Pranithi Hongsprabhas MD Division of Clinical Nutrition, Department of Medicine, Faculty of Medicine...

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Pranithi Hongsprabhas MDPranithi Hongsprabhas MDDivision of Clinical Nutrition, Division of Clinical Nutrition,

Department of Medicine, Department of Medicine, Faculty of MedicineFaculty of Medicine

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Update in Clinical Update in Clinical NutritionNutrition

Case Case discussion in discussion in

nutritionnutrition

Critical illness/Acute Critical illness/Acute pancreatitispancreatitis 45 yr old, previously healthy man was

ssssss sssssssss sssss ss sssssss ssssssss .,.

120, 100/60 25 /. ssssss,. >2000 135, 3, 11 /, 25000, 4.5 450, 36/, . ss sssssss ssssssss: 70 . 1.8

Critical illness/Acute Critical illness/Acute pancreatitispancreatitis What would be your strategy for fluid Rx

at this stage? s ssss sssssss ss sss ssssssss ssssssss ss

urse are potentially relevant for metaboli sm and nutrition?

What is his nutritional status?: is he nutritional depleted, or at risk?

sss sssss sssssssss ssssssss ss ss s, es, why and how?

Fluid Rx considerationFluid Rx considerationCritical illness/Acute pancreatitisCritical illness/Acute pancreatitis

maintenance + ECF resuscitation

considersequestration --> hypovolemiaprerenal vs acute renal failure impending lung injury / ARDS

Case StudyCase StudyCritical illness/Acute pancreatitisCritical illness/Acute pancreatitis

Foreseen clinical course potentially relevant for nutrition and metabolism

Hyper metabolic/catabolic ileus electrolyte imbalance: hyponatremia,

hypo/hyperkalemia hyperglycemia hypertriglyceridemia: decreased LPL

activity

Patient’s nutritional status: Not depleted but at risk

Nutritional screening BMI: normal: 0 no weight loss: 0 nearly no food intake: 1 hypermetabolic/catabolic:2

Score:3 previously normal status Close F/U if not improve: perform

nutrition assessment

Hierarchy of Vital Organ Hierarchy of Vital Organ SystemSystem

Immediately relevant for survival circulation CNS respiratory system

Relevant for survival with delay splanchnic organ metabolism

Rational for early ANSPancreatitis: hypermetabolic/catabolic prolonged inadequate food i

ntake risk of nutritional deterioratio

nMalnutrition: adverse effect on host defen

se, immune competence worsen outcome: 25MR . vs

214. in pt unable to achieve +s sssssss Sitzmann JV, et al. Surg Gynecol

Obstet 1989

Rational against early ANS No PRCT exists to show t

hat early ANS reduces th e duration or lessens the

severity of disease when compare to no NS

Early NS(TPN) is associat ed with complications. Sa

x et al. Am J Surg 1987.

Early return of oral diet o r displacement of jej fee

ding back to stomach as sociates with exacerbati

on of pancreatitis. s sssssss SA, et al. JPEN 1 9 9 7

progressive deterioration of clinical

CT performed D 3 of admission

Percutaneousaspirationofnecr osi s f or C/S, G/S Ant i bi ot i c st ar t ed

Would you startSNS , and if yes,

why and how? What are the ris

ks of PN vs EN a t this stage?

Critical illness/Acute pancreatitis Critical illness/Acute pancreatitis 5D ARF, ARDS, C/S reveals E coli. 5D ARF, ARDS, C/S reveals E coli.

sssssss sssssss,sssss ssssss

hypermetabolic/catabolic

sss ssss-ssssssssss y: elemental or po

l ymer i c but smals ssssss

combined PN

D9 surgical removal of

infected necrosis was done due to persistent ileus and progressive sepsis.

Jejunostomy and ileostomy

Regular HD worsening ARDS/ on

PCV/PEEP

sssss sss sssss SNS already?

s sss ss ssss sssss sss sssssssss ’

TEE? How much N/d is t

he patient likely to lose, if not fed?

Nitrogen and energy balance response to Nitrogen and energy balance response to nutritionnutrition

Energy intake -->

Energy balance

Depleted

Energy balance

Argument for parenteral Argument for parenteral nutritionnutrition Need to reduce stimulation and

secretion of proteolytic enzymes

PN least likelihood of pancreatic stimulation

easily access

Nutritional goal achieved quickly and easily

Argument for enteral Argument for enteral nutritionnutrition

Without EN associates with Gut atrophy may be source for syst

emic endotoxin and sepsis Winsor AC. Gut

bacterial translocation to pancreati c tissue. RusselJC. AmJSurg1983.

