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Nutrition in CRRT Do the losses exceed the delivery?. Timothy E. Bunchman. Nutrition in MOSF. What are the needs of the patient due to presence of MOSF? Protein Carbohydrate Lipids What are the losses of the patient due to the therapy of CRRT?. Protein & Amino Acid Metabolism.
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Nutrition in CRRTDo the losses exceed the delivery? Timothy E. Bunchman
Nutrition in MOSF • What are the needs of the patient due to presence of MOSF? • Protein • Carbohydrate • Lipids • What are the losses of the patient due to the therapy of CRRT?
Protein & Amino Acid Metabolism • Clinically seen as • Hyper catabolic • E.g. Rapidly rising BUN • Over time loss of lean body mass
Protein & Amino Acid Metabolism • Mechanisms • Increase in muscle catabolism • Decrease in muscle protein synthesis • Increase in hepatic • gluconeogenesis • Ureagenesis • Protein synthesis • Altered AA transport (cellular) • Decrease in renal peptide catabolism
Protein & Amino Acid Metabolism • Potential causes • Insulin resistance • Metabolic acidosis • Inflammation • Catabolic hormones • Growth hormone/factor resistance • Substrate deficiencies • Malnutrition prior to illness • Loss on dialysis
Carbohydrate metabolism • Clinical findings • hyperglycemia
Carbohydrate metabolism • Mechanisms • Insulin resistance • Increase in hepatic gluconeogenesis
Carbohydrate metabolism • Potential causes • Stress hormones • Inflammatory mediators with increase in cytokine (e.g. TNF) expression • Metabolic acidosis • Pre-existing hyperparathyroidism
Lipid Metabolism • Clinical findings • Hypertriglyceridemia
Lipid Metabolism • Mechanisms • Inhibition in lipolysis • Increase in hepatic triglyceride secretion
Lipid Metabolism • Potential causes • Unknown inhibitor to lipoprotein lipase • Inflammatory mediators
Nutrition in PCRRT • CRRT allows solute clearance • uremic solutes • small molecular sized nutrients (eg oligosaccharides) • amino acids and small peptides • electrolytes
Is malnutrition an independent predictor of survival in ARF? • Energy Balance studies • Cumulative energy deficits associated with increase mortality • Bartlett et al, Surgery 1986 • 48% mortality in malnourished • 29% mortality in non malnourished • Fiaccudori et al, J Am Soc Neph 1996
Nutritional Factors in ARF • Increase in protein catabolism • underlying and cause of ARF • cytokine effects • uremia • increase in gluconeogenesis and protein degradation • hormonal • Insulin resistance, diminished protein synthesis • metabolic acidosis
Nutritional Factors in ARF • Dialysis losses • protein losses in PD • amino acid losses in PCRRT • Diminished nutrient utilization • Inadequate supplementation • failure to measure needs • side effects of nutrition supplementation
Dialysis Losses • Peritoneal Dialysis • albumin, protein, immunoglobulin and amino acid losses • Katz et al, J Peds
Dialysis Losses • CRRT • small peptide and amino acid • Mokrzycki and Kaplan, J Am Soc Neph 1996
Protein losses on CRRT • Range of amino acid and protein losses • 7-50 gms/day • Factors effecting AA/protein losses • hemofilter size (surface area) and composition • nature of solute (molecular size) • total ultrafiltration • plasma concentration of amino acids/protein
Protein losses on CRRTMokrzycki and Kaplan, J Am Soc Neph 1996 • CVVH and CVVHDF • Polysulfone membranes • (Amicon 20 and Fresenius F-80) • BFR 100-300 mls/min • Dx FR 1000 mls/hr with net u/f/hr 1600 mls • 1.2 - 7.5 gms/day of protein losses
Protein losses on CRRTDavies et al, Crit Care Med, 1991 • CAVHD • AN-69 (0.43 m2; PAN membrane) • BFR MAP dependent (80 mls/min) • Dx rate @ 1 l/hr; net u/f/hr 340 mls • AA losses at 1 liter Dx: 9% of total intake • Dx rate @ 2 l/hr; net u/f/hr 340 mls • AA losses at 2 liter Dx:12% of total intake
Protein losses on CRRTDavenport et al, Crit Care Med 1989 • CVVH • Polyamide FH 55 (Gambro) • BFR 140 mls/min • Net u/f/hr 1000 mls • Amino Acid losses/day by diagnosis • Cardiogenic shock- 7.4 gms • Sepsis-3.8 gms
