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Nutrition in critical care

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Title: Nutrition in critical care


1
Nutrition in critical care
  • Pratthana Srisangthong,MD

2
Scope
  • Metabolic response in critical illness
  • Assessment of nutritional status
  • Enteral nutrition
  • Parenteral nutrition
  • Immunonutrition and antioxidant

3
Background
  • 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.

4
Metabolic response in critical illness
  • 2 principal metabolic response
  • 1 response to starvation
  • 2 response to stress

Proceedings of the Nutrition Society (2007), 66,
1624
5
Metabolic 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
6
Metabolic 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)

7
Metabolic response to starvation
  • Starvation in critically ill patients leads to
    accelerated protein-calorie malnutrition.
  • These alterations caused by inflammatory
    mediators.

8
Metabolic response to stress
  • 1 energy metabolism
  • - increased REE

9
Metabolic 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

10
Metabolic 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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Metabolic 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
13
Metabolic 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 )

14
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15
A.S.P.E.N. Nutrition Support Practice Manual 2nd
Ed.
16
Consequences of protein catabolism
17
Metabolic 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

18
Metabolic response to stress
  • carbohydrate metabolism
  • substrate of gluconeogenesis
  • glycerol from adipose tissue
  • alanine from skeletal muscle
  • lactate from peripheral tissue and
    skeletal muscle

19
Metabolic 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

20
Metabolic 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

21
Metabolic response to stress
  • 6 fluid and electrolyte

depending on the patients underlying medical
problems, nutritional status, and drug or
resuscitative therapy.
22
Assessment 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.
23
Assessment 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.

24
Assessment 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

25
Purpose of nutrition support
  • 1 safe life
  • 2 speed recovery by reducing neuropathy and
    maintain muscle mass and function

26
Route 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
27
Is 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)

29
Effects 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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Is 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

33
How 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

34
How 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.

35
Caloric 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
36
Which route is preferable for EN?
  • There is no significant difference in the
    efficacy of jejunal versus gastric feeding in
    critically ill patients

37
Protein 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.

38
Lipid 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

39
Lipid 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

40
Parenteral 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?

41
Complications 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

42
Complications 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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44
n engl j med 35518 november 2, 2006
45
Complications 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

46
Complications of PN
  • Hypertriglyceridemia
  • Patients at risk
  • sepsis
  • multiorgan failure
  • diabetes
  • liver disease
  • renal failure
  • pancreatitis.

47
Complications 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

48
Immunonutrition 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.

51
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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
55
Function of arginine
56
Metabolism of arginine
57
Metabolism 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

59
Antioxidants
  • 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
60
Selenium 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
61
Selenium 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.

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