep fat wasting, and temporal muscle wasting. V. Nutrition Intervention 14. Outline the appropriate nutrition support plan for Mr. Maddox. When enteral access is available, recommend starting Nepro in order to meet kcalorie and protein needs. In order to avoid electrolyte imbalances, start very slowly at 10 mL/hr and advance by 10 mL q 6 hours/as tolerated to goal rate of 70 mL/hr (based on 22 hours per day to account for interruptions in the ICU). This will provide 1540 ml, 2772 kcal, 125 grams protein, and 1120 mL free water (33 kcal/kg, 1.5 g protein/kg). Provide approximately 1652 mL free water via maintenance IV or divided flushes. 15. Should any micronutrients be supplemented for the AKI patient treated with CRRT? Are there other micronutrients that should be avoided during an episode of AKI treated with CRRT? • K, Mg, PO4, and Ca should be added/replaced based upon the diuretic phase of the CRRT and the patients serum levels. • Deficiencies of Se, Cu, thiamin may also occur • It is suggested to provide daily supplementation of 1 mg folate, 10 mg pyridoxine, the age and sex appropriate DRI for vitamin C (prevent oxalosis), 100 μg Se, and a daily renal multivitamin for AKI patients receiving CRRT • Vitamin A should probably not be supplemented due to the potential for toxicity • Vitamin D supplementation may be needed if secondary parathyroidism is present due to CKD or levels are low in the critically ill • Vitamin K should be supplemented if the patient is on PN and receiving antibiotic medication VI. Nutrition Monitoring and Evaluation 16. Write your ADIME note for the nutrition support recommendations. Date Time A: 67 yo male DX: AKI s/p CABG  3 on 10/9 PMH: CAD, s/p MI  15 years ago, HLD, DM2 Skin: 3+ peripheral edema; Braden 13. No wounds noted. Abdomen: Soft, obese appearance, active and audible bowel sounds in all quadrants I/O  24 hours: 730 mL/295 mL (net: + 5,295 mL) Labs: K 5.7, BUN 38, Cr 6.62, GFR 8, Glu 123, Phos 5.3, Ca 8.6, Alb 2.5, Prealb 12, RBC 2.95, Hgb 9.1, Hct 28.6 Urine: cloudy/amber; UOP dec significantly since admission (past 24 hrs: 75 mL) Ht: 6’2” Wt: 225#, Adm Wt: 208#, IBW: 190#, %IBW: 109%, Admission BMI: 26.7 kg/m2 EER: 2600-3000 kcal (30-35 kcal/kg IBW), EPR: 155-173 g PRO (1.8-2.0 g/kg IBW) D: Malnutrition related to critical illness/hypercatabolism as evidenced by inadequate energy intake for previous 7 days, preorbital and tricep fat wasting, and temporal muscle wastingI: I: When enteral access is available via NG tube, recommend starting Nepro: 20 mL/hr and advance by 20 mL q 4 hours/as tolerated to goal rate of 70 mL/hr (based on 22 hours per day to account for interruptions in the ICU). This will provide 1540 mL, 2772 kcal, 125 grams protein, and 1120 mL free water (33 kcal/kg, 1.5 g protein/kg). Provide approximately 1652 mL free water via maintenance IV or divided flushes to meet hydration needs if this is consistent with his CRRT plan. Assure HOB elevated 30-45 degrees. Suggest a daily MVI with CRRT – may require additional micronutrient supplementation. Recommend Accuchecks q 6 hours with insulin therapy. Communicate with team and patient’s family the nutrition support recommendations per above. M/E: Monitor TF tolerance. Monitor electrolytes, vitamin, mineral levels. Monitor weight status, pertinent labs (e.g. BG, BUN), I/O, and skin integrity. Solution Manual for Medical Nutrition Therapy: A Case-Study Approach Marcia Nahikian Nelms 9781305628663, 9780534524104, 9781133593157