NUTRITION - University of British...
Transcript of NUTRITION - University of British...
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
• 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
Stress Hypermetabolism
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
Stress Hypermetabolism
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
Stress Hypermetabolism
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
Stress Hypermetabolism
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
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 +++ +
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
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
Energy and Substrate Requirements
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
Energy and Substrate Requirements
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
Energy and Substrate Requirements
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
Energy and Substrate Requirements
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
Energy and Substrate Requirements
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
Gramlich L et al. Nutrition 20 : 843-48, 2004
Meta-analysis of 13 RCT Enteral Vs Parenteral nutrition
EN vs PN
No differences in ventilator days, LOS More hyperglycemia with PN EN cheaper
Gramlich L et al. Nutrition 20 : 843-48, 2004
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
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:
Enteral Nutrition Formulas
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
Enteral Nutrition Formulas
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:
Enteral Nutrition 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
Enteral Nutrition Formulas
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
Enteral Nutrition Formulas
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
Enteral Nutrition Formulas
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
Enteral Nutrition Formulas
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
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
Novak F et al, Crit Care Med 2002, 30 2022-9
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
Novak F et al, Crit Care Med 2002, 30 2022-9
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
Novak F et al, Crit Care Med 2002, 30 2022-9
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
Novak F et al, Crit Care Med 2002, 30 2022-9
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
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 & 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”
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
Heyland DK et al. JPEN 2002, 26 : supp 51-5
• Small bowel feeding associated with increased protein and caloric delivery and shorter time to target nutrient delivery
Heyland DK et al. JPEN 2002, 26 : supp 51-5
Aspiration Pneumonia
Aspiration Pneumonia
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