Nutritional Support in the Perioperative Period

Topic 17

Module 17.5

The Traumatized Patient

CHC Dejong

Learning Objectives

Understand the mechanisms behind the metabolic effects of trauma;

How does the stress response after traumatic injury lead to hypermetabolism;
What does this mean for protein metabolism;
Can certain aspects of the stress response after acute non-surgical trauma be avoided and how
can they be treated;
Insights into the relationship between hypermetabolism, alterations in protein metabolsim and
complications in surgery for trauma.

Contents

1. Introduction
2. What happens after trauma?
3. Clinical symptoms
4. Protein kinetics
5. Why is there increased protein degradation during trauma?
6. Minimizing unwanted effects of trauma and its treatment: hypothermia
7. Proactive approach to prevent unnecessary aspects of the surgical stress response
8. What is the actual substrate mix used by the body after trauma?
9. What metabolic goals should be achieved in traumatized patients?
10. Assessment of efficacy of treatment

Key Messages

Trauma leads to overall catabolism in the body;

Anabolism occurs in splanchnic organs, immune system and in wounds;
Nutrition should support these processes;
Specific nutrients like glutamine may be considered.

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1. Introduction
This chapter discusses the effects
of acute un-anticipated traumatic Long bone fracture
injury on human metabolism. This
is to make a distinction with
surgical trauma as well as with the
critically ill. In elective surgery, Isolated extremity
the trauma inflicted by the surgical injury as e.g. Long
procedure is foreseeable and bone fractures cause
therefore, appropriate measures catabolism due to
can be taken to counteract any immobilization, direct
unwanted effects of the host injury and remote
effects on kidney and
response to trauma. This is not the
lungs
case in acute traumatic injury,
such as a long bone fracture due o
a traffic accident (Fig. 1, Fig. 2).
It is not intended to give an Fig. 1
extensive review of various types
of trauma, such as single versus
multiple injuries blunt versus
penetrating, hypothermia versus
burns or fractures versus soft tissue Long bone fracture
trauma. The scope is to focus on
skeletal muscle injury and its
effects on metabolism.
Adequate treatment
2. What happens after allows for early
trauma? mobilization avoiding
extensive muscle
From observations in traumatized wasting and prevents
wild animals in their natural remote damage due to
surroundings, three distinct e.g. fat embolism and
features become clear. The animal muscle necrosis
retreats into a hiding place and
exhibits little mobility.
Fig. 2
A second striking phenomenon is
anorexia, not exclusively due to
the inability to catch food, but also
present when easy access to food is
offered. Finally the animal exhibits
a catabolic state, reflected in loss Weight loss after major trauma
of weight, largely consisting of loss
of muscle (Fig. 3, Fig. 4).
When the trauma is not too Where?
extensive, the traumatized area Mainly muscle
heals, where after the animal
resumes normal activity, starts Less pronounced in fat
eating and regains muscle mass and Why?
function. In the following, we will
explain why these adaptations
Reduced food intake
after trauma are a logic and Increased energy expenditure
obligatory event. Metabolic Error in Protein/Fat metabolism
Fig. 3

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 Effects of major trauma on homeostasis The response of the human
being to acute trauma is
of the organism essentially the same as in
animals. It differs from surgical
trauma in that it is
unanticipated and therefore,
many of its effects can not be
prevented, although we can
treat them.
Accidental trauma may range
from a simple long bone
fracture to any combination of
injuries in multiple trauma
Trauma is victims (Fig. 5). As such,
accompanied by a symptoms may vary widely and
pronounced negative many organs may be affected.
nitrogen balance The general principle in treating
Fig. 4 these patients is to protect life
and preserve function of vital
organs. Once this has been
achieved, nutritional support
Multiple trauma may be started. Obviously, the
route of administration may be
affected by the specific trauma
Multiple trauma (1, 2).
differs from simple
extremity trauma 3. Clinical symptoms
in that several
organ systems
Symptoms of accidental injury
may become
involved directly
are mainly related to the local
or indirectly (e.g. effects of trauma, such as a
muscle necrosis fracture, and the systemic
and subsequent effects of a particular injury
renal injury) (3). Pain and shock are two
dominant features that initiate
and sustain a chain of adverse
Fig. 5 events that may be described as
the stress response.
Two different phases are
distinguished in shock after
Changes in body composition trauma: an initial hypodynamic
phase and a later hyperdynamic
following trauma phase (4).
The initial hypodynamic phase
may be quite pronounced after
Decrease in total
body protein and
trauma and leads to
potassium (TBP hypoperfusion of all organs.
and TBK) Subsequent transmembrane
fluid shifts will lead to
intracellular dehydration and
Decrease in subsequent acidification, which
intracellular water precludes adequate cell
(ICW) and function including regulation of
intracellular protein turnover (5) (Fig. 6).
potassium (ICK)
Fig. 6

