NUTRITION - University of British Columbiagsresidency.surgery.med.ubc.ca/files/2012/12/Nutrition_Yahya... · Enterla nutrition is more physiologic, less expensive and associated with

NUTRITION

Dr. Yahya Almarhabi. MD Trauma surgery

Question-1

  A patient recovering from sepsis and acute lung injury (admission weight 75 kg) is difficult to wean from the ventilator. Minute ventilation is 15 L/min. RQ is 1.15. He is receiving 3,000 kcals/day (80%from CHO and 20% from lipid) as TPN.

The most appropriate nutritional modification is:

1-increase the proportion of fat to 50% of calories

2-decrease calories to 2250 kcal/day

3-increase calories to 4000 kcal/day

4-substitute protein calories for part of carbohydrate calories

Malnutrition in Hospitalized Patients

•  Malnutrition –  A disorder in body composition reflected in decreased body

mass, decreased organ mass resulting in compromised organ function

–  Protein/ caloric malnutrition –  Specific nutrition deficiency –  Altered metabolism resulting from a disease process

•  Incidence: –  25-50% on admission –  25-30% during hospital stay

•  Morbidity : 25% •  Mortality : 5%

Starvation Vs Stress Hypermetabolism

Starvation

•  A clinical situation that develops whenever nutrient supply is inadequate to meet nutrient demand

•  Characterized by a specific metabolic adaptive response aimed at preserving the lean body mass

•  The metabolic response is characterized by decreased energy expenditure, utilization of alternative fuel sources and reduced protein wasting

Metabolic Adaption to Starvation

•  Initial fuel sources: •  Glycogen for 1st 24h •  Glucose from amino acids via gluconeogenesis for 3-4

days •  Fatty acids, ketones and glycerol become primary fuel

sources in all but obligate glucose using tissues (beyond 5-7 days of starvation)

•  R/Q- 0.6 to 0.7 •  Decreased net protein catabolism and ureagenesis

in the fully adapted starved state

Stress Hypermatabolism (SIRS)

•  A generalized response whereby energy and substrate are mobilized to support inflammation, immune function and tissue repair

•  Occurs at the expense of the lean body mass •  Occurs in response to a variety of stimuli such as

sepsis, trauma, burns ,pancreatitis and BMT •  Usually associated with some degree of perfusion

deficit (shock) and resultant microcirculation injury

Stress Hypermetabolism-SIRS

  Clinical characteristics:   Increased oxygen consumption   Increased cardiac index and decreased SVR   Increased minute ventilation  hyperglycemia, elevated lactate and increased urinary

nitrogen excretion  R/Q- 0.08 to 0.85

Stress Hypermetabolism

•  Carbohydrate Metabolism: –  Hyperglycemia “insulin resistance”

•  Decreased insulin mediated glucose uptake •  Increased gluconeogensis that is poorly suppressed by

glucose infusion

–  Increased glucose oxidation •  Increased non-insulin mediated glucose uptake •  Maximum rate of gluocse oxidation- 5mg/kg/min

–  Increased Cori Cycle activity with conversion of lactate to glucose


  Fat Metabolism:   Increased oxidation of all chain lengths  Decreased essential fatty acids in the plasma, in part

due to hyperinsulinemia, resulting in suppression of fat mobilization

 Ketonemia usually absent  With progression to multiple organ failure, triglyceride

clearance decreases


  Protein Metabolism   Increased total protein synthesis and catabolism with a

net increase in protein catabolism   Increased muscle release and decreased uptake of

amino acids  Rapid decrease in the lean body mass  Decreased albumin and transferrin synthesis   Increased ureagenesis and urinary nitrogen losses


  What becomes of the amino acids?  Extrahepatic oxidation ( branched chains:Valine;

Leucine; Isoleucine)  Redistribution to viscera, wounds and WBC  Gluconeogenic substrate (Alanine)  Hepatic synthesis of acute phase reactant proteins

  Skeletal muscle becomes the substrate for processes of inflammation and tissue repair


Mediator Effect

Insulin Glucose uptake and metabolism, protein synthesis, lipogenesis

Cortisol and Glucagon Gluconeogenesis ,protein catabolism

Catecholamines Glycogenolysis, gluconeogenesis, lipolysis

Tumor Necrosis Factor Stress protein catabolism, increased energey expenditure, inhibition of lipoprotein lipase

Interleukin-1 Stimulate ACTH; increased cortisol and glucagon ; gluconeogenesis, protein catabolism

Interleukin-2 Lipolysis

Platelet Activating Factor Gluconeogenesis

Long CL et al. JPEN 1979.

