Metabolic Stress

NFSC 370
McCafferty
Stress: Any threat to a persons 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 bodys 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
hasnt 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 bodys 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. Dont 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.