Argument for enteral Argument for enteral nutritionnutritionEN pancreatic stimulation?

Pancreatic exocrine function reduces CCK stimulated secretion be abolished recovery of secretory function takes time feeding low in GI(distal to ligament of Trei

tz) does not stimulate pancreatic secretio n 1987 1Grant JP. JPEN . , Keith RG.Surg Gynecol Obstet980.

Comparison of the safety of early enteral Comparison of the safety of early enteral vs parenteral nutrition in mild acute vs parenteral nutrition in mild acute pancreatitis.pancreatitis. RESULTS:

no differences on admission in mean age, Ranson criteria, MOF, or APACHE III score

no differences between groups in serial pain scores, days to normalization of amylase, days to diet by mouth, serum albumin levels, or percent nosocomial infection. However, the mean cost of TPN/pt was x 4 than TEN (p < .001).

Mean serial Ranson criteria, APACHE III, and MOF decreased in the TEN , whereas increase in the TPN group.

Difference in the 3rd Ranson criteria (mean 6.3 days) for the TEN and TPN groups (0.5 vs 2.8, respectively) (p = .002).

Stress-induced hyperglycemia worse in the TPN group, (p < .02), whereas no significant change in the TEN group.

CONCLUSIONS: TEN is as safe and effective, may promote more rapid resolution of the toxicity and stress response.

TEN via jejunal feeding should be used preferentially in this disease setting.

McClave, S. A. et al. JPEN J Parenter Enteral Nutr. 1997.

Evidence based data

Compare with PN, EN attenuates the acute phase Compare with PN, EN attenuates the acute phase response and improves disease severity in acute response and improves disease severity in acute pancreatitispancreatitis

Windsor ACJ, et al. BMJ 1998; 42(3) 431-5

Enteral (16) Parenteral (18)

Age 63 63

Severity

Severe

Mild/ moderate

CT score 156 (117-222) 125 (49-168)

Enteral Parenteral

SIRS 11 pre

2 post

12 pre

10 post

Sepsis 0 3

MOF 0 5

Operativeintervention

1 cystogastrostomy 1 cystogastrostomy

2 necrosectomy

Mortality 0 3

Enteral nutrition is superior to parenteral Enteral nutrition is superior to parenteral nutrition in severe acute pancreatitis: Results of nutrition in severe acute pancreatitis: Results of a randomized prospective trial. a randomized prospective trial.

Kalfarentzos F, et al. Br J Surg 1997; 84: 1665-9

38 pts with acute severe pancreatitis were randomized into 2grs. ss ss - (n= 18) r ecei ved ENt hr ough a NJ wi t h a semi el

ement al di et ss ss 20(n = ) received PN through a central venous

catheter. Safety, Nbal ance,cost RESULTS

ss sss ssss sssssssss sssssss sssssss sssssss ss sss ssssss sss ssssssss .

ssssss sssssssssssss ss s sssss ssss sssss sssssssss (<0.05) ( < 0.01) parenteral nutrition.

ss sssssssssss sssssss ssss sssss ssssss ss ss sss3. CONCLUSIONThi s st udy suggest s t hat ear l y ent er al nut r i t i on shoul d

be used preferentially in patients with severe acute pancreatitis.

Randomized controlled trial of the effect of early Randomized controlled trial of the effect of early enteral nutrition on markers of the inflammatory enteral nutrition on markers of the inflammatory response in predicted severe acute pancreatitis response in predicted severe acute pancreatitis

Powell JJ, et al. Br J Surg 2000; 87: 1375-81

admission Day 2 Day4

Conventionaltreatment

admission Day4

Conventionaltreatment

Clinical trials of EN in Clinical trials of EN in severe pancreatitissevere pancreatitis

Reference Time offeeding

outcomeResults

Kalfarentzos F.N= 38 RCT

48 hr Morbid Decreased: Total Septic Hyperglycemia CostsNS: N balance

Nakad A.N= 20 Prosp

72 hr Morbid Technical complicationPancreatic complication

Winsor ACN= 34 RCT

48 hr SIRS Decreased SIRS CRP Endotoxin Antioxidant capacity

Enteral vs. parenteral Enteral vs. parenteral nutrition for acute pancreatitisnutrition for acute pancreatitis