Malnutrition

Characteristic Starvation Hypermetabolism

Energy expenditure Decreased Increased

Respiratory quotient Low (0.7) High (0.85)

Mediator activation + +++

Primary fuels Fat Mixed

Gluconeogenesis + +++

Proteolysis + +++

Protein synthesis + ++

Ureagenesis?UUN + +++

Ketone formation ++++ +

Response to feeding +++ +

Recommendations for Nutrition Support

Nutrition Support in ICU

  Who?  Malnourished patients  Patients in whom malnutrition is likely to occur  Patients who have not eaten for 7 days

  When?  Start nutrition support as soon as need is recognized

and patient is hemodynamically stable, but always within 7 days

 Probably no benefit in previously healthy patients expected to eat within 7 days

EN alone often does not meet caloric goals for Crit. Care pts ? When start TPN? •  ESPEN: within 2 days of ICU admission •  ASPEN: after 7 days of admission RCT TPN=>Early ( within 48 h) Vs Late (day 8) to achieve caloric goal

HR=1.06; 95% confidence interval [CI], 1.00 to 1.13;

P = 0.04

HR=1.06; 95% confidence interval [CI], 1.00 to 1.13;

P = 0.04

Delayed PN associated with..

  More likely to be “discharged alive earlier” from ICU & from hospital ( HR 1.06 for each)

  Reduced ICU infection & cholestasis   Reduced MV

Nutrition Support in ICU

  What can we do and not do?  Can minimize starvation effects  Can prevent specific nutrient deficiencies  May modulate, to some extent, the metabolic processes

of the disease  Cannot abolish the ongoing protein breakdown and

wasting of the lean body mass associated with catabolic illness

Energy and Substrate Requirements

  Calories:  Estimated from Harris-Benedict equations

 BEE X stress factor of 1.2-2.0

 Measured using expired gas analysis  BEE or REE - no stress factor required

  Excess calories  Hyperglycemia, excess CO2 production, lipogenesis

and hepatic steatosis

  Recommend of 25-30 kcal/kg/day


  Glucose:  Maximum rate of oxidation-5mg/kg/min (7.2 gm/kg/

day)  Stress gluconeogenesis (2-4 mg/kg/min) is poorly

suppressed by the provision of calories or glucose  Excess glucose –hyperglycemia, excess CO2 production,

hyperinsulinemia, suppression of lipolysis and hepatic steatosis

 Recommend 60-70% of calories, or 20 kcal/kg/day or 5 gm/kg/day as glucose


  Fat:  Essential fatty acid deficiency

 Starvation – develops in 6-8 weeks  Stress – develops as early as 10 days

 Fat calories minimize CO2 production  Excess fat – hyperlipemia, impaired immune function

and hypoxemia  Recommend

 Stravation – 2 to 5% of calories as fat  Stress – 15 to 40 % of calories as fat   Limit fat to 1 gm/kg/day


  Protein  Protein catabolism is not suppressed by the provision of

adequate calories, protein or amino acids  Attainment of nitrogen balance requires the support of

stress protein synthesis (inflammation, immune function and tissue repair)

 Recommend – 1.2 to 2.0 gm/kg/day (nitrogen balance)  Non-protein calories/ Nitrogen ration

 Starvation 150/1  Hypermetabolism 80/1


  Electrolytes, Vitamins and Trace Elements   Intracellular ions (K,PO4 and Mg) are required for the

attainment of nitrogen balance  Vitamin and trace element requirement in critical illness

are unknown  Recommend electrolytes to achieve normal levels

considering excess losses or impaired excretion and with special attention to intracellular ions

 Provide RDA for vitamins and trace elements


Nutrition General recommendation

Total calories 25-30 kcal/kg/day

Glucose 5 gm/kg/day 20 kcal/kg/day 60-70% of calories

Fat 15-40% of calories Less than 1 gm/kg/day

Amino acids or protein 1.2-2.0 gm/kg/day

Trace elements and vitamins RDA*

Electrolytes Maintain normal levels

Route of Administration Enteral vs Paentral Nutrition

Route of Administration Enteral vs Paentral Nutrition

Gramlich L et al. Nutrition 20 : 843-48, 2004

Meta-analysis of 13 RCT Enteral Vs Parenteral nutrition

Infection

RR=0.64, P=0.004


Mortality

RR=1.08, P= 0.7


EN vs PN

  No differences in ventilator days, LOS   More hyperglycemia with PN   EN cheaper


Enteral Vs Parentral Nutrition

  Summery   Indication for TPN are few (short bowel, bowel

obstruction, proximal high output enterocutaneous fistula)

