Chapter 39

Medical Nutrition
Therapy for Metabolic
Stress: Sepsis,
Trauma, Burns, and
Surgery

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Metabolic response to Stress

! Sepsis (infection)
! Trauma (including burns)
! Surgery
! When the systemic response is activated,
the physiologic and metabolic changes that
follow are similar and may lead to septic
shock

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 Metabolic Response to Stress

! Involves most metabolic pathways

! Accelerated metabolism of lean body
mass (LBM)
! Negative nitrogen balance
! Muscle wasting

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Ebb Phase
! Immediate: hypovolemia, shock, tissue
hypoxia
! Decreased cardiac output
! Decreased oxygen consumption
! Lowered body temperature
! Insulin levels decrease because glucagon
is elevated

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 Flow Phase
! Follows fluid resuscitation and restoration of
oxygen transport
! Increased cardiac output begins
! Increased body temperature
! Increased energy expenditure
! Total body protein catabolism begins
! Marked increases in glucose production, FFA
release, circulating insulin, catecholamines,
glucagon, and cortisol
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Hormonal and Cell-Mediated

Response
! Hormones cause protein catabolism
! BCAA to synthesize glutamine
! Mobilization of acute-phase proteins
causes rapid loss of LBM and negative
nitrogen balance
! Increased circulation of FFAs
! Hyperglycemia
! Sodium and water retention
! Cytokines
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 ! Counterregulatory hormones, which are elevated
after injury and sepsis, play a role in the accelerated
proteolysis.
! Glucagon promotes gluconeogenesis, amino acid
uptake by the liver, ureagenesis, and protein
catabolism.
! Cortisol, which is released from the adrenal cortex in
response to stimulation by adrenocorticotropic
hormone ACTH secreted by the anterior pituitary
gland, enhances skeletal muscle catabolism and
promotes hepatic use of amino acids for
gluconeogenesis, glycogenolysis, and acute-phase
protein synthesis

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Metabolic Responses During

Sepsis
Organ Response
Liver ↑ Glucose production
↑ Amino acid uptake
↑ Acute-phase protein synthesis
↑ Trace metal sequestration
Central nervous system Anorexia, fever
Circulation ↑ Glucose
↑ Triglycerides
↑ Amino acids
↑ Urea
↓ Iron
↓ Zinc

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 Metabolic Responses During
Sepsis (cont’d)
Skeletal muscle ↑ Amino acid efflux (especially glutamine),
leading to loss of muscle mass
Intestine ↓ Amino acid uptake from both luminal and
circulating sources, leading to gut mucosal
atrophy
Endocrine ↑ Adrenocorticotropic hormone
↑ Cortisol
↑ Growth hormone
↑ Epinephrine
↑ Norepinephrine
↑ Glucagons
↑ Insulin (usually)
From Michie HR: Metabolism of sepsis and multiple organ failure, World J Surg 20:461, 1996.

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Starvation Versus Stress

! Metabolic response to stress differs from
the responses to starvation
! Starvation = decreased energy
expenditure, use of alternative fuels,
decreased protein wasting, stored
glycogen used in 24 hours
! Late starvation = fatty acids, ketones, and
glycerol provide energy for all tissues
except brain, nervous system, and RBCs

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 Metabolic Changes in Starvation

From Simmons RL, Steed DL: Basic science review for surgeons, Philadelphia, 1992, WB Saunders.

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Comparison of Starvation and Stress

Starvation Stress Hypermetabolism
Resting energy Decreased Increased
expenditure
Respiratory quotient (0.6–0.7) (0.8–0.9)

Mediator activation — +++

Primary fuels Fat Mixed
Proteolysis + +++
Branched-chain + +++
oxidation
Hepatic protein + +++
synthesis
Ureagenesis + +++
Urinary nitrogen loss + +++

Gluconeogenesis + +++
Ketone body ++++ +
production
From Barton RG: Nutrition support in critical illness, Nutr Clin Pract 9:127, 1994. Modified from the American Society for Parenteral
and Enteral Nutrition (ASPEN).
*Patients fall in a continuum between the extremes of starvation and stress hypermetabolism.

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 Systemic Inflammatory Response
Syndrome
! SIRS is the inflammatory response that
occurs in infection, pancreatitis, ischemia,
burns, multiple trauma, hemorrhagic shock,
and organ injury
! Common complication: multiple-organ
dysfunction syndrome (MODS)
! Patients are hypermetabolic
! Ileus (lack of peristalsis); enteral feeding
restores gut function

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Diagnosis of Systemic
Inflammatory Response Syndrome
! Site of infection established and at least
two of the following are present
– Body temperature >38! C or <36! C
– Heart rate >90 beats/min
– Respiratory rate >20 breaths/min (tachypnea)
– PaCO2 <32 mm Hg (hyperventilation)
– WBC count > 12,000/mm3 or <4000/mm3
– Bandemia: presence of >10% bands (immature
neutrophils) in the absence of chemotherapy-
induced neutropenia and leukopenia.

