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Metabolic Stress
NFSC 370
McCafferty
Stress: Any threat to a person’s well being
 Pathological stresses:

disease and trauma (physical insult such as
bone fractures, wounds, burns, and surgery)
 Severe pathological stresses:

cause hormonal and metabolic changes that
alter nutrient needs. (serious infections, major
tissue damage, extensive surgery and severe
burns)
The Stress Response:

The body’s adaptive response to severe
stress, mediated by immune, inflammatory,
and hormonal mechanisms.
Ebb Phase



Flow Phase
 Acute phase =
(hypermetabolism, hormonal shift to
catabolism, and inflammatory response)
 Adaptive phase =
I. Acute Phase Response
A. Hypermetabolism – Increased
metabolic rate
•
•
•
believed to contribute to the GI tract
changes, anorexia, fever and malaise that
accompany the inflammatory response
B. Hormonal Shift to Catabolism
1. Insulin to glucagon/
counterregulatory hormone
ratio decreases
• Remember:
• The counterregulatory hormones promote
–
–
–
– (Most important AAs in glu production are
alanine and glutamine: synthesized from
BCAAs)
2. Glucose and amino acids are
mobilized to synthesize stress
factors
Specific factors synthesized depend on
type of stress (ie broken bone vs. fighting
infection = different factors)
C. Immune and Inflammatory
Responses
1. Immune system fights off
infections/pathogens Remember: insulin
promotes CHO/TG storage and protein
synthesis.
2. Inflammatory response to tissue injury:
inactivates/removes invaders and repairs
tissue.
At the injury site:
a. Capillaries dilate and become more permeable
b. Blood, protein, and immune system factors flow
to injured area
c. Fluid enters interstitial spaces: edema
(Eventually blood flow slows; clots form
around injured area and contain it)
d. Redness, swelling, heat, and pain
e. Increased HR, body T, respiration (and WBCs if
bacterial infection)
f. Decreased serum iron and zinc
g. Anorexia
h. If infection remains localized: abscess or
granuloma
i. If infection enters bloodstream: sepsis
Can cause multiple organ failure and death
D. Clinical findings typical of Stress
Response (acute phase)
1.
2.
3.
4.
5.
II. Effects of Stress/PEM on
Nutrition Status

Both deplete energy reserves, cause
protein catabolism, impair nutrient
absorption, and tax the immune system.

Stress increases protein needs.
(hormones, tissue repair, immune
factors, etc.)
A. Acute Malnutrition
1. Previously healthy +
acute/prolonged stress = acute
malnutrition.
2. Nutrients used for stress factors 
depletion
3. Protein-sparing use of ketone bodies
impeded by stress. (hormonal
picture -- also body hasn’t had time
to begin making ketone bodies)
B. Chronic Malnutrition
1. Inadequate reserves to mount
stress/immune response
2. Body has adapted to prolonged
energy and protein deficit
(conserving lean mass and using fat
stores)
C. Mixed Malnutrition
1. Chronic malnutrition + extreme or
prolonged stress
2. Stress + inadequate nutrients
3. Acute malnutrition may  mixed
malnutrition
D. Decreased Nutrient Absorption
1.
2.
E. Decreased GI Motility
(book says gastric, x it out)
1. Stress 
2. Slows motility (no oral diets in acute
phase)
3. Worsened by lack of enteral
nutrients
4.
F. Anorexia (already mentioned)
and then of course if the trauma is to
the GI tract, that worsens everything
as well.
III. Effects of Stress/PEM on
GI Tract Immune Function
A. Immune Fx. of GI Tract
1. Mucosal barrier contains antimicrobial
chemicals/protective enzymes
(Slippery: prevents invaders from
“sticking” to lining)
2. Gastric acid
3. Intestinal Barrier: villi are crowded close
together forming physical barrier.
Damaged cells may allow entrance of
harmful particles.
4. Immune System Cells: Mucus
containing and lymph cells: 70-80% of
the body’s immunologic-secreting cells
are located in the intestine.
5. Intestinal Flora: Inhibit growth of
pathogenic bacteria by competing for
space and nutrients and producing
SCFAs which prevent bacteria from
adhering to intestinal surface.
IV.Secondary Effects on Nutr.
Status
A. Decubitus Ulcers
1.
Immobility/bedrest causes
2.
Poor nutritional status exascerbates decubes 
3.
Most at risk:
B. Calcium Stones
1. Prolonged immobility 
C. Drug Interactions
1. Drug therapy may affect nutr. status (esp.
if multiple drugs)
2. PEM/Stress  intestinal changes  effect
on nutrient and drug absorption
3. Severe stress/PEM  decreased albumin
 slowed drug transit to site of action
and slowed transit to liver/kidneys for
detoxification/excretion
V. Medical Nutrition Therapy
A. Goals of Nutrition Therapy:
1. Prevent acute malnutrition
2. Preserve organ function/immune
function
3. Minimize nutrient losses
4. Prevent “Refeeding Syndrome”


Physiologic and metabolic complications
associated with introducing nutrition too
rapidly to a person with severe PEM.
Complications may include hepatic steatosis,
hyperglycemia, cardiac insufficiency,
respiratory distress, CHF, convulsions, coma,
and death.
B. Nutrient Needs
1. Fluid and electrolytes (lost through
bleeding, wound exudate, v/d, fever).
a. Fluid needs are based on blood volume
(clinical measures include BP, HR,
urinary output, etc.)
b. Intracellular electrolytes (K, P, Ca, Mg)
move into serum during catabolism.
 During adaptation, serum levels may
plummet. Life-threatening:
2. Energy: needs depend on severity of stress,
organ fx, metabolic state and nutrition status
a. Harris-Benedict equation with stress factor
of 1.3 (unless direct or indirect calorimetry
is available). Careful: H-B equation tends
to overestimate kcalorie needs.
b. Or, 25-30 nonprotein kcals/kg
c. Closely monitor pt. to prevent
overfeeding.
i.
ii.
iii.
d.
e.
3. Protein:
a.
b. 1.5-2 g prot/kg body wt., depending on stress.
Up to 3g/Kg for extensive burns.
c. Don’t forget protein sparing effect of adequate
kcalories.
d. Specific Amino Acids:
i. Supplementing BCAAs may minimize
negative N balance
ii. Glutamine: may become conditionally
essential during stress: provides fuel for
intestinal cells and helps maintain their
structure and function
iii. Glutamine and arginine may
improve immune function (both are
synthesized from BCAAs)
4. CHO and Fat: Protein sparing
a. Excess carbohydrate can contribute to
b. Excess fat can interfere with the
c. Nonprotein kcals: 60-70% glucose and
25-30% fat
d. In burns: only 15-20% fat
e. Fatty acids
i. w6FAs in excess of EFA needs
decrease immune fx (TPN/TF
formulas)
ii. Use of w3FAs (fish oil) for stressed
patients is being studied.
5. Micronutrients
a. Specific requirements during stress are
unknown
b. B vitamins:
c. Antioxident nutrients become depleted
(no proven benefit yet of
supplementation)
d. Zinc and vitamins A & C are important
in wound healing
C. Providing Nutrients During Stress
1. Oral diets: As appropriate when bowel
sounds return. Begin with cl. liquids and
progress to full liquids, soft, and regular as
tolerated.
2. Nutrition Support:
3. TF –
a.
b. Early enteral feeding (36h post stress)
stimulates intestinal blood flow,
adaptation, and function, and minimizes
hypermetabolism. May help prevent
bacterial translocation.