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The
Hypermetabolic State: A Special Challenge
The impact
of the hypermetabolic state on patient nutritional requirements
is often understated or overlooked. Hypermetabolism
typically occurs after significant insult to the body.
In hospitals and institutions, the most common causes
are infections, sepsis, burns, multiple trauma, fever,
long-bone fractures, hyperthyroidism, prolonged steroid
therapy, surgery and bone marrow transplants.
Patients progress through a well-defined sequence of
metabolic stages following such insults as illustrated
in the charts below.
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Hypermetabolism:
A Real Marathon for Patients
Frank N. Konstantinides,
MT, MS
Clinical Associate Professor
College of Pharmacy
University of Minnesota
St. Paul, Minnesota
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Metabolic Stages Following Trauma
|
| Day |
Phase |
Characteristics |
| 1-2
|
Ebb (or Shock)
|
Low metabolism
|
| 2-25 |
Catabolic Flow |
Extremely high metabolism
Extremely high nitrogen consumption
Redirection of protein synthesis
|
| 25+ |
Anabolic Flow |
Lower metabolism
Return to normal protein synthesis pattern
|
Changes in Metabolic Rate and Nitrogen Excretion with
Various Types of Physiologic Stress
Reproduced with permission
from Long CL, Schaffel N, Geiger JW, et al. Metabolic
response to injury and illness: Estimation of energy
and protein needs from indirect calorimetry and nitrogen
balance.
JPEN. 1979; 3:452-456.
Adapted
from Long CL, Schaffel N, Geiger JW, et al. Metabolic
response to injury and illness: Estimation of energy
and protein needs from indirect calorimetry and nitrogen
balance. JPEN. 1979; 3:452-456.
During the
acute phase, the liver redirects protein synthesis,
up-regulating certain proteins and down-regulating others.
Measuring the serum level of proteins that are up- and
down-regulated during the acute phase can reveal extremely
important information about the patient's nutritional
state. The most important up-regulated protein is C-reactive
protein, which can rapidly increase 20- to 1,000-fold
during the acute phase.
Negative
Acute Phase Proteins
|
| Protein |
Half-Life |
Binds
With |
2-Day
Trauma Response |
| Albumin
|
20 Days |
Anions, Drugs, Free Fatty
Acids
|
Negative Acute Phase |
| Transferrin |
8 Days |
Iron |
Negative Acute Phase |
| Ceruloplasmin |
5-7 Days |
Copper |
Weak Acute Phase Reactant |
| Prealbumin |
2 Days |
Thyroxine Retinol-
Binders |
Negative Acute Phase |
| Retinol-Binding Protein |
12 Hours |
Vitamin A |
Negative Acute Phase |
Positive
Acute Phase Proteins
| Protein |
Half-Life |
Binds
With |
2-Day
Trauma Response |
| a1-Antitrypsin |
16 Days |
Proteases |
Strong Positive Acute
Phase |
| a1-Acid
Glycoprotein |
6 Days |
Drugs |
Strong Positive Acute
Phase |
| a2-Macroglobulin |
2-4 Days |
Endopeptidases and Proteases |
Neutral- No Change in
Concentration
|
| C-Reactive Protein |
5 Hours |
Damaged Cells, Bacteria,
Platelets,
Lymphocytes |
Very Strong, Rapid
Increase (Usually
20-to 1,000-fold)
|
The
Prognostic Inflammatory & Nutrition Index (PINI),
developed by Ingenbleek et al. (1984) is calculated
using the following equation:
PINI = [ a1-acid glycoprotein
] x [C-reactive protein] / [albumin] x [prealbumin]
The
PINI Value Indicates the Risk of Malnutrition
| PINI
Value |
Malnutrition Risk |
| < 1 |
No Risk |
| 1 - 10 |
Low Risk |
| 11 - 20 |
Moderate Risk |
| 21+ |
High Risk |
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