Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
in the ICU
Sandra L Schoepfel MS RD RN CNSD
Karl D Pilson MD
Suresh Agarwal MD FACS
Boston Medical Center
Boston, MA
Slide 5
Invalidation
Weight (BMI)
Anthropometrics
Albumin, Pre-Albumin
Nitrogen Balance
Slide 7
Malnutrition
Recent surveys suggest that 33-53% of
hospitalized patients suffer from moderate to
severe malnutrition
Souba W. N. Eng J Med 1997;336-41
Atalay BG. JPEN 2008 Jul-Aug;32(4):454
Delgado AF. Clinics 2008;63(3):357
Slide 10
Slide 11
Slide 12
Slide 13
Greenfield
1997
Response to Stress/Injury
Neurohormonal - "Counterregulatory hormones"
Glucagon
Epinephrine
Glucocorticoids
Inflammatory mediators
IL-1, IL-2, IL-6
TNF-a
IFN-g
Slide 14
Greenfield
1997
Slide 17
Adult males
106 lb (48 kg) for the first 60 inches (152 cm) = 6 lbs
(2.7 kg for every inch > 60
Ex: Ht. 510 (180.3 cm) = IBW of 166 lb or 75.4 kg)
Slide 20
Conditions
Energy Requirement
~ Kcal/kg/day
~Protein gm/kg/day
Elective Surgery
1.00-1.25 x BEE
25-30
1.0-1.2
Multiple Trauma
1.25-1.5 x BEE
25-35
1.4-1.5
Sepsis/Peritonitis
1.5 x BEE
25-35
1.4-2.0
1.75-2.0 x BEE
35-40
1.8-2.5
Slide 22
A=age
W=wt in kg
S=sex (1=male, 0=female)
T=trauma (1=yes, 0=no)
B=burns (1= yes, 0 = no)
(This is the 1992 version)
Nitrogen Balance
Used to reflect the balance between exogenous nitrogen
intake and renal removal of nitrogen-containing
compounds through stool, urine, skin, fistulas, wounds,
etc.
Measurement of nitrogen balance is most accurate in
patient who receive a defined nutrient intake such as is
in the case in those receiving enteral or parenteral
nutrition
Urea nitrogen urine concentration increases dramatically
in the sickest of patients reflecting catabolism of protein
associated with systemic inflammation
Slide 25
Slide 26
Greenfield 1997
Slide 27
0.6-0.7 starvation/underfeeding
0.84-0.86 desired range/mixed fuel utilization
0.9-1.0 carbohydrate metabolism
1.0+ overfeeding / lipogenesis
Slide 29
Slide 34
Slide 35
Slide 36
Late
Feeding
ICU Mortality
18.10%
21.40%
0.01
Hospital Mortality
28.70%
33.90%
0.001
10.9 8.1
10.2 7.7
NS
~58%
~52%
0.001
Outcomes
p Value
Slide 38
Slide 39
Where to start?!
Determine number of calories needed
Use predetermined feeding weight whether actual, ideal,
adjusted or usual body weight first
Utilize predictive equations, indirect calorimetry
Level of evidence
Large, randomized trials with clear-cut results; low risk of falsepositive (alpha) error or false-negative (beta) error
Small, randomized trials with uncertain results; moderate to high
risk of false-positive (alpha) and/or false-negative (beta) error
Slide 43
Arginine
Omega-3 fatty acids
Nucleotides
+ / - Glutamine
Antioxidants
Slide 49
Slide 50
Immunonutrition
Glutamine Most abundant AA in plasma and skeletal muscle; nonessential, but may be conditionally essential during catabolic stress. Has
shown to be of benefit in burn, and trauma patients, but evidence is lacking
in other critically ill patients.
Arginine conditionally essential amino acid thought to enhance the
depressed immune responses associated with trauma, sepsis, or
malnutrition.
Nucleotides precursor of DNA and RNA that are necessary for most cell
functions, including protein synthesis. Demands during catabolic stress may
exceed production.
Omega-3 FAs fish oil with beneficial effects in septic patients, including
modulating of leukocyte function and regulation of cytokine release through
nuclear signaling and gene expression. The enhance the production of
prostaglandin derivatives which play a role in accelerating the resolution of
the pro-inflammatory state. IV omega-3 fatty acids are currently unavailable
in parenteral emulsions in the United States.
Antioxidants thought to be of some benefit in severely stressed and septic
patients, but exact amounts and combinations have yet to be determined for
this population
Slide 51
What Is An Appropriate
Gastric Residual Volume (GRV)?
Threshold level of GRV tolerated by clinicians is
of great debate!
No clinical significance of GRV < 200 ml
Stomach is a distensible container in which GRV
measurements dont account for
Aspiration of TFs is associated with a low morbidity
and an even lower mortality risk
Patients with high GRV >400 ml or who demonstrate
GI intolerance => consider NJT
Slide 52
Slide 53
Hemodynamic Instability
High risk guidelines for a hypoperfused GI
tract:
FiO2 >60
PEEP >5
Mean Arterial Pressure 75 mmHg
? high dose pressors
NG output increases
New abdominal pain
Abdominal distention
Cessation of flatus, stool
Slide 55
Refeeding Syndrome
Metabolic response caused by either enteral or
parenteral nutrition
Shift from stored body fat to CHO as primary fuel after
prolonged NPO status
Feeding causes insulin levels to rise creating intracellular
movement of electrolytes
Mg, K, PO4 levels may fall; can lead to arrhythmias,
respiratory and cardiac failure, and death
Prevention and therapy:
Correct electrolyte abnormalities BEFORE initiating nutrition
support, avoid overfeeding, and provide appropriate vitamin
supplementation
Slide 56
Amino Acids
Dextrose
Fat
10% Lipids
20% Lipids
30% Lipids
4 kcal / g
3.4 kcal / g
10 kcals / g
1.1 kcal / mL
2 kcal / mL
3 kcal / mL
Slide 57
Amino Acids
Dextrose
Lipids
Total Volume
4%
15%
2%
2000 mL
Trace Elements
Chromium, Copper, Zinc, Manganese, Selenium, Iron
Electrolytes
Usually in the form of NaCl, NaAc, NaPO4, KCL, KAc,
KPO4, MgSO4, CaGluc
Miscellaneous
H2 blockers, Heparin, Insulin, Glutamine
Slide 59
*Patients should be monitored closely for refeeding syndrome for the first week
of PN therapy.
