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

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

Is malnutrition an independent predictor of survival in ARF?

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

IgG levels in Infants(Katz et al, J Peds 117:258-261, 1990)

IgG Albumin

Loss (mg/kg)

3.6 + 2.94

284 + 176

Loss(mg/

1.73m2)

114.3 + 93

9301 + 3725

IgG levels in Infants(Katz et al, J Peds 117:258-261, 1990)

0

200

400

600

800

1000

1200

1400

1 2 3 4 6 7 10 12 24

+ PD

- PD

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

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 CRRT Mokrzycki and Kaplan, J Am Soc Neph 1996

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 CRRT Davies et al, Crit Care Med, 1991

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

Protein losses on CRRT Davenport et al, Crit Care Med 1989

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

Nutritional losses Replacement fluid vs dialysateMaxvold et al, Crit Care Med 2000 Apr;28(4):1161-5

Comparison of Total Amino Acid losses: CVVH vs CVVHD(Maxvold et al, Crit Care Med 2000 Apr;28(4):1161-

5 )

12.4 11.6

0

2

4

6

8

10

12

14

16

CVVH CVVHD

Am

ino

Aci

d L

oss

es

(g

/day

/1.7

3 m

2)

NS

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

Nutritional losses Replacement fluid vs dialysateMaxvold et al, Crit Care Med 2000;28(4):1161-5

24 Hr Nitrogen Balance: CVVH vs CVVHD(Maxvold et al, Crit Care Med 2000 ;28(4):1161-5 )

-3.68 -0.44

-10

-8

-6

-4

-2

0

2

4

24 h

r N

itro

gen

Bal

ance

(g/d

ay/1

.73

m2)

NS

? 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)

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

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