 Enterla nutrition is more physiologic, less expensive and associated with fewer metabolic derangements and complications than TPN

 Enteral nutrition may reduce infectious complications compared to parentral nutrition

 Use enterla nutrition whenever possible

Question-1

  A patient recovering from sepsis and acute lung injury (admission weight 75 kg) is difficult to wean from the ventilator. Minute ventilation is 15 L/min. RQ is 1.15. He is receiving 3,000 kcals/day (80%from CHO and 20% from lipid) as TPN.

The most appropriate nutritional modification is:

1-increase the proportion of fat to 50% of calories

2-decrease calories to 2250 kcal/day

3-increase calories to 4000 kcal/day

4-substitute protein calories for part of carbohydrate calories

Types of Enteral Formulas

Enteral Nutrition Formulas

  Intact Formulas   Contain intact protein as

caseinate or soy isolate (15-20% of kcals).

  Lactose and gluten free

  Carbohydrate as oligosaccharides (46-60% of kcals)

  Lipid as long chain fats (20-35% of kcals)

  Usually isosmotic   Low residue or with fat

  Hydrlyzed Formulas   Provide protein as peptides or

amino acids

  Carbohydrate as mono or disaccharides

  Low in fat (medium Triglyceride)   For feeding intolerance

  Elemental Formulas   Provide protein as crystalline

amino acids

  Carbohydrate as mono or disaccharides

  No fat

Classified according to protein form:


  Standard formulas:   For starved patients who can’t

eat   150/100

  High protein formulas:   Contain 45-60 g protein/

1,000 kcal.

  For hypermetabolic patients

  Caloric dense formulas:   Contain 2 kcal/ml   For fluid restricted patients   Most are relatively low in

protein

  Organ specific formulas:   For specific organ failures

  Immunity enhancing formulas   Designed to alter immune

function and reduce inflammatory response

Classified according to Clinical Use


  Pumonar failure:   For acute respiratory failure   Contain 50 % fat for lower CO2 production   Avoiding overfeeding is more important

  Hepatic Failure:   Contain high branched chain and low aromatic amino acid concentrations   Will correct amino acid profile but probably not encephalopathy.

  Renal failure   Contain low protein,K,and PO4   For patients with renal failure and not being dialyzed   Protein too low for stressed patients being dialyzed

  Non of proven benefit

Organ specific formulas:


  Immunity enhancing Enteral formulas:   Arginine

  Nonessential,   NO precursor, nonspecific immune stimulant, enhanced wound

healing   Glutamine

  Conditionally essential*   Fuel for entrocytes, lymphocytes, macrophages, improve gut

barrier function   Omega-3 polyunsaturated fatty acids:

  Metabolized via cycloxygenase and lipxygenase to trienoic prostaglandins and petaenoic leukotrienes which are less “inflammatory” than Omega-6 products


  Meta-analysis of 22 RCTs (n=2419)   Comparing nutrition supplemented with some combination

of arginine,glutamine,omega-3 fatty acids and nucleotides to standard enteral formula in terms of mortality and infectious complications

Heyland DK et al . JAMA 286: 944-53,2001

Mortality

RR=1.10; 95% CI= 0.93-1.31 Heterogeneity P = .54

Infectious Complications

RR=0.66; 95% CI=0.54-0.80 Heterogeneity ,P<.001

Length of Hospital Stay

ES= −0.63; 95 % CI= −0.94 to −0.32 Heterogeneity (P<.001)


  RCT (n=597 adult ICU patients)   Immunonutrition Vs isocaloric control formulas

 No differences in mortality, infectious complications , ventilator days or LOS

Keift H et al. intesive Care Med 2005, 31:501-3


  RCT, multi-institutional trial   Comparing a high fat, low carbohydrate diet

containg eicosapentaenoic acid, gamma-linolenic acid and antioxidants Vs isonitrogenous, isocaloric enetral formulas

  N=146 patients wit ARDS  Significantly improve PaO2/FiO2 with lower FiO2,

PEEP and Minute Ventilation  Study diet associated with significantly fewer vent.