Nutritional losses Replacement fluid vs dialysateMaxvold et al, Crit Care Med 2000 Apr;28(4):1161-5 • Prospective crossover study to evaluate nutritional losses of CVVH vs CVVHD • Study design • Fixed blood flow rate-4 mls/kg/min • HF-400 (0.3 m2 polysulfone) • Cross over for 24 hrs each to pre filter replacement or Dx at 2000 mls/hr/1.73 m2
Nutritional losses Replacement fluid vs dialysateMaxvold et al, Crit Care Med 2000 Apr;28(4):1161-5 • Indirect calorimetry to measure REE • TPN source of nutrition @ 120% of REE • 70% dextrose • 30% lipids • Insulin to maintain euglycemia when needed • 10% Aminosyn II • 1.5 gms/kg/day of protein
Comparison of Total Amino Acid losses: CVVH vs CVVHD(Maxvold et al, Crit Care Med 2000 Apr;28(4):1161-5) NS Amino Acid Losses (g/day/1.73 m2)
Nutritional losses Replacement fluid vs dialysateMaxvold et al, Crit Care Med 2000;28(4):1161-5 • Amino acid and protein losses with this prescription represent between 10-12% of total delivered nutritional proteins • Glutamine loss accounted for approximately 20% of total AA loss • Some Amino Acid preparations for TPN are deficient in glutamine
24 Hr Nitrogen Balance: CVVH vs CVVHD(Maxvold et al, Crit Care Med 2000 ;28(4):1161-5 ) NS 24 hr Nitrogen Balance (g/day/1.73 m2)
? Glucose loss in the Dialysate • 90 kg BMT tx pt with MOSF • Begun on CVVD at 2.5 liters of Normocarb • Due to acidosis 2 liters of Normocarb added as a prefilter replacement fluid therefore the child is now on CVVHDF • Normocarb is glucose free • What is the caloric impact of this?
? Calorie deficient due to no glucose in the Dialysate-2 • Ultrafiltrate glucose is measured at 109 mg/dl • 4.5 liters/hr x 24 hrs = 108 liters uf/day • 109 mg/dl = 1090 mg/l = 1.09 gms/l • 1.09 gms/l x 108 liters = 117 gms of glucose lost • 117 gms x 4 cals/gm = 470 cals lost
Is this significant? • IVFs are • TPN giving 2500 cals/day • 5 IVFs for meds, drips, etc all in D5 with a total rate of 200 ccs/hr • 200 ccs/hr x 24 hrs = 4800 ccs of D5 • D5 has 5 gms/100ccs or 50 gms/1000 • 50 gms x 4.8 liters = 24 gms • 24 gms x 4 cal = 96 cals (cals not thought of)
Intensive Insulin therapy(Van den Berghe et al NEJM 345:1359-67, 2001)
Intensive Insulin therapy(Van den Berghe et al NEJM 345:1359-67, 2001)
Intensive Insulin therapy(Van den Berghe et al NEJM 345:1359-67, 2001)
Intensive Insulin therapy(Van den Berghe et al NEJM 345:1359-67, 2001)
Trace elements and Vitamins • Trace elements are poorly cleared due to protein binding • Water soluble vitamins are well cleared and the child is at risk for deficiency
Trace elements and Vitamins • Vitamin A may be retained and cause toxicity manifested as hypercalemia • Vitamin K is not cleared but in patients with MOSF on antibiotics will become deficient and will need supplementation • Vitamin D may be depressed if pt had pre existing renal insufficiency • Vitamin E levels are depressed in MOSF but are not cleared
So what do we do? • 1. Keep glucose under control • Use insulin freely (yes some of the insulin is cleared ?? How much?) • If using ACD-A citrate the D stands for Dextrose • (I missed that but I was educated by a NICU nurse)
So what do we do? • 2. Keep lipids as part of the formulation but be aware that both glucose and lipids effect triglycerides
So what do we do? • 3. Protein load as an amino acid needs to be targeted • Local standard is to target to a BUN of 40-60 mg/dl • Some NICU babies on the current M-60 AN-69 membrane of the PRISMA require 7-9 gms/kg/day to reach a target of BUN to 30 mg/dl
Urea Levels: HD vs. HFMehta et al, Kid Int, 2001, 60:1154-1163
So what do we do? • 4. Use the gut whenever possible • Benefit of immune function of enteral formulas • Decreases risk of TPN line induced sepsis • Bacterial • fungal
A Study to do • Serial nitrogen balance, REE, glucose metabolism studies throughout the course of the child’s illness • Impact upon balance of catabolism to anabolism as one increases the protein/AA exposure