Title: Nutrition in critical care
1Nutrition in critical care
- Pratthana Srisangthong,MD
2Scope
- Metabolic response in critical illness
- Assessment of nutritional status
- Enteral nutrition
- Parenteral nutrition
- Immunonutrition and antioxidant
3Background
- Adequate nutrition is essential to the
- critically ill patient.
- It helps support
- anabolism
- uncontrolled catabolism
- maintain a competent immune system
- improve patient outcome.
- Severe trauma, burns, sepsis, and head injury are
associated with marked - hypermetabolism and hypercatabolism,
- ? metabolic alterations.
4Metabolic response in critical illness
- 2 principal metabolic response
- 1 response to starvation
- 2 response to stress
Proceedings of the Nutrition Society (2007), 66,
1624
5Metabolic response to starvation
- Typical setting ? patient with chronic disease
- During the first 12 24 hr of acute starvation
- mobilization of hepatic glycogen stores
- 24 72 hr
- stimulation of gluconeogenesis
- After 72 hr
- - increase in hepatic ketone bodies
production - - reduction of gluconeogenesis
- - decreased protein breakdown
- Subsequently, as starvation progresses
- decrease lean body mass and BMR
-
Nutrition 13(Supp1)45S-51S, 1997
6Metabolic response to starvation
- Several features distinguish the metabolic
response of starved, critically ill patients. - As starvation progresses
- increased loss of lean body mass
- energy expenditure is not decrease.
- Continuation of starvation beyond 3 d
- not accompanied by a stimulation of both
- ketogenesis and ketone body oxidation
(with their normally concomitant suppression of
gluconeogenesis and protein breakdown)
7Metabolic response to starvation
- Starvation in critically ill patients leads to
accelerated protein-calorie malnutrition. - These alterations caused by inflammatory
mediators.
8Metabolic response to stress
- 1 energy metabolism
- - increased REE
-
9Metabolic response to stress
- Factor influenced energy expenditure
- 1 effect of illness
- - stage and length of illness
- - fever lt each 1 c ? increase 10 15 of
EE gt - - pain , physical activity , agitation ,
abnormal posturing , increase muscle tone ,
seizure
10Metabolic response to stress
- 2. effect of treatment
- - cathecholamine ? EE
- - beta blocker ? EE
- - sedative drug ? EE
- Supportive treatment can limit level of
metabolism
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12Metabolic response to stress
- 2 protein metabolism
- - protein catabolism gt protein synthesis
- ? net negative nitrogen balance
- - loss of muscle mass and protein degradation
in vital organ - - immobilization causes atrophy of skeletal
muscle ?negative nitrogen balance
Nutrition Vol. 13, No. 9(Suppl), 1997
13Metabolic response to stress
- protein metabolism
- - movement of amino acid ( alanine,
glutamine ) for gluconeogenesis - decreased intramuscular of glutamine
- - BCAA metabolism
- - liver reprioritized protein synthesis
- positive acute phase protein
- ( CRP , alpha 1 antitrypsin )
- negative acute phase protein
- ( albumin , prealbumin )
-
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15A.S.P.E.N. Nutrition Support Practice Manual 2nd
Ed.
16Consequences of protein catabolism
17Metabolic response to stress
- 3 carbohydrate metabolism
- - increased couterreguratory hormone and
cytokines - GH, cortisol, glucagon, cathecholamine
- IL-1, IL-6, TNF, LTS, prostanoids
- endogeneous glucose production
- - insulin resistance hyperglycemia
18Metabolic response to stress
- carbohydrate metabolism
- substrate of gluconeogenesis
- glycerol from adipose tissue
- alanine from skeletal muscle
- lactate from peripheral tissue and
skeletal muscle -
19Metabolic response to stress
- 4 lipid metabolism
- effect of catecholamines and cytokines
- mobilization of glycerol and free fatty acid
- increased lypolysis
- increased fatty acid oxidation
- reduced energy store
20Metabolic response to stress
- 5 Changes in endocrine system
- The response is essential for maintainance of
cellular and organ hemeostsis - - activation of hypothalamic pituitary adrenal
axis - - release cortisol from adrenal tissue
-
21Metabolic response to stress
depending on the patients underlying medical
problems, nutritional status, and drug or
resuscitative therapy.
22Assessment of nutritional status
- History include medical, surgical and dietary
history -
A history of acute or chronic weight loss or gain
before hospital admission is an essential
indicator of the patients nutritional status.
23Assessment of nutritional status
- 2 Anthropometric parameters
- unreliable and seldom used because the
patients positioning and fluid status affect
their accuracy. - 3. Visceral protein levels
- affected by stress, fluid shifts, and other
factors - limit their specificity and sensitivity.