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Also, hypovolemic shock affects
intestinal barrier and this may
facilitate translocation of bacteria
Mechanism of sepsis/MOF
or their components and a
subsequent generalized
inflammatory response (6-8) (Fig. Trauma Severe SIRS (Early) sepsis/MOF
7).
The clinical picture of the stress
response, including increased GALT
LPS translocation
Immune supression
capillary leakage, the development Gut Barrier

of tissue edema, increased cardiac Inflammation

output and vasodilatation is
generally considered a harmful side Hemorrhage Bacterial translocation
effect of trauma. It leads to Laparotomy
(Late) sepsis/MOF
ICU-therapy
compromised alveolar diffusion of Infection
oxygen, to intravascular
hypovolemia, renal insufficiency
and many other disturbances of Fig. 7 Moore et al, Annals of Surgery 2000 Vol 231 No 1, 9-10

organ function (3).

4. Protein kinetics
During acute disease and following
trauma, growth is inhibited and the Trauma Protein kinetics
organism becomes catabolic, which
is specifically exemplified by Immobilization
muscle breakdown and atrophy (9).
It is now clear that the Muscle protein breakdown
neuroendocrine response including
the cytokine response to disease Protein synthesis in liver, wound and
leads to an obligatory loss of immune system
muscle that cannot be blocked by
nutrition alone (10).
Anabolism and catabolism occur
In fact, the normal response to simultaneously
moderate trauma or disease
includes immobility, anorexia, and
Overall result: Body weight loss
catabolism (Fig. 8).
Muscle tissue disappears, but at the Fig. 8
site of injury or in tissues such as
liver and the immune system, there is protein accumulation that is modulated by pro-inflammatory
cytokines. Although the individual is anorectic, the anabolic accumulation of tissue in the liver,
immune system, and site of injury can only occur with substrate that is derived from other tissues
such as muscle. This is an easily detectable situation, and it clearly indicates that muscle
catabolism during acute trauma or disease is a useful adaptive phenomenon because the substrate
derived from this catabolism is utilized for the healing response. As a consequence, modulation of
the catabolic hormonal pattern with the intention of blocking muscle catabolism should not block
the anabolic actions in the wound and immune system (11).
During pure starvation, the reutilization of amino acids derived from protein degradation is
efficient. Essential amino acids are degraded to a very limited degree and are reused for protein
synthesis. Whole-body protein turnover decreases, and very little protein is lost at the whole-body
level.

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 Following trauma, amino acids
derived from muscle catabolism
are not released in the circulation
Trauma Amino acid kinetics as such, but a large part
(especially the branched-chain
amino acids (BCAAs)) are
Muscle protein breakdown irreversibly degraded to yield other
Muscle: BCAA conversion to glutamine amino acids such as glutamine and
and alanine alanine, which are avidly used at
the site of injury and in the liver
Glutamine consumption in gut, liver, wound and immune system (11) (Fig. 9).
and immune system This precludes efficient
As BCAA are essential amino acids, this reutilization of amino acids and
process means catabolism obligatorily leads to increased
protein catabolism at the whole-
Overall result: Body weight loss body level.
It follows that the substrate mix
Fig. 9
and specifically the amino acid mix
that is utilized during disease is
essentially different from the substrate mix that is used during pure starvation. This may have
consequences for subsequent treatment.

5. Why is there increased protein degradation during trauma?

In traumatized animals, muscle protein synthesis rates are not decreased, but remain stable or are
even slightly increased. In view of the fact that muscle protein loss occurs, this must imply that
muscle protein degradation increases to an even greater degree. However, muscle protein turnover
contributes only 40% to total body protein turnover and this figure may even be less in the stressed
condition.
It has already been mentioned that in the stressed condition liver protein synthesis is greatly
enhanced. The increase in muscle protein degradation may furnish amino acids from peripheral
tissues to central tissues to sustain synthesis of crucial proteins. Visceral protein synthesis is
increased in response to trauma and these proteins are functional like e.g. clotting factors,
fibrinogen, complement factors and many others.