Days , ICU days and new organ failure

Gatek,JE et al . Crit Care Med 1999,27:1409-20


  RCT   Multi-center trial   EPA+GAL + Antioxidants Vs

isocaloric,isonitrogenous control diet   N= 163 patients with severe sepsis and septic shock

 Significant decreases in mortality, vent. Days, ICU days and new organ failures with study formulas

Pontes-Arruda et al. Critical Care 34: 2325-33,2006

Pontes-Arruda et al. Critical Care 2011, 15:R144

RCT 115 Pts EPA/GLA Vs isocaloric, isonitrogenous

P=0.0217

Primary outcome

Pontes-Arruda et al. Critical Care 2011, 15:R144

Enteral Nutrition Formulas Secondary outcome

Glutamine Supplementation

  Meta-analysis of 14 RCT   Comparing Glutamine supplementation to standard

care in surgical and critically ill patients with respect to outcomes

Novak F et al, Crit Care Med 2002, 30 2022-9

Mortality

surgical pts, RR, 0.99; 95% CI, 0.27–3.58 critically ill patients, RR, 0.77; 95% CI, 0.57–1.03


Infectious Complication

Surgical pts, RR=0.36; 95% CI, 0.14 – 0.92 Critically ill pts, RR=0.86; 95% CI, 0.68 – 1.08


LOS

surgical pts= -3.54 days; 95% CI, -5.3 to -1.76 critically ill pts = 0.9 days; 95% CI, -4.9 to 6.8

P-homogen =0.0001


Glutamine Supplementation

  Glutamine use associated with decreased infectious complications (RR=0.81, 95%CI 0.64- 1.00)

  Treatment benefits more pronounced with parenteral nutrition, high-doses glutamine and in surgical patients


Summary for Enteral Formulas

  Immunity Enhancing Enteral Formulas:  More than 300 abstracts/articles and 25 RCTs, many in

elective surgery and cancer patients, not critically ill patients

  Immunity enhancing enteral formulas may reduce infectious morbidity but have not been shown to improve mortality in critically ill patients

  Glutamines Supplementation  May be beneficial, particularly in parnterally fed

patients

Summary for Enteral Formulas

  Inflammation Modulating Enteral Formula:  Appear to improve oxygenation and reduce mortality,

ventilator days, ICU LOS and organ failures in patients with sepsis or ARDS

Nutritional Assessment and Monitoring

Assessment and Monitoring

  History and physical

  Anthropometric measurements (little utility in ICU)

  Visceral proteins:   albumin, transferrin, retinol binding protein, transthyretin (many non-

nutritional influences)

  Glucose- every 6 hrs initially and as needed

  Electrolytes- daily and as needed (particularly K,Mg & PO4)

  Coagulation parameters-weekly

  Nitrogen balance- weekly and as needed

  Indirect calorimetry- weekly and as needed

Nitrogen balance

  Nitrogen balance= Nitrogen in – Nitrogen out   Nitrogen in= protein in (gm/24hr) / 6.25 (gm

protein/gm N2)   Nitrogen out = UUN (mg/dl) x dl of urine/24 hr x

2.1   (multiply UUN x 1.2 to account for non-measured,

non-urea nitrogen, e.g uric acid, creatinine, creatine)

Indirect Calorimetry- what does it mean?

  Determines oxidative heat production based on oxygen consumption and carbon dioxide production.

  Energy expenditure calculated by modified Wier equation

Indirect Calorimetry

RQ Fuel Source Condition

0.60-0.7 Fat Starvation

0.80-0.95 Mixed Ideal

1.0 Carbohydrate Excess carbohydrate

>1.0 Fat synthesis Overfeeding

Complications of Nutrition Support and Their Prevention

Complications & Prevention

  Complications of TPN:  Complications related to central line placement-

pneumothorax, vascular injury, arrhythmia  Prevention- U/S guidance, confirm line position with CXR,

PICC line

  Infectious Complications:  Prevention- dedicated port for TPN, standarized dressing

change protocols, avoid hyperglycemia, antibiotic impregnated catheters.