24Assessment of nutritional status
- 4 Delayed hypersensitivity skin testing
- - limits in the critically ill patients
- - many nonnutritional factors such as acute
hemorrhage, hypovolemic shock, surgery, and the
use of steroids and immunosuppressants
depress immune function. - 5 Gold standard ? indirect calorimeter
25Purpose of nutrition support
- 1 safe life
- 2 speed recovery by reducing neuropathy and
maintain muscle mass and function
26Route of supplement
- EN vs PN
- Patients who can be fed via the enteral route
should receive EN - Indication of EN in ICU patients
- All patients who are not expected to be
- on a full oral diet within 3 days should
receive EN
Clinical Nutrition (2006) 25, 210223
27Is early EN (lt 2448 h after admission to ICU)
superior to delayed EN in the critically ill?
28- Effects of Early Enteral Feeding on the
- Outcome of Critically Ill Mechanically
- Ventilated Medical Patients
- large multi-institutional ICU database.
- 4,049 patients requiring mechanical ventilation
for gt 2 days. - overall ICU and hospital mortality
- were lower in the early feeding group (18.1 vs
21.4, p 0.01 - early feeding was found to be
- independently associated with an increased risk
of ventilator-associated pneumonia (VAP)
29Effects of Early Enteral Feeding on theOutcome
of Critically Ill MechanicallyVentilated Medical
Patients
CHEST / 129 / 4 / APRIL, 2006
30- Prospective ,controlled, clinical trials
- - 150 patients were enrolled.
- 75 pt ? early feeding
- 75 pt ? late feeding
- Patients in early feeding had greater incidence
of VAP.49.3 vs 30.7 p 0.020 and longer ICU
days. - No statistic difference in mortality
- Aggressive early EN in mechanical ventilator
medical patients is associated with greater
infection and prolong length of stays.
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32Is early EN (lt2448 h after admission to ICU)
superior to delayed EN in the critically ill?
- The expert committee, however favours view that
critically ill patients, who are haemodynamically
stable and have a functioning gastrointestinal - tract, should be fed early (lt 24 h), if
possible, using an appropriate amount of feed
33How much EN should critically ill patients
receive?
- - During the acute and initial phase of
- critical illness an exogenous energy supply
- in excess of 2025 kcal/kg BW/day may be
associated with a less favourable outcome - - During recovery (anabolic flow phase), the
- aim should be to provide 2530 total kcal/kg
- BW/day
34How much EN should critically ill patients
receive?
- Patients with a severe undernutrition should
- receive EN up 2530 total kcal/kg BW/day. If
these target values are not reached supplementary
parenteral nutrition should be given.
35Caloric Intake in Medical ICU Patients
- Prospective cohort study.
- Patients with an ICU length of stay of at least
96 hr. - Study participants were underfed relative to ACCP
targets. moderate caloric intake (9 to 18 kcal/kg
per day) was associated with better outcomes than
higher levels of caloric intake.
CHEST / 124 / 1 / JULY, 2003
36Which route is preferable for EN?
- There is no significant difference in the
efficacy of jejunal versus gastric feeding in
critically ill patients
37Protein requirement
- 1.5 g/kg/day.
- 2 g/kg/day in patients with trauma, severe burns,
and head injury - 2.5 g/kg/day in adult patients treated with
continuous renal replacement therapy - (CRRT)
- nutritional support can only limit the loss
- of the bodys protein and calorie stores.
- The goal is to administer sufficient nitrogen to
provide a positive or neutral - nitrogen balance.
38Lipid requirements
- 0.5 1 g/kg/d 20-40 of energy
- Lipid clearance is reduced in stressed patients
due to decreased activity of lipoprotein lipase
(LPL), - infusion rate should not exceed 0.12 g/kg/hr to
avoid the development of elevated triglyceride
levels. - Source of essential fatty acid, fat soluble
vitamin. - Avoid omega 6 linoleic is precursor of
arachinodic acid precursor of PG,TXA,LT
39Lipid requirements
- 0.5 1 g/kg/d 20-40 of energy
- Lipid clearance is reduced in stressed
- patients due to decreased activity of
- lipoprotein lipase (LPL),
- infusion rate should not exceed 0.12
- g/kg/hr to avoid the development of
- elevated triglyceride levels.
- Source of essential fatty acid, fat soluble
- vitamin.
- Avoid omega 6 linoleic is precursor of
arachinodic acid ? precursor of - PG,TXA,LT
40Parenteral nutrition
- Indication
- In patients who cannot be fed
- sufficient enterally the deficit.
- intolerant to EN
- Beware
- Overfeeding
- PN should not be used to correct acute
- fluid and electrolyte deficiencies?
