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Medical Nutrition Therapy for Metabolic Stress and Critical Care

Medical Nutrition Therapy for
Metabolic Stress and Critical Care


Objectives
• Describe the metabolic response to
critical illness
• Describe role of nutrition therapy for
critically ill patients
• Describe how to assess nutrient
needs for a critically ill patient


Metabolic Stress
• Stressors:
– Sepsis
– Surgery
– Trauma (includes burns)

• These stressors activate a particular
systemic response, leading to a

number of physiologic and metabolic
changes


What happens during metabolic stress?
• Metabolic alterations to meet the body’s
needs for survival
– hypermetabolism
– hypercatabolism
– hyperglycemia
– sodium & water retention
– increased heart rate & cardiac output
– hypercoagulability & increased platelet
aggregation
– increased sympathetic tone
• controls “fight or flight” response


Metabolic Response to Stress
• Involves most metabolic pathways
• Accelerated metabolism of lean body
mass
• Negative nitrogen balance
• Muscle wasting
Hypercatabolism!


Ebb Phase
• Usually restricted to the first 24-48 hours
• Immediate response






Hypovolemia and tissue hypoxia
Decreased cardiac output
Decreased oxygen consumption
Lowered body temperature
Decreased insulin and increased glucacon
levels


Flow Phase
• Follows fluid resuscitation and improved
O2 transport
• Increased cardiac output begins
• Increased body temperature
• Increased energy expenditure
• Total body protein catabolism begins
•  glucose production, free fatty acids,
circulating insulin, catecholamines,
glucagon, & cortisol


Figure 89.2. Neuroendocrine and metabolic consequences of
injury. ACTH, adrenocorticotropic hormone. From: Lowry SF &
Perez JM. The hypercatabolic state. In Shils ME, et al. (eds) Modern
Nutrition in Health & Disease. Lippincott, Williams & Wilkins, 2006.


Metabolic Responses During Sepsis
Organ
Liver

Response
 Glucose production
 Amino acid uptake
 Acute-phase protein
synthesis
 Trace metal sequestration

Central nervous system
Circulation

Anorexia, fever
 Glucose
 Triglycerides
 Amino acids
 Urea
 Iron
 Zinc


Metabolic Responses During Sepsis
(continued)

Skeletal
muscle

 Amino acid efflux (especially glutamine),

Intestine

 Amino acid uptake from both luminal and

leading to loss of muscle mass
circulating sources, leading to gut mucosal
atrophy



Endocrine

 Adrenocorticotropic hormone
 Cortisol

 Growth hormone
 Epinephrine
 Norepinephrine
 Glucagon
 Insulin initially, then  levels & insulin resistance
From Michie HR: Metabolism of sepsis and multiple organ failure, World J Surg 20:461, 1996.


Hormonal and Cell-Mediated Response
• Causes energy metabolism to shift to protein
as a primary fuel
–The body needs glucose, so protein is used for
gluconeogenesis

• Increase in hepatic amino acid uptake for
protein synthesis
–“Acute phase proteins” are made instead of visceral
proteins

• Lean body mass may be mobilized as a
protein source


Skeletal Muscle Proteolysis


Hormonal Stress Response Specifics
• Conserve fluid & sodium to maintain
blood volume:
– Aldosterone
• Corticosteroid that causes the kidney to retain
sodium

– Antidiuretic hormone
• Stimulates renal tubular water absorption


Hormonal Stress Response Specifics
(continued)

• Simulate metabolism:
– Adrenocorticotropic hormone (ACTH)
• Acts on adrenal cortex to release cortisol
• Mobilize amino acids from skeletal muscle

– Catecholamines
• Epinephrine & norepinephrine from renal medulla
• Stimulate hepatic glycogenolysis, fat
mobilization, gluconeogenesis

From: http://health-pictures.com/gland/adrenal-gland.htm accessed 2/28/09


Acute Phase Response
• Occurs when a patient is very stressed
• See increased production of cytokines
– Protein mediators secreted by
macrophages in response to tissue
damage, infection, inflammation, and some
drugs and chemicals
– Hormone regulators of the immune system
– Stimulate production of inflammatory
mediators associated with shock & sepsis


Actions of Specific Cytokines
• Tumor necrosis factor (TNF)
– Increased catabolism of lean body mass
– Causes anorexia
– Activates the hypothalamic-pituitaryadrenal axis

• Interleukin-1
– Mediates the acute phase response
– Associated with fever, hypotension,
inflammation, protein catabolism

• Interleukin-6
– Release of hepatic acute phase proteins


Response at the Cellular Level
• Eicosanoids are produced in response
to this stress
– These are lipid mediators of inflammation
– Three major types:
• Prostaglandins
• Leukotrienes
• Thromboxanes


Immune Cell Saturated with
omega-6 Fat

AA

Phospholipid
Membrane

AA

AA

AA
AA

AA

AA

AA

AA

Slide courtesy Abbott Nutrition

Proinflammatory
compounds


Prostaglandins
• Prostaglandins
– Modulate intensity & duration of inflammatory &
immune responses
– 2 series derived from arachidonic acid (n-6)
– PGE2 has significant pro-inflammatory function





Induction of fever & erythema
Increased vascular permeability
Vasodilation
Enhancement of pain & edema in response to
histamine
• Inhibition of B-cell & T-cell proliferation


Prostaglandins
(continued)

• The 3 series is less inflammatory
– Derived from omega-3 fatty acids:
eicosapentaenoic acid (EPA) and
docosahexaenoic acid (DHA)
– Thromboxanes are derived from PGH
• These are similar to PG in that
– 2 series is pro-inflammatory
– 3 series is much less active


Leukotrienes
• Primary mediators of inflammation &
allergic reactions
• Also increase microvascular permeability
• Promote arteriolar constriction
• Promote bronchoconstriction and
increase bronchial mucous production


Leukotrienes
(continued)

• The 4 series, derived from AA, is
proinflammatory
• LTB4 has the most significant action

– Potent chemoattractant & chemokinetic action
toward leukocytes
– Inhibition of T-cell mitogenesis
– Stimulation of PMN cells to aggregate & adhere to
endothelial cells
– Promote secretion of inflammatory products by
neutrophils
– Synergy with other mediators to increase vascular
permeability

• The 5 series, made from EPA & DHA, is less
active


Thromboxanes





Similar function to leukotrienes
Derived from PGH
Involved in platelet aggregation
TXA2 stimulates formation of plateletderived growth factor
– Stimulates blood clotting

• 2-series is inflammatory & 3-series is
less so


Influencing Eicosanoid Production
• Arachidonic acid comes from omega-6 fatty
acids
– Example: corn oil is high in omega-6 fatty acids

• Feeding more omega-3 fats may help push
production of the anti-inflammatory (or less
active) eicosanoids
– Example: enteral formulas with fish oil are
promoted as “immune modulating”


Metabolic Response in
Starvation vs. Stressed
State


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