Al Omran M, Groof A, Wilke D. Cochrane Review. In: The Cochrane Library, Issue 3, 2002

EN vs. PN

Death 0.56 (0.05 to 5.62)

LOHS -2.2 (-3.6 to -0.78)

Systemic infection 0.61 (0.29 to 1.28)

Local septic complication 0.56 (0.12 to 2.68)

Other local infection 0.16 (0.01 to 2.86)

Favor EN Favor PN1

Death 0.56 (0.05 to 5.62)

LOHS -2.2 (-3.6 to -0.78)

Systemic infection 0.61 (0.29 to 1.28)

Other local infection 0.16 (0.01 to 2.86)

Local septic complication 0.56 (0.12 to 2.68)

Enteral vs. parenteral nutrition for Enteral vs. parenteral nutrition for acute pancreatitisacute pancreatitis

Al Omran M, Groof A, Wilke D. Cochrane Review. In: The Cochrane Library, Issue 3, 2002

Safety of Early enteral Safety of Early enteral nutrition (EEN)nutrition (EEN) No significant difference in medical outcome PN vs EN

Days to normalize amylase, oral diet, LOS, ICU stay and mortality

Site of feeding lower in GI invoke fewer stimulation of pancreatic

secretion (stimulate inhibitory factors: PIP, PP, bile salt)

Decrease SIR markers Nutrients and pancreatic stimulation:

Fat > fat free LCT > MCT intact protein> peptides

Tolerance: variable, depends on severity, necrosis Gut integrity: largest immune organ

Mucosa, blood flow, GALT can be maintained by EN Local immune response

Acute pancreatitisAcute pancreatitisESPEN 2002ESPEN 2002 Nutrient requirements:

25 35 12energy B – kcal/kg BW/day;protein . 15– . g/kg BW/day;

CHO 3 6– g/kg BW/day corresponding to blood glsssss sssssssssssss

lipidsup t o 2 g/ kg BW/ day cor r espondi ng t o bl ood T G

SNS: start with TF by a jejunal feeding (when cal oric goal cannot be reached, give additional PN)

nutrition with a small content of an elemental (1 0–30 ml/h)

continuously perfused to the jejunum. When EN is not possible, give PN

ESPEN Guideline 2006 in acute ESPEN Guideline 2006 in acute pancreatitis: Indicationpancreatitis: Indication Mild acute:

nutrition support is unnecessary if resume normal diet after 5-7 d (B)

EN within 5-7 d, no +ve impact (A) TF if oral diet not possible >5 d (C)

Severe necrotizing: EN is indicated if possible (A) EN should be supplemented by PN if

needed (C) With complicated disease (fistula,

pseudocyst) TF can be performed successfully

ESPEN Guideline 2006: ESPEN Guideline 2006: applicationapplication

TF is possible in major of diseases, but may need PN supplement (A)

Oral feeding can be progressively progress once gastric outlet obstruction, complication under control (C)

Severe case: continuous EN in all who tolerate it (C)

ESPEN Guideline 2006 for ESPEN Guideline 2006 for routeroute

Jejunostomy feeding is preferred if gastric feeding cannot be tolerated (C)

ESPEN Guideline 2006 for ESPEN Guideline 2006 for formulaformula Peptide base formula can be used safely (A) Standard formula can be tried if tolerated (C)

Critical illness/Acute Critical illness/Acute pancreatitispancreatitis D11-20 patient has

improved lung function and gas exchange still on heavy sedation

EN has been started but retention remains a problem

What are the potential metabolic effect of sedative agents, and are there different between drug in this aspect?

Would you use prokinetic agent? If so, are there any risks associated with prokinetic?

Sedation: decrease REE propofol contain lipid and

give high calorie probably use prokinetic

with caution evidence of bowel

necrosis with using prokinetic

Critical illness/Acute Critical illness/Acute pancreatitispancreatitis D25 His clinical improved

but lost substantially his muscle mass and the FVC was markedly reduced

Would either of these findings have any consequences for the nutrition strategies?

Which factors can contribute to the deterioration of muscle function?

What is the clinical relevance of deteriorated muscle function in this setting:

proteincat abol i c, CIP/CIM -- difficultweaning>VAP, r epeat ed SI RS

Case StudyCase StudyCritical illness/Acute Critical illness/Acute pancreatitispancreatitis D33 Pt remain on MV

with unsuccessful weaning attempts. Infection was under controlled

which metabolic factors could contribute to difficult weaning/

Would you modify your feeding strategy during weaning?

