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
KKUKKU
Update in Clinical Update in Clinical NutritionNutrition
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Case Case discussion in discussion in
nutritionnutrition
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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
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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?
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Fluid Rx considerationFluid Rx considerationCritical illness/Acute pancreatitisCritical illness/Acute pancreatitis
maintenance + ECF resuscitation
considersequestration --> hypovolemiaprerenal vs acute renal failure impending lung injury / ARDS
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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
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Case StudyCase StudyCritical illness/Acute pancreatitisCritical illness/Acute pancreatitis
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
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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
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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
Case StudyCase StudyCritical illness/Acute pancreatitisCritical illness/Acute pancreatitis
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Case StudyCase StudyCritical illness/Acute pancreatitisCritical illness/Acute pancreatitis
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
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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
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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
Case StudyCase StudyCritical illness/Acute pancreatitisCritical illness/Acute pancreatitis
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?
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Nitrogen and energy balance response to Nitrogen and energy balance response to nutritionnutrition
Energy intake -->
N in
take
---
>
N b
ala
nce
Energy balance
0
0
Depleted
Energy balance
0
0
MOFS
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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
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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
1998
bacterial translocation to pancreati c tissue. RusselJC. AmJSurg1983.
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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.
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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
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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
6
10
7
11
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
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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.
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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
2000
2200
2400
2600
admission Day 2 Day4
EN
Conventionaltreatment
TN
F
0
100
200
300
400
500
600
700
800
admission Day4
EN
Conventionaltreatment
IL 6
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Clinical trials of EN in Clinical trials of EN in severe pancreatitissevere pancreatitis
Reference Time offeeding
1o
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
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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)
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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
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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
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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
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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
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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)
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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)
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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
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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:
No
proteincat abol i c, CIP/CIM -- difficultweaning>VAP, r epeat ed SI RS
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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
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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
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Respiratory Quotient (RQ)Respiratory Quotient (RQ)
RQ =VCO2
VO2
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
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Metabolic Response to Metabolic Response to OverfeedingOverfeeding
• Hyperglycemia• Hypertriglyceridemia• Hypercapnia• Fatty liver• Hypophosphatemia, hypomagnesemia,
hypokalemia
Barton RG. Nutr Clin Pract 1994;9:127-139
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Advance Pulmonary Advance Pulmonary DiseaseDisease ASPEN 2002ASPEN 2002
Effect of Feeding
At 1.3 REE
Fixed CHO: fat
Talpers S.Chest 1992;102:551
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Adult Renal Adult Renal failurefailure
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ARFARF
General: Fluid:
Overload Electrolytes:
K, P retention
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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
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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
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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
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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
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Liver DiseasesLiver Diseases
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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
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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
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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
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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)
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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
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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
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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
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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
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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
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OutcomeOutcome
Improves nutritional status Improve liver functionProlonged survival
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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
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Nutrition in Nutrition in CancerCancer
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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
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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
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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
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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
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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
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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
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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%
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CHO MetabolismCHO Metabolism
Gluconeogenesis: increased Lactate, glycerol, alanine Cannot be suppressed by glucose
supplement Decreased glucose tolerance: insulin
resistance
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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)
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Protein MetabolismProtein Metabolism
Increased protein metabolism Whole body protein turnover:
unchanged Muscle tissue: largest pool
Muscle protein loss, muscle wasting Decreased protein synthesis
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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
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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
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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
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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
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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
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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
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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
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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
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Special situationSpecial situation
Perioperative ENRadiotherapyChemotherapyTransplantationAdvance stage/ incurable
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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)
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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?
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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
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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
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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
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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
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““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
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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.
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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
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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
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Hyperparathyroidism Hyperparathyroidism
Impaired protein metabolism
Insulin resistance impaired protein metabolism
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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
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Effects of Nutritional Therapy on Effects of Nutritional Therapy on the Progression of Renal the Progression of Renal InsufficiencyInsufficiency
Non diabeticDiabetic
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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
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Decl
ine in
G
FR(m
l/m
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
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Klahr S. N Engl J Med 1994; 330: 877.
Modification of Diet in Renal Disease StudyLPD vs. normal protein
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LPDVLPD
ESR
D o
r death
% o
f pati
ents
RR 0.93[.65-1.33]
P value=0.6
Klahr S. N Engl J Med 1994; 330: 877.
Modification of Diet in Renal Modification of Diet in Renal Disease StudyDisease Study
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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 Diabetic Renal Disease: the Progression of Diabetic Renal Disease: LPD vs. normal proteinLPD vs. normal protein
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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
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Management of Management of MalnutritionMalnutrition Early Adequate dialysis enteral supplement intraperitoneal nutrition management of inflammation: elevate
CRP Anabolic factors
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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
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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)
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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
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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
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FormulaFormula
Standard Nephro formula: high concentration, low
in electrolytes
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Intensive careIntensive care
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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
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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
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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
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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
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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