The document discusses the relationship between trauma and diseases. It covers several key points: 1) Trauma can indirectly impact diseases by activating or accelerating latent conditions, especially if accompanied by infection, reduced exercise, weight gain or overeating. 2) Major injuries are associated with an inflammatory response that can lead to multiple organ failure and death if not properly treated. 3) The metabolic response to trauma involves neuroendocrine and immune system changes that mobilize energy stores and substrates. This response aims to aid recovery but can damage distant organs if severe. 4) Specific diseases that can be impacted by trauma include post-traumatic stress disorder, diabetes, rhabdomyolysis (muscle breakdown),

1. Relationship between Trauma
and diseases
Presented by
Dr. Said K. M. Dessouki

2.  INTRODUCTION
 CLASSIFICATION (Metabolic-Immunological- Neuroendocrinal)
 FEATURES OF METABOLIC RESPONSE
 FACTORS MEDIATING METABOLIC RESPONSE
 CONSEQUENCES OF METABOLIC RESPONSE
 FACTORS MODIFYING METABOLIC RESPONSE
 Immune response to trauma
 APPLIED ASPECTS:
 1- Post-traumatic stress disorder (PTSD)
 2- Diabetes
 3- Rhabdomyolysis
 4- Coagulopathy after traumatic brain injury.
 5- Multisystem organ failure

3. • A single injury (non-recurrent trauma) may fall into one of five different
categories in its relation-ship to a disease,
• (1) direct;
• (2) temporarily aggra-vating;
• (3) accelerating;
• (4) precipitating symp-toms of a latent preexistent process;
• (5) bringing the patient’s attention to a previously unrecognized condition.
- Conversely, The preexistence of disease may also lead to trauma, as in the
instance of syncope resulting in injury.
• (1) diseases directly due to trauma, (fractures, wounds and infec-tions)
• (2) diseases that are never due to a single in-jury, (measles or arteriosclerosis)
• (3) diseases usually occurring without trauma, some-times trauma may be a
causative factor.(Renal abscess, exophthalmic goiter and the arthritides).

4. • Following accidental or deliberate injury, a characteristic series of
changes occurs, both locally at the site of injury and within the body
generally; these changes are intended to restore the body to its pre-
injury condition.
• The magnitude of the metabolic response is generally proportional to
the severity of tissue injury and the presence of ongoing stimulation but
can be modified by additional factors such as infection
• The response to injury has probably evolved to aid recovery, by
mobilizing substrates and mechanisms of preventing infection, and by
activating repair processes
• Although the metabolic response aims to return an individual to
health, a major response can damage organs distant to the injured site
itself.
• In modern surgery, a major goal is to minimize the metabolic response
to surgery in order to shorten recovery times.
Introduction cont.

5. • Classically, these responses have been described as stress response, a
term coined by the scottish chemist CUTHBERTSON in 1932.
• Intial response is directed at maintaining adequate substrate suppy to
the vital organs, in particular oxygen and energy
• When the inflammatory response impairs function of organs or organ
systems, the term multiple organ dysfunction syndrome is applied
(MODS).
• Systemic Inflammatory Response Syndrome (SIRS,) is a the term used
to describe the body’s response to infections and noninfectious
causes and consists of two or more of the following, Hyper/hypo
thermia, Leukopenia/ leukocytosis, Tachycardia, Tachyapnea.

6. Injury (surgery, Burn, trauma
& infections): Alteration of
neuro-endocrine system,
metabolic and immunology
----> causes disequilibrium of
internal environment & tries to
return to homeostasis.
•Minor Injuries: is usually
followed by functional
restoration w/ minimal
intervention.
•Major injuries: associated
with inflammatory response ---->
failure to give appropriate
intervention ----> multiple organ
failure -----> DEATH

7. Classification
• The "Ischemia/Reperfusion Phenotype” –phenotype represents the
immediate, nervous system-related alteration in response to injury, in which
neuronal and humoral responses and edema formation predominate.
• This phase is characterized by regulating the metabolic supply to cells via the least
elaborate mechanism: diffusion.
• The "leukocytic phenotype“ – is characterized as the intermediate (or
"immune") phase of the metabolic response to trauma.
• This phase is characterized by leukocytic and bacterial infiltration of previously
damaged tissues, which occurs in an edematous, oxygen-poor environment.
• The resulting post-shock hypercatabolism and hypermetabolism is related to a
hyperdynamic response with increased body temperature, increased oxygen
consumption, glycogenolysis,lipolysis, proteolysis and futile substrate cycling
• The “ Angeogenic phase “- third ("angiogenic") phenotype is defined as the late
(or"endocrine") phase of systemic response to injury.
• This phase is characterized by a return of oxidative metabolism, favoring
angiogenesis in damaged tissues and organs. This process creates a capillary bed that
facilitates tissue repair and regeneration

8. The stress response is a
neuroendocrine process.

9. Ebb and Flow
phases
• Trauma causes major alterations in energy and protein metabolism.
• The response to trauma can be divided into the ebb phase and the flow
phase.
• The ebb phase (Stress Phase) occurs immediately after trauma and lasts
from 24-48 hours followed by the flow phase (after operation phase).
• After this, comes the anabolism phase and finally, the fatty-replacement phase.
• During the anabolic phase (recovery from operation phase ) glycogen
and protein are resynthesized. This causes rapid reuptake of K+
.This may lead to
hypokalaemia

10. Metabolic Response to Trauma:
Ebb Phase (24 upto 48 hours after trauma)
• Characterized
• Hypovolemic shock
• reversible
• Irreversible
• Release of Catacholamines/ vasoactive hormones
• ↑ Cardiac Output
• Peripheral Vasoconstriction
• ↑ Respiratory Rate
• Delivery of Maximum oxygen Levels
• ↑ Blood Glucose
• Mobilization of free Fatty acids

11. Metabolic Response to Trauma: Flow
Phase (may last for weeks)
∀↑ Catecholamines
∀↑ basal metabolic Rates
∀↑ Glucocorticoids
∀↑ Glucagon
• Release of cytokines, lipid mediators
• Acute phase protein production
• Catabolic stage
Fonseca : Oral and Maxillofacial Trauma Vol.1

12. Anabolic phase
• Recovery
• restoration of lean body mass, weight and well being

13. Metabolic Response to Trauma
Fatty Deposits
Liver & Muscle
(glycogen)
Muscle (amino
acids)
Fatty Acids
Glucose
Amino Acids
Endocrine
Response
Endocrine response in the form of increased catecholamines,
glucocorticoids and glycogen, leads to mobilization of tissue energy
reserves. These calorie sources include fatty acids and glycerol from lipid
reserves, glucose from hepatic glycogen (muscle glycogen can only
provide glucose for the involved muscle) and gluconeogenic