Overfeeding -->+VCO2

hypermetabolic-->+VO2

look for overfeeding explore for muscle

wasting patient (clinically)--> put to respirator, respiratory rehabilitation

Nutrition in Ventilatory FailureNutrition in Ventilatory Failure

Ventilator dependency mismatch between ventilatory

demand and capacity to perform work of breathing

overfeeding worsening mismatch: increased VCO2

underfeeding may worsen mismatch:

loss of muscle

Respiratory Quotient (RQ)Respiratory Quotient (RQ)

RQ =VCO2

RQ: Respiratory QuotientVCO2: CO2 ProducedVO2: Oxygen Consumed

RQ• Glucose oxidation 6/6 = 1.0

1 glucose + 6 O2 = 6 CO2 + 6 H20

• Fat oxidation 16/23 = 0.71 palmitate + 23 O2 = 16 CO2 + 16 H2O

• Protein oxidation 4.1/5.1 = 0.81 amino acid + 5.1 O2 = 4.1 O2 + 2.8 H2O

• Lipogenesis > 1.0 – 8.0

Metabolic Response to Metabolic Response to OverfeedingOverfeeding

• Hyperglycemia• Hypertriglyceridemia• Hypercapnia• Fatty liver• Hypophosphatemia, hypomagnesemia,

hypokalemia

Barton RG. Nutr Clin Pract 1994;9:127-139

Advance Pulmonary Advance Pulmonary DiseaseDisease ASPEN 2002ASPEN 2002

Effect of Feeding

At 1.3 REE

Fixed CHO: fat

Talpers S.Chest 1992;102:551

Adult Renal Adult Renal failurefailure

ARFARF

General: Fluid:

Overload Electrolytes:

K, P retention

ARF: ARF: dialysis supportdialysis support

PD not commonly used IHD/ CRRT

HD 3/wk, 3-4 hr/session CRRT causes less hemodynamic

changes, grater clearance, tight control metabolic derangement

Hybrid dialysis: Slow, low efficiency dialysis (SLED): 6-12

hr/session, 6-7 d/wk

ARF: ARF: nutrition aspectsnutrition aspects

Metabolism: Effects of underlying disease/co morbidities Effects of treatment Effects of other organ dysfunction

GI function: motility, absorption, bleeding Energy: according to underlying causes CHO:

High insulin resistance: gluconeogenesis hyperglycemia

Fat: Impairment of lipolysis

ARF: ARF: nutrition aspectsnutrition aspects

Protein Increased protein catabolism: breakdown of

muscle protein and abnormal use of aa by muscle

Accelerated protein breakdown Gluconeogenesis Insulin resistance Acidosis Cytokines Counter regulatory hormone

Abnormal aa metabolism by ARF: Glutamine, arginine,histidine

Acute renal failureAcute renal failureNutritional requirement in ARFNutritional requirement in ARF

EnergyEnergy 20-30 kcal/kg/d

CHO 3-5 (max7) g/kg/d

Fat 0.8-1.2 g/kg/d

Protein (EAA/NEAA)Protein (EAA/NEAA)

Conservative 0.6-0.8 g/kg/d

Extracorporeal Rx 1-1.5 g/kg/d

CCRT, in hypercatabolism

Up to maximum 1.7g/kg/d

ESPEN Guideline on EN: Adult Renal Failure. Clin Nutr 2006

Liver DiseasesLiver Diseases

Liver diseasesLiver diseases

Prevalence uncommon in non

cirrhotic/compensated cirrhosis common in decompensated

cirrhosis, severity correlates with liver dysfunction

Characteristic of PEM are influenced by etiology

Pattern of Malnutrition in Chronic Pattern of Malnutrition in Chronic Liver DiseaseLiver Disease

Muscle wasting

Fat loss Reduced synthetic function

Alcohol Severe Mild Moderate

Viral Moderate Moderate Mild

Promary biliary cirrhosis

Severe Severe Mild

Primary sclerosing cholangitis

Moderate Mild Mild

Protein Energy Malnutrition in Protein Energy Malnutrition in Liver DiseasesLiver Diseases

Reduced intake anorexia satiety nausea and vomiting unpalatable (protein, salt restriction

Malabsorption bile salt def pancreatic def enteropathy

Altered metabolism

alcoholic toxicity to E and P metabolism protein break down and aa oxidation accelerate fat oxidation gluconeogenesis

