Transcript Nutrition in Acute Renal Failure

Nutrition in CRRT
Do the losses exceed the
delivery?
Timothy E. Bunchman
Nutrition in MOSF
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What are the needs of the patient due
to presence of MOSF?
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Protein
Carbohydrate
Lipids
What are the losses of the patient due
to the therapy of CRRT?
Protein & Amino Acid Metabolism
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Clinically seen as
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Hyper catabolic
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E.g. Rapidly rising BUN
Over time loss of lean body mass
Protein & Amino Acid Metabolism
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Mechanisms
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Increase in muscle catabolism
Decrease in muscle protein synthesis
Increase in hepatic
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gluconeogenesis
Ureagenesis
Protein synthesis
Altered AA transport (cellular)
Decrease in renal peptide catabolism
Protein & Amino Acid Metabolism
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Potential causes
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Insulin resistance
Metabolic acidosis
Inflammation
Catabolic hormones
Growth hormone/factor resistance
Substrate deficiencies
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Malnutrition prior to illness
Loss on dialysis
Carbohydrate metabolism
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Clinical findings
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hyperglycemia
Carbohydrate metabolism
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Mechanisms
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Insulin resistance
Increase in hepatic gluconeogenesis
Carbohydrate metabolism
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Potential causes
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Stress hormones
Inflammatory mediators with increase in
cytokine (e.g. TNF) expression
Metabolic acidosis
Pre-existing hyperparathyroidism
Lipid Metabolism
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Clinical findings
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Hypertriglyceridemia
Lipid Metabolism
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Mechanisms
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Inhibition in lipolysis
Increase in hepatic triglyceride secretion
Lipid Metabolism
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Potential causes
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Unknown inhibitor to lipoprotein lipase
Inflammatory mediators
Nutrition in PCRRT
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CRRT allows solute clearance
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uremic solutes
small molecular sized nutrients (eg
oligosaccharides)
amino acids and small peptides
electrolytes
Is malnutrition an independent
predictor of survival in ARF?
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Energy Balance studies
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Cumulative energy deficits associated with
increase mortality
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Bartlett et al, Surgery 1986
48% mortality in malnourished
29% mortality in non malnourished
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Fiaccudori et al, J Am Soc Neph 1996
Nutritional Factors in ARF
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Increase in protein catabolism
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underlying and cause of ARF
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uremia
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increase in gluconeogenesis and protein
degradation
hormonal
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cytokine effects
Insulin resistance, diminished protein synthesis
metabolic acidosis
Nutritional Factors in ARF
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Dialysis losses
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protein losses in PD
amino acid losses in PCRRT
Diminished nutrient utilization
Inadequate supplementation
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failure to measure needs
side effects of nutrition supplementation
Dialysis Losses
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Peritoneal Dialysis
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albumin, protein, immunoglobulin and
amino acid losses
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Katz et al, J Peds
IgG levels in Infants
(Katz et al, J Peds 117:258-261, 1990)
IgG
Loss
(mg/kg)
Loss
(mg/1.73m2)
Albumin
3.6 + 2.94 284 + 176
114.3 +
93
9301 +
3725
IgG levels in Infants
(Katz et al, J Peds 117:258-261, 1990)
1400
1200
1000
800
+ PD
- PD
600
400
200
0
1
2
3
4
6
7
10
12
24
Dialysis Losses
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CRRT
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small peptide and amino acid
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Mokrzycki and Kaplan, J Am Soc Neph 1996
Protein losses on CRRT
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Range of amino acid and protein losses
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7-50 gms/day
Factors effecting AA/protein losses
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hemofilter size (surface area) and
composition
nature of solute (molecular size)
total ultrafiltration
plasma concentration of amino
acids/protein
Protein losses on CRRT
Mokrzycki and Kaplan, J Am Soc Neph 1996
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CVVH and CVVHDF
Polysulfone membranes
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(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 CRRT
Davies et al, Crit Care Med, 1991
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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
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AA losses at 1 liter Dx: 9% of total intake
Dx rate @ 2 l/hr; net u/f/hr 340 mls
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AA losses at 2 liter Dx:12% of total intake
Protein losses on CRRT
Davenport et al, Crit Care Med 1989
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CVVH
Polyamide FH 55 (Gambro)
BFR 140 mls/min
Net u/f/hr 1000 mls
Amino Acid losses/day by diagnosis
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Cardiogenic shock- 7.4 gms
Sepsis-3.8 gms
Nutritional losses
Replacement fluid vs dialysate
Maxvold et al, Crit Care Med 2000 Apr;28(4):1161-5
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Prospective crossover study to evaluate
nutritional losses of CVVH vs CVVHD
Study design
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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 dialysate
Maxvold et al, Crit Care Med 2000 Apr;28(4):1161-5
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Indirect calorimetry to measure REE
TPN source of nutrition @ 120% of REE
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70% dextrose
30% lipids
Insulin to maintain euglycemia when
needed
10% Aminosyn II
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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 )
16
12.4
11.6
Amino Acid Losses
(g/day/1.73 m2)
14
12
NS
10
8
6
4
2
0
CVVH
CVVHD
Nutritional losses
Replacement fluid vs dialysate
Maxvold et al, Crit Care Med 2000;28(4):1161-5
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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 )
4
-0.44
24 hr Nitrogen Balance
(g/day/1.73 m2)
-3.68
2
0
-2
-4
-6
-8
-10
NS
? Glucose loss in the Dialysate
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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
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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?
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IVFs are
TPN giving 2500 cals/day
5 IVFs for meds, drips, etc all in D5
with a total rate of 200 ccs/hr
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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)
Patients
557
544
Glucose target
level
180-220
mg/dl
80-110
mg/dl
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
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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
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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?
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1. Keep glucose under control
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Use insulin freely (yes some of the insulin
is cleared ?? How much?)
If using ACD-A citrate the D stands for
Dextrose
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(I missed that but I was educated by a NICU
nurse)
So what do we do?
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2. Keep lipids as part of the
formulation but be aware that both
glucose and lipids effect triglycerides
So what do we do?
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3. Protein load as an amino acid needs
to be targeted
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Local standard is to target to a BUN of 4060 mg/dl
Some NICU babies on the current M-60
AN-69 membrane of the PRISMA require 79 gms/kg/day to reach a target of BUN to
30 mg/dl
Urea Levels: HD vs. HF
Mehta et al, Kid Int, 2001, 60:1154-1163
So what do we do?
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4. Use the gut whenever possible
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Benefit of immune function of enteral
formulas
Decreases risk of TPN line induced sepsis
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Bacterial
fungal
A Study to do
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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