6. Minimizing unwanted effects of trauma and its treatment: hypothermia

More often than not, a laparotomy is part of the treatment of major trauma patients. The open
abdomen is a site of major fluid and heat loss, and this is potentially harmful to the patient.
Prevention of (intraoperative) hypothermia reduces the severity of the endocrine-metabolic
response and sympathetic reflexes, and changes the fibrinolytic-coagulatory balance resulting in
reduced bleeding. Several randomised trials have demonstrated that preservation of normothermia
by infusion of fluids, heated to body temperature and using an upper body forced-air heating cover
reduces wound infections, cardiac complications and bleeding, and transfusion requirements (12).

7. Proactive approach to prevent unnecessary aspects of the surgical stress

response
Increased whole body protein degradation partly reflects the increased degradation of muscle
protein, and partly increased turnover of visceral proteins, that play crucial functional roles in the
response to trauma and other diseases.
Protein synthesis rates should be stimulated by nutritional support to synthesize new muscle protein
and to meet the demand of crucial visceral protein and proteins in wounds, white cells and
macrophages. So essentially, new therapeutic interventions should be more tailored to organ needs
and thereby supply organs with their specific needs.

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8. What is the actual substrate mix used by the body after trauma?
One of the major reasons why reutilization of amino acids derived from muscle proteolysis leads to
net catabolism at the whole-body level is that the increased glutamine and alanine efflux from
muscle following trauma (13) is derived in part from the irreversible degradation of the BCAAs.
This precludes reutilization of BCAAs for protein synthesis and leads to a catabolic rate that is more
pronounced than during starvation unaccompanied by disease or trauma. The observation that more
glutamine (and alanine) is released from peripheral (muscle) tissues (14) implies that more
glutamine is consumed in central organs such as liver, immune system, and possibly the site of
injury (Fig. 9).

9. What metabolic goals should be achieved in traumatized patients?

As stated, the acutely traumatized
organism increases its protein
turnover and becomes catabolic.
Although plasma concentrations of
Multiple Trauma Glutamine-
albumin decrease, fractional enriched enteral nutrition
synthesis rates of albumin and
fibrinogen increase after trauma Reduction in morbidity (28%) in multiple
(11). The accumulation of white
cells, macrophages, granulation
trauma patients
tissue, collagen, and bone matrix
at fracture sites is also proof of
increased synthetic processes at
May be mediated via arginine production in
the site of injury and in the the kidney
immune system following trauma.
These considerations imply that
one of the metabolic goals of
therapeutic intervention should be Houdijk et al, Lancet 1998;352:772-776
to support increased protein Fig. 10
turnover.
Another goal is to exogenously
furnish the specific nonessential
amino acids that the previously Early enteral feeding and gut permeability
healthy organism produces in
excess after trauma and acute Early enteral feeding may have beneficial effects on intestinal
illness. Glutamine would seem to permeability (as assessed by the lactulose/mannitol test)
be a good candidate for this in the
traumatized patient, because it has 0,07
been shown to reduce 0,06
complications in trauma victims 0,05
(15) (Fig. 10). 0,04 EN< 6hr
Early enteral nutrition may be 0,03 EN> 24hr
beneficial if tolerated (Fig. 11). 0,02
Finally, we should preserve the 0,01
differential changes in protein 0
kinetics as observed in the L/MDay2 L/MDay 4
previously healthy organism subject
to trauma or acute disease.
Endeavors to inhibit net muscle Intensive Care Med 1999;25:157-161

catabolism in patients with burns

by the use of growth hormone have
been reasonably successful (16) and therefore, preservation of the central anabolic responses and
inhibition of muscle catabolism may be a future treatment option, but only when this does not
interfere with the central response.

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10. Assessment of efficacy of treatment
Essentially, growth stops when organisms are traumatized (11) and all substrate is directed to the
healing response. Although the response to trauma is obligatorily catabolic despite nutritional
support, nutrition may limit nitrogen losses by increasing the protein content of the food to
1.5 g of protein/kg/24 h limits nitrogen losses.
Glutamine enrichment may limit nitrogen losses and may improve outcome for trauma patients (15).
The increased flux and rate of appearance of glutamine from peripheral to central tissues after
trauma is such that supplementing the nutritional regimen with as much as 20 or even 40 g/d can
still be considered in the physiological range and safe.
Clinically, it is clear that healthy granulation tissue, solid epithelialization of granulating defects,
growth of hair, loss of tissue edema, and regaining of muscle tonicity are all convincing signs of
benefit.

References

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