Fasting diagnostic test GIB HE

Metabolic alteration in Metabolic alteration in cirrhosiscirrhosis Accelerated starvation: fat oxidation Protein imbalance

Skeletal muscle breakdown HE: 3rd most common of death (20%)

Subclinical HE 70%, not require specific Rx HE (NH3, mercaptans, FA, - aminobutyric,

altered aa, endogenous BZD) Overt HE

95% has precipitating factors 5% pp by protein

95% tolerate diets of proteins (upto 1.5g/kg/d)

Metabolic alteration in ALDMetabolic alteration in ALD

AlcoholAlcohol has deleterious effects no muscle protein inhibit meal stimulated hepatic protein

synthesis increase intestinal permeability provide empty calorie

7kcal/g Replace nutrient energy Induce cirrhosis

Objectives of nutritional RxObjectives of nutritional Rx

Prevent of slow catabolism to prevent or correct PCM

Attain optimal glucose control Sustain energy balance Correct or prevent vitamin/trace

element deficiencey Improve hepatic function/regeneration

Reversla of existing HE, and prevention Reduction of ascites and edema

Preparation for transplant

BackgroundBackground

SNS is less relevant if acute liver failure than chronic liver disease

GI functions: adequately in most allowing correction of nutritional deficits

Fat oxidation predominant profile of cirrhosis: should avoid fasting

Diet composition depends on type of liver diseases Mildly decompensate: high cal-prot, low

Na TF inmprove liver function and HE

ESPEN Guideline for SNS: ESPEN Guideline for SNS: alcoholic hepatitisalcoholic hepatitis

Recommend Energy: 35-40 kcal/kg/d Protein: 1.2-1.5 g/kg/d

ONS recommended Type of formula

Whole protein formula Consider more concentrated high energy

formulae in pt with ascites BCAA formula in HE arising during EN

ESPEN Guidelines on EN: Liver disease. Clin Nutr 2006

Recommend Energy: 35-40 kcal/kg/d Protein: 1.2-1.5 g/kg/d

Use supplement when cannot meet requirement (ONS or TF)

Type of formula Whole protein formula Consider more concentrated high energy

formulae in pt with ascites BCAA formula in HE arising during EN

ESPEN Guideline for SNS: ESPEN Guideline for SNS: CirrhosisCirrhosis

ESPEN Guidelines on EN: Liver disease. Clin Nutr 2006

OutcomeOutcome

Improves nutritional status Improve liver functionProlonged survival

Nutrition recommendationNutrition recommendation

Cachexia 120% of estimated EE, increased cal if malabsorption or malnutritionamall, frequent meals

HE Maximize medical Rx, identify and Rx PP factorRestrict protein only if protein sensitive (0.5-0.7 g/kg/d) and increase to tolerance up to 1.5g/kg/dConsider nutritional supplement BCAA if intolerance to std protein

Ascites/Edema

Na restriction

Hyponatremia

Restrict water 1-1.5l/d

Hyperglycemia

CHO control meal/ insulin

Hypoglycemia

Frequent meals or snack

Steatorrhea Restrict fat, try MCT, supplement fat soluble vitamin

Osteopenia Maintain appropriate wt, balance dietProvide enough protein to maintain muscle massCa 1.5g/d, enough vitamin DAvoid alcohol

Nutrition in Nutrition in CancerCancer

Weight Loss in Cancer PatientsWeight Loss in Cancer Patients

80% of cancer pt lose wt Wt loss is prognostic significant

Kondrup AJCN 2002, De Wys et al. Am J Med 1980, Andreyev et al. Eur J Cancer 1998

CancerCancer Cachexia: MythCachexia: Myth

Anorexia-cachexia syndrome is due to the host lack of appetite and or starvation

Anorexia-cachexia happens because of tumor consumes the host nutrients

Cancer CachexiaCancer Cachexia

Syndrome of combined physiologic, metabolic and psychological factors

Manifestations: anorexia progressive involuntary wt loss, wasting,

tissue depletion Fatigue, poor performance Anemia

More advance disease: higher risk of wt loss

Cancer Cachexia Anorexia Cancer Cachexia Anorexia Syndrome (CACS)Syndrome (CACS)

Cachexia

Abdominal pain

Depression

Constipation

Radio/chemotherapy, surgery side effects

Taste alteration

Malabsorption

Intestinal obstruction

Derangement of Metabolism

Lipolysis

TNF-, IFN- increase of leptin

LIF, TGF-β

Increased

• Lipolysis/lipid metabolism

• Proteolysis

• REE

Decreased

• Lipogenesis

• LPL activity

• Protein synthesis

Does nutritional status influence Does nutritional status influence the clinical course and the the clinical course and the prognosis?prognosis?Reduce QOLLower activity levelIncrease treatment related

adverse reactionsReduce tumor response to

treatmentReduce survival

Does cancer influence energy Does cancer influence energy expenditure?expenditure?

Cancer itself does not have consistent effect on REE Increased ~ ¼ had 10% higher

than predicted Unchanged Decreased ~ ¼ had 10% lower

than predicted

Carbohydrate MetabolismCarbohydrate Metabolism

1925 Cori & Cori demonstrate decreased glucose level

High anaerobic glycolysis Glucose to lactate

Increased lactate level Lactate

Oxidized 15 % Regenerate to glucose 85%

CHO MetabolismCHO Metabolism

Gluconeogenesis: increased Lactate, glycerol, alanine Cannot be suppressed by glucose

supplement Decreased glucose tolerance: insulin

resistance

Lipid MetabolismLipid Metabolism

Depletion of fat store The proportion of wt loss: fat loss Associated with

hypertriglyceridemia Increased lipolysis, FFA and glycerol

turnover Normal or increased lipid oxidation Decreased lipid clearance

Decreased lipoprotein lipase (LPL)

Protein MetabolismProtein Metabolism

Increased protein metabolism Whole body protein turnover:

unchanged Muscle tissue: largest pool

Muscle protein loss, muscle wasting Decreased protein synthesis

Energy requirementEnergy requirement

If REE cannot be measured, use rule of thumb

Ambulant pt: 30-35 kcal/kg/d Bedridden pt: 20-25 kcal/kg/d

Oncological Rx may modulate EE

Do cancer patients require a Do cancer patients require a distinct nutrient composition?distinct nutrient composition?

Standard formula are recommended for EN of cancer pt Protein 1 g/kg/d (minimum) 1.2-2 g/kg/d Supplement with electrolyte, vitamins

and trace element acording to RDA

What are specific nutritional What are specific nutritional goals in cancer patients?goals in cancer patients?

Prevent and treating undernutrition

Enhancing anti-tumor treatment effects

Reducing adverse effects of anti-tumor Rx

Improve QOL

When should EN be When should EN be started?started? If undernutrition already exists If it is anticipated that Pt will be unable

to eat for > 7 d If an inadequate food intake (<60%) to

eat for > 10 d

Can EN maintain or improve Can EN maintain or improve nutritional status in cancer nutritional status in cancer patients?patients?Yes : In wt lost patients from

insufficient intake: Gain more wt, lost less wt1

improve or maintain nutritional status2 maintain QOL

1. Systematic review of ONS, counceling Baldwin et al, 20042. Cancer cachexia and GI cancer Bozzetti F1989 and Lindh A 1986.3. GI and H& neck cancer. Isenring EA, 2004

Can EN maintain or improve Can EN maintain or improve nutritional status in cancer nutritional status in cancer patients?patients?In the presence of inflammation

Extremely difficult to achieve anabolism

Without effective antitumor Rx, it is impossible to reverse this process

At least to maintain wt or minimize wt loss

Additional intervention pharmacological effort recommended to modulate inflammatory response

Can metabolic modulators Can metabolic modulators increase nutritional intakeincrease nutritional intake Steroids (short term)

Improve appetite Nausea Pain

Progesterone Improve appetite Wt gain QOL

ω-3 fatty acid: less active pro-inflammatory midiators Improve appetite and body weight

Does supplementation with Does supplementation with ωω-3 fatty -3 fatty acid have beneficial effect in cancer acid have beneficial effect in cancer patients?patients?

RCT : contradictory/controversial Evidence level C RCT :

improve survival/Non significant effect on wt Did not improve wt or appetite

Non RCT: improve survival, side effect of CTX Recent RCT: high dose EPA: wt stabilization,

wt gain Unlikely to prolong survival in advance

cancer The result of further trials are awaited

Special situationSpecial situation

Perioperative ENRadiotherapyChemotherapyTransplantationAdvance stage/ incurable

Is there indication for EN during Is there indication for EN during radiotherapy (XRT)or combined radiotherapy (XRT)or combined radiotherapy(cXRT)?radiotherapy(cXRT)?