 Routine line changes not effective

Question-2

  A 39 y.old woman is recovering after multiple surgical debidements for necrotizing pancreatits. She is on enteral feeds and is having severe diarrhea. Workup for C.diff. has been negative on several occasions. Management options include all of the following except:

  1-start metronidazole   2-change to a different enteral formula   3-add supplemental pancreatic enzymes to feeds   4-D/C enteral feeding and strat TPN

Answer-2

  A 39 y.old woman is recovering after multiple surgical debidements for necrotizing pancreatits. She is on enteral feeds and is having severe diarrhea. Workup for C.diff. has been negative on several occasions. Management options include all of the following except:

  1-start metronidazole   2-change to a different enteral formula   3-add supplemental pancreatic enzymes to feeds   4-D/C enteral feeding and strat TPN

Diarrhea

  Fresh approach to every case, consider:  C.difficile  Hyperosmolar agents (hypertonic elixirs, sorbitol‐

containing meds  Antibiotics, other medications  Try continuous instead of bolus feeding  Try a formula with lower osmolality  Consider soluble fiber-containing or small peptide

formulations, but avoid if at high risk for bowel ischemia or dysmotility

Complications & Prevention

  Complications of Enteral Nutrition:  Complication related to access (tube misplacement, GI

perforation, sinusitis, nasal septal ulceration, tube dislodgement)  Prevention- confirm tube position with X-ray, place with

fluoroscopic guidance, soft silastic tubes, secure tubes, care in turning/ moving patients

 Gastrointestinal complications ( vomiting, diarrhea)  Prevention- prokinetic agents, small bowel feeding, change

in formula, avoid anti-anaerobic antibiotic, diagnose and treat infectious causes , imodium ,TPN

Hepatobiliary Complications

  Hepatic steatosis- fatty infiltration:  Occurs early (7-21 days)  Elevated aminotransferases  Due to excess glucose, hyperinsulinemia

  Intra or Extra hepatic cholestasis:  Occurs later (>21 days)  Elevated cannilicular enzymes and bilirubin  Gallbladder sludge and gallstones  Due to lack of enteral feeding

  Prevention- avoid overfeeding and excess glucose, enteral feeding

Question-3

  An elderly man presents to the ER with several days of crampy abdominal pian, vomiting and abstipation. After 3 days of expectant Rx for bowel obstruction, he is operated upon for lysis of adhesions. On PO#7 , bowel function has not returned and he is started on TPN. On PO# 8, he is at risk for all of the following except:

1-Cardiac arrhythmia 2-Hemolysis 3-Rhabdomyolysis 4-Metastatic calcification

Answer-3

  An elderly man presents to the ER with several days of crampy abdominal pian, vomiting and abstipation. After 3 days of expectant Rx for bowel obstruction, he is operated upon for lysis of adhesions. On PO#7 , bowel function has not returned and he is started on TPN. On PO# 8, he is at risk for all of the following except:

1-Cardiac arrhythmia 2-Hemolysis 3-Rhabdomyolysis 4-Metastatic calcification

Complications

  Intracellular Electrolytes (K,PO4 &Mg)  Required for protoplasm repletion and the retention of

other nutritients  Feeding, particularly glucose, leads to rapid uptake of

intracellular electrolytes with resultant depletion of serum levels

 Acute depletion of serum levels of intracellular electrolytes “Refeeding Syndrome”

Aspiration Pneumonia


Heyland DK et al. JPEN 2002, 26 : supp 51-5

RR-0.76; 95%CI 0.59-0.99 Hetrog. (P=0.89)

VAP Meta-analysis of 10 RCTs Comparing small bowel Vs gastric feeding


RR=0.93, 95%CI(0.72-1.20) Hetrogen. (P=0.99)

Mortality


•  Small bowel feeding associated with increased protein and caloric delivery and shorter time to target nutrient delivery




  86 mechanically ventilated pateints   RCT (semi-recumbent Vs supine body position)   Pneumonia

  semirecumbent 5% vs supine 23% P=0.018

  Incidence of pneumonia 50% when supine and enterally fed

Drakulovic MB et al , Lancet 1999, 354: 1851-8

Summary

  Distinguishing stress from starvation metabolism is critical to the provision of nutrition support in the ICU

  Critically ill patients may require more energy but are less able to tolerate glucose and require fat to meet energy requirements

Summary

  Critically ill patients require more protein to achieve nitrogen balance

  Enteral nutrition is the preferred route for nutrition support, but TPN is acceptable if glucose is colntrolled

  Nutrition support must be monitored to achieve nutritional goals and minimize complications

Documents

NUTRITION - University of British Columbiagsresidency.surgery.med.ubc.ca/files/2012/12/Nutrition_Yahya... · Enterla nutrition is more physiologic, less expensive and associated with