**Essential Fatty Acid Deficiency (EFAD) may develop when no source of fatty
acid is supplied for > 14 days. Minimum lipid requirements to prevent EFAD
is 500 mL of a 20% fat emulsion (100 grams) over 24 hours given once a
week
Slide 60
Overfeeding Consequences - 1
Azotemia Patients >65 years and patients given >2 gm/kg
protein are at risk.
Fat-overload syndrome Recommended maximum is 1 gm
lipid/kg/d. Infuse IV lipid slowly over 24 hours.
Hepatic steatosis Patients receiving chronic highcarbohydrate, very low fat TPN are at risk.
Hypercapnia Makes weaning difficult.
Hyperglycemia Increases risk of infection. Intake should
not exceed 5 mg CHO/kg/min (4 mg/kg/min for diabetics).
Slide 61
Overfeeding Consequences - 2
Hypertonic dehydration Can be caused by
high-protein formula with inadequate fluid
provision.
Hypertriglyceridemia Propofol, high TPN lipid
loads, and sepsis increase the risk. If the
patient is hypertriglyceridemic, decrease lipid to
an amount to prevent EFAD and monitor.
Slide 62
Consequences of Overfeeding-3
Metabolic acidosis Patients receiving low
ratios of energy to nitrogen are at risk. Acidosis
can cause muscle catabolism and negative
nitrogen balance.
Refeeding syndrome Common in
malnourished patients or those held NPO prior
to initiation of feeding. Start feedings
conservatively, advance gradually, and monitor
Mg, Ph, and K closely.
Slide 63
Intensive treatment
96
92
Conventional treatment
ONLY REACHED
SIGNIFICANCE for patients
in the SICU for
5 days or longer
88
42.5% reduction in
mortality with
intensive treatment;
P<.04
84
80
0
A
Admission
100
96
Intensive treatment
92
Conventional treatment
88
34% reduction in
mortality with
intensive treatment;
P<.01
84
80
0
50
100
B
Days
250 After
Admission
Slide 65
150
200
International multi-center
6104 ICU patients were randomized
Conventional insulin group (n = 3054 assigned => 3010 after 90 days)
Maintain 80-110 mg/dL
Intensive insulin group (n = 3050 assigned => 3012 after 90 days)
Maintain < 180 mg/dL
The NICE-SUGAR Study Investigators. N Engl J Med 2009;360:1283-97
Slide 66
NICE-SUGAR RESULTS
No difference
ICU LOS
Hospital LOS
Ventilator days
Renal replacement
therapy
Severe hypoglycemia
Conventional insulin group 0.5%
Intensive insulin group 6.8%
90-day mortality
in conventional insulin group
Slide 67
NICE-SUGAR
> 70% nutrition received
from EN
Larger sample size
Mixed medical / surgical
Slide 68
Self Assessment
Ready to test your knowledge?
Take the Review
Slide 69
References
References
Slide 72
References
Slide 73
References
Kieft H, Roos A, Bindels A, et al. Clinical outcome of an
immune enhancing diet in a heterogeneous intensive
care population. Intensive Care Med. 2005;31:524-532.
McClave SA, et al. Poor validity of residual volumes as a
marker for risk of aspiration in critically ill patients. Crit
Care Med. 2005;33;449-450.
Choban PS, Dickerson RN. Morbid obesity and nutrition
support: is bigger different? Nutr Clin Pract.
2005;20:480-487.
Dellinger RP, Carlet JM, Masur H, et al; Surviving Sepsis
Campaign Management Guideline Committee. Surviving
Sepsis Campaign guidelines for management of severe
sepsis and septic shock. Crit Care Med. 2004;32:858873.
Slide 74
References
McClave SA, Chank WK. Feeding the
hypotensive patient: does enteral feeding
precipitate or protect against ischemic bowel?
Nutr Clin Pract. 2003;18:279-284.
Montejo JC, Zarazaga A , Lopez-Martinez J, et
al. Immunonutrition in the intensive care unit: a
systematic review and consensus statement.
Clin Nutr. 2003;22:221-233.
Wooley, JA, Sax HC. Indirect Calorimetry;
Applications to Practice. Nutr Clin Pract.
2003;18:434-439.
Slide 75
References
Van den Berghe G, Wouters P, Weekers F, et al.
Intensive insulin therapy in the critically ill patient. New
Engl J Med. 2001;345:1359-1367.
Marik PE, Zaloga GP. Early enteral nutrition in acutely ill
patients: a systematic review. Crit Care Med.
2001;29:2264-2270.
Souba WW, Austen WG. Nutrition and metabolism. In:
Greenfield LJ, Mulholland MW, Oldham KT, et al.
Surgery: Scientific Principles and Practice. 2nd ed. New
York, NY: Lippincott-Raven; 1997.
Souba WW. Nutritional Support. N. Engl J Med.
1997;336:41-48.
Slide 76