Yes, use intensive counceling and ONS to increase intake (A) to prevent Rx associated wt loss To prevent interuption of XRT

in GI, head and neck area If obstructive H&N or esophageal CA interferes

with swallowing: tube feeding is preferred TF is preferred if local mucositis is expected (c) Routine EN is not indicated during XRT of other

body regions (c)

No Routine EN during CTX has no

effect on tumor response nor CTX associated unwanted effects (b)

Is there indication for EN Is there indication for EN during chemotherapy?during chemotherapy?

ConclusionConclusion

Complete improvement of nutritional state is not attained in short time

Cancer Rx should not be postponed until nutritional rehabilitation achieved

Nutritional Rx should be incorporated in to the overall Rx as early as possible

Effort to improve nutritional and metabolic status may decrease morbidity and mortality in pts who need surgery, XRx, CRx

Chronic renal failure:Chronic renal failure: ScopeScope

Protein energy malnutrition in CKD Effect of nutritional Rx on progression of

CKD Nutritional therapy: predialysis

avoid uremic toxicity avoid malnutrition

Prevalence of PEMPrevalence of PEM

PEM common in advance stage of CKD 40% sss. 199561386 - 10 70 of MHD. .1993; 43:39.

- 1851% CAPD 1993 4Bergstrom J. Kid Int ;

339 or 40% and 8% severe. .1991; 17 46:-2 4 7 1 .

s ss-ss ssssss<510/ Characteristics of PEM in CKD

Relationship Between Malnutrition Relationship Between Malnutrition and Morbidity and Mortalityand Morbidity and Mortality

PEM in CKD is related to poor clinical outsss s

body protein reserve < 80% had 1 year mortality rate > normal ~ 41. x

Low albumin: stros gest predictor of deats ssss albumin 3.51- 4.0 = 2.21 albumin < 2.5 = 7.45

300Prealbumin < mg /l associated wit h higher mortality

““Malnutrition Syndrome” Malnutrition Syndrome” in ESRDin ESRD ESRD pts develop a state similar to

chronic malnutrition Not appear to be corrected simply by

adequate dialysis. Malnutrition and uremia have

synergistic effect on lymphocyte function and cytokine response

Effect of PEM on Renal Effect of PEM on Renal FunctionFunction

Impaired ability to eliminate acid and solute load

Reduced renal plasma flow

Reduced GFR and urine concentrating ability

Klahr S. Effect of malnutrition and of changes in protein intake on renal function.in Nutritional management of renal disease. 1997:229.

Mechanism Responsible With PEM Mechanism Responsible With PEM in Chronic Kidney Disease: in Chronic Kidney Disease: Multifactorial Multifactorial

Poor intake abnormal lipid and CHO metabolism amino acid imbalance abnormal hormonal response loss of nutrients in dialysis (4-10g

aa/HD, 5-15g prot/d in PD) uremic toxicity and metabolism

Metabolic Metabolic AAcidosiscidosis

Increased cortisol, BCKA dehydrogenase activity

proteolysis protein breakdown, aa oxidation negative N balance decreased albumin synthesis impaired insulin activity and glu utilization correction of MA improves N and nutritional

status

Hyperparathyroidism Hyperparathyroidism

Impaired protein metabolism

Insulin resistance impaired protein metabolism

Proposed Features of Malnutrition Proposed Features of Malnutrition TypesTypes Stenvinkel P, et al. Nephrol Dial Transplant 2000;15:953-Stenvinkel P, et al. Nephrol Dial Transplant 2000;15:953-6060

Type 1 Type 2

Serum albumin Normal/low low

Co-morbidity uncommon Common

Presence of inflammation

No Yes

Food intake low Low/normal

REE Normal Elevated

Oxidative stress Increased Markedly increased

Protein catabolism decreased Increased

Reversed by dialysis or nutrition support

yes no

Effects of Nutritional Therapy on Effects of Nutritional Therapy on the Progression of Renal the Progression of Renal InsufficiencyInsufficiency

Non diabeticDiabetic

Effects Effects on on Progresion of Renal Progresion of RenalInsufInsuffficiencyiciency: Non-Diabetic: Non-Diabetic

*Ziller K N Engl J Med 1991; 324:78. Ciavarella et al 1987, Walker et al 1989, Dullaarr et al 1991

no definitively established whether

protein restriction in CRF slow the

progression of RF

ine in

P = 0.004P = 0.009

P = 0.3

Normal proteinLPD

Klahr S. N Engl J Med 1994; 330: 877.