41Complications of PN
- PN associated with a more pronounced
proinflammatory response than EN harmful in
patients with severe inflammation. - Complications of excess dextrose infusion
- hyperglycemia
- hypertriglyceridemia
- hepatic steatosis,
- respiratory decompensation
- depression of immune function
42Complications of PN
- Hyperglycemia
- depression of immune function
- increase infection risk
- impair cellular and humoral host defenses
- reducing phagocytosis
- inhibiting
- complement fixation
- Controlling hyperglycemia has resulted in
- improved phagocytic function as well as
- improved patient outcome.
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44n engl j med 35518 november 2, 2006
45Complications of PN
- Hypertriglyceridemia
- due to dextrose overfeeding or excess lipid
infusion. - Stressed patients are at higher risk for
hypertriglyceridemia due to - 1 increased lipolysis and hepatic fatty acid
reesterification - 2 increased hepatic triglyceride synthesis
from dextrose infusion - 3 decreased LPL enzyme activity
- 4 medications such as corticosteroids
46Complications of PN
- Hypertriglyceridemia
- Patients at risk
- sepsis
- multiorgan failure
- diabetes
- liver disease
- renal failure
- pancreatitis.
47Complications of PN
- hypercapnia
- - result from total energy and dextrose
overfeeding - patient at risk ? borderline respiratory
function and limited - pulmonary reserve.
- excess carbon dioxide is produced
- increased respiratory workload and minute
ventilation
48Immunonutrition and antioxidant
- Growth hormone
- Arginine
- Antioxidant
- Selenium
49- The negative nitrogen balance in critically
- ill patients is partly due to resistance to
growth hormone and the decreased production and
action of IGF-I - prospective, multicenter, double-blind,
randomized, placebo-controlled trials - 247 Finnish patients and 285 patients in other
European countries who had been in an - ICU for 5 to 7 days
N engl j med 35518 www.nejm.org november 2, 2006
50- The in-hospital mortality rate was higher in the
patients who received growth hormone than in
those who did not (Plt0.001) - Among the survivors, the length of stay in ICU
and in the hospital and the duration of
mechanical ventilation were prolonged in - the growth hormone group.
- In patients with prolonged critical illness,
- high doses of growth hormone are associated with
increased morbidity and mortality.
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52- The reason for the increased morbidity and
mortality is unclear - Modulation of immune function may be involved
multiple-organ failure and septic shock or
uncontrolled infection as causes of death in GH - Fluid retention abnormal fluid
distribution - Hyperglycemia increase risk of infection
- GH prevents the mobilization of glutamine from
muscle - Stimulation of lipolysis
53- The reason for the increased morbidity and
mortality is unclear - Modulation of immune function may be involved
multiple-organ failure and septic shock or
uncontrolled infection as causes of death in GH - Fluid retention ? abnormal fluid distribution
- Hyperglycemia ? increase risk of infection
- GH prevents the mobilization of glutamine from
muscle - Stimulation of lipolysis
54- Is essential amino acid for adult in injured or
stress state - Is less available in body under these conditions
- Function of arginine
- Protein synthesis substrate of urea cycle
- Production of nitric oxide
American journal of critical care,Jan 2004,vol
13, No 1
55Function of arginine
56Metabolism of arginine
57Metabolism of arginine
- Proline ? hydroxyproline ? collagen
- substrate for wound healing
- Nitric oxide
- Decreased acute injury
- Decreased wound infection
- Vascular relaxation ? regulate blood pressure
58- Clinical improvement in surgical patient fewer
infection complications - But increased mortality in patients with shock,
sepsis, organ failure
59Antioxidants
- Critical illness is associated with the
generation of oxygen free radicals and low
endogenous antioxidant capacity leading to a
condition of oxidative stress - overall antioxidants were associated with a
significant reduction in mortality RR 0.6 but
had no effect on infectious complications - the mortality effect was mediated other
mechanisms, perhaps related to improved organ
function
Intensive Care Med (2005) 31327337
60Selenium in intensive care Probably not a magic
bullet but an important adjuvant therapy
- multiple-center prospective, randomized,
controlled supplementation trial in patients with
severe sepsis - no significant difference in intention-to treat
mortality rate (p .109) - But significant reduction of 28- day mortality
rate in the patients with high APACHE score - Improving selenium status reinforce the
endogenous AOX defenses
Crit Care Med 2007 Vol. 35, No. 1
61Selenium in intensive care Probably not a magic
bullet but an important adjuvant therapy
- The possibility of deleterious toxic effects, and
AOX may be pro-oxidant. - Selenium is beneficial in some of the
- most critically ill patients. is likely to be
- through its antioxidant activities,not all of
which have antioxidant activity. - Other modes of action may explain some of the
inconsistent effects of AOX supplements this
clearly requires further investigation.
62THE END