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 Tight Junction

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Factors to Consider in Screening

an Intensive Care Unit Patient

• Preadmission nutrition status

• Organ function
• Use of pharmacologic agents, vasopressors, and
other paralytic agents
• Ability to predict clinical course
(i.e., length of intubation or ventilator dependence)
• Need for enteral or parenteral nutrition

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 Medical Nutrition Therapy for
SIRS and MODS
! Goals
– Minimize starvation
– Prevent or correct specific nutrient deficiencies
– Provide adequate kilocalories
– Manage fluid and electrolytes
– Begin enteral feeding when hemodynamically
stable
! Nutrition support alone cannot abolish
hypermetabolism

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Energy Requirements in
SIRS and MODS
! 25 to 30 kcal/kg
! Avoid overfeeding
! Glycemic control
! Equations and indirect calorimetry
! “Permissive underfeeding”
-14 to 18 kcal/kg/day of actual weight
- 22 kcal/kg/day of ideal body weight

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 Nutrient Requirements in
SIRS and MODS
! Protein
– 1.2 to 2 g/kg
! Vitamins, minerals, and trace elements
! Feeding strategies
! Timing and route of feeding
! Formula selection
– MCT, BCAA, glutamine, arginine, omega-3 fatty
acids, dietary fiber

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Major Body Burns

! Severe trauma: skin as protective organ
can no longer prevent infectious agents
from invading the body
! Fluid and electrolytes most essential
! Wound management depends on the
depth and extent of injury: check staging
! Weight loss is common
! Wound healing can only occur in anabolic
state
! Success of early enteral feeding
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 Abdominal Compartment
Syndrome
! Can be a complication of major abdominal
trauma, bowel distension, and shock
! Caused by increased intraabdominal
pressure
! Hemodynamic instability; respiratory ,
renal, and neurologic consequences
! Elevated nutritional and fluid needs
! Enteral nutrition

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Interpretation of Burn Classification

Based on Damage to the Integument

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 Nutritional Care Goals for
Burned Patients
Minimize metabolic response by
Controlling environmental temperature
- Maintaining fluid and electrolyte balance
- Controlling pain and anxiety
- Covering wounds early
2. Meet nutritional needs by
§ Providing adequate calories to prevent weight loss of
>10% of usual body weight
§ Early enteral nutrition
§ Providing adequate protein for positive nitrogen
balance and maintenance or repletion of circulating
proteins
§ Providing vitamin and mineral supplementation as
indicated
3. Ancillary measures

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Energy Requirements in Major

Burns
! Ireton-Jones calculation for estimated
energy expenditures
EEE = 1784 – 11(A) + 5(W) + 244(G) + 239(T) +
804(B)
A = age
W = weight (kg)
G = gender (female = 0; male = 1)
T = diagnosis of trauma (absent = 0; present = 1)
B = diagnosis of burn (absent = 0; present = 1)

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 Protein in Major Burns
! Protein losses occur from urine, wounds,
healing process, and increased
gluconeogenesis
! 20% to 25% kcal as protein needed; high
BV
! Adequacy best evaluated by monitoring
wound healing and graft take
! Accurate weights and nitrogen losses are
difficult to obtain

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Energy and Protein Adequacy in

Major Burns
! Monitor wound healing, graft take, and basic
nutritional assessment parameters
! Estimation of wound nitrogen losses when
calculating nitrogen balance
– <10% open wound = 0.02 g N/kg/day
– 11% to 30% open wound = 0.05 g N/kg/day
– >31% open wound = 0.12 g N/kg/day

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 Vitamins and Minerals in
Major Burns
! Vitamin C for collagen synthesis and
immune function: some centers use 500
mg 2× daily
! Vitamin A for immune function and
epithelialization: 5000 IU per 1000 kcal of
enteral nutrition
! Hyponatremia and hypokalemia can occur
! Hypocalcemia seen in burns >30% TBSA
and accompanies hypoalbuminemia
! Minerals: low Mg, PO4, Zn, can occur;
monitor carefully
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Methods of Nutrition Support in

Major Burns
! Burns <20% TBSA: regular, high-
kilocalorie, high-protein diet
! Patients with major burns with very high
energy needs or poor appetites may
require enteral feeding and occasionally
parenteral nutrition

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 Surgery
! Well nourished patient tolerates surgery
better than poorly nourished patient
! When possible, replete before surgery
! Enteral feeding or PN as needed
! Empty stomach at time of surgery
! Postoperative nutrition support if unable to
meet nutrient needs orally for 7 to 10 days
! Addition of omega-3 fatty acids
! Introduce solid food when GI tract is ready;
advance quickly from liquids to solids
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Focal Points
! The combined impact of metabolic alterations that occur in
stress and bed rest can lead to rapid and severe depletion of
LBM.
! Nutrition support cannot fully prevent or reverse the
metabolic alterations and disruptions in body composition
associated with critical illness; however, nutrition support
likely ameliorates the rate of net protein catabolism.
! Clinical judgment is paramount in making decisions about
the need to initiate nutrition support.
! For patients who will require enteral nutrition, it should begin
as soon as hemodynamic stability is achieved.
! Enteral nutrition is preferred because of its role in
maintaining gut integrity and immunity.
! Critically ill patients who are injured, septic, or bedridden
cannot be expected to gain weight, LBM, or strength until the
hypermetabolism resolves and physical therapy, exercise,
and rehabilitation begin.
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