Modification of Diet in Renal Disease Study:LPD vs. normal protein

Modification of Diet in Renal Disease StudyLPD vs. normal protein

LPDVLPD

r death

f pati

RR 0.93[.65-1.33]

P value=0.6

Modification of Diet in Renal Modification of Diet in Renal Disease StudyDisease Study

Pedrini MT. Ann Int Med 1996; 124: 627.

The Effect of Dietary Protein Restriction on The Effect of Dietary Protein Restriction on the Progression of Diabetic Renal Disease: the Progression of Diabetic Renal Disease: LPD vs. normal proteinLPD vs. normal protein

Non DM

Pedrini MT. Ann Int Med 1996; 124: 627.

The Effect of Dietary Protein Restriction on The Effect of Dietary Protein Restriction on the Progression of Non Diabetic Renal the Progression of Non Diabetic Renal Disease: Disease: LPD vs. normal proteinLPD vs. normal protein

Management of Management of MalnutritionMalnutrition Early Adequate dialysis enteral supplement intraperitoneal nutrition management of inflammation: elevate

CRP Anabolic factors

Adequate dialysis Adequate rx of MA Anemia treatment Prevent infection Adequate protein/energy intake Avoid medication interfering food intake, GI

function Oral supplement / EN If all fail, no improvement in status and no RRF, pt

should be transferred to HD

Strategies for Treating Malnutrition in Strategies for Treating Malnutrition in CAPDCAPD

Criteria for MalnutritionCriteria for Malnutrition

Albumin < 4.0 g/dL decrease in EDW nPCR< 0.8g/kg/day low Cr, BUN without

RRF Decreased

anthropometrics

(IGF-1 < 300 g/L) low predialysis

serum K and phos (prealbumin<30

mg/dL)Tchol < 150 md/dLTFN < 150 mg/dL

(Wolfson, 1997)

Nutritional requirement in CRF Nutritional requirement in CRF (non dialysis)(non dialysis)

ESPEN NKF

GFR 25-70 ml/min 0.55-0.6 (2/3 HBV)

GFR <25 ml/min 0.55-0.6 (2/3 HBV)Or 0.28 +EAA or EAA+KA

0.6 Or 0.75 (intolerance or inadequate energy

Mineral requirementMineral requirement

P 600-1000 mg

K 1500-2000 mg

Na 1.8-2.5 g

Nutritional requirement in CRF Nutritional requirement in CRF (non dialysis)(non dialysis)

ESPEN NKF

Protein intakeProtein intakeHDPD

1.2-1.4 (>1/2 HBV)1.2-1.5 (>1/2 HBV)

1.2 (>1/2 HBV)1.2-1.3 (>1/2 HBV)

EnergyHDPD

35 <60 35<60 30

Mineral requirementMineral requirement

P 800-1000 mg

K 200-2500 mg

Na 1.8-2.5 g

FormulaFormula

Standard Nephro formula: high concentration, low

in electrolytes

Intensive careIntensive care

IndicationIndication

All pt who are not expected to be on a full oral diet within 3 d should receive EN

Hemodynamically stable critically ill patients who have a functioning GI tract should be fed early (<24hr) using an appropriate amount

ApplicationApplication

No general amount can be recommended as EN, adjusted to progression/course of diseases and GI tolerance

Exogenous energy Acute and initial phase of critical illness

20-25 kcal/kg/d During anabolic recovery phase

25-30 kcal/kg/d Severe undernutrition

25-30 kcal/kg/d Consider prokinetics in pt with intolerance

ESPEN Guideline on EN: Intensive Care. Clin Nutr 2006

RouteRoute

Use EN in pt who can be fed No significant diff between jejunal feed

and gastric feed Use supplemental PN in pt who cannot

be fed sufficiently

FormulaFormula

Whole protein formula IMN

Arginine Gluctamine Ribonucleic acid N-3 fatty acid

In elective upper GI pt Mild sepsis (APACHEII <15) Trauma ARDS: formula containing n-3 FA

ESPEN Guideline on EN: Intensive Care. Clin Nutr 2006

Formula Formula

No recommendation of IMN in Burned Severe sepsis (APACHEII > 15) ICU pt cannot tolerate > 700 ml receive

IMN Glutamine should be added to standard

EN in (A) Burned pt Trauma pt

Pranithi Hongsprabhas MD Division of Clinical Nutrition, Department of Medicine, Faculty of Medicine...

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