Nutrition in critical care

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Nutrition in critical care

• Pratthana Srisangthong,MD

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Scope

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

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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.

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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
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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
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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)

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Metabolic response to starvation

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

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Metabolic response to stress

• 1 energy metabolism
• - increased REE

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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

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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
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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 )

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A.S.P.E.N. Nutrition Support Practice Manual 2nd
Ed.
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Consequences of protein catabolism
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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

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Metabolic response to stress

• carbohydrate metabolism
• substrate of gluconeogenesis
• glycerol from adipose tissue
• alanine from skeletal muscle
• lactate from peripheral tissue and
  skeletal muscle

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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

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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

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Metabolic response to stress

• 6 fluid and electrolyte

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

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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

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Purpose of nutrition support

• 1 safe life
• 2 speed recovery by reducing neuropathy and
  maintain muscle mass and function

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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
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Is early EN (lt 2448 h after admission to ICU)
superior to delayed EN in the critically ill?
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• 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)

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Effects of Early Enteral Feeding on theOutcome
of Critically Ill MechanicallyVentilated Medical
Patients
CHEST / 129 / 4 / APRIL, 2006
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• 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

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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

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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.

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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
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Which route is preferable for EN?

• There is no significant difference in the
  efficacy of jejunal versus gastric feeding in
  critically ill patients

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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.

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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
  

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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

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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?

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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

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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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n engl j med 35518 november 2, 2006
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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

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Complications of PN

• Hypertriglyceridemia
• Patients at risk
• sepsis
• multiorgan failure
• diabetes
• liver disease
• renal failure
• pancreatitis.

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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

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Immunonutrition and antioxidant

• Growth hormone
• Arginine
• Antioxidant
• Selenium

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• 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
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• 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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• 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

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• 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

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• 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
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Function of arginine
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Metabolism of arginine
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Metabolism of arginine

• Proline ? hydroxyproline ? collagen
• substrate for wound healing
• Nitric oxide
• Decreased acute injury
• Decreased wound infection
• Vascular relaxation ? regulate blood pressure

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• Clinical improvement in surgical patient fewer
  infection complications
• But increased mortality in patients with shock,
  sepsis, organ failure

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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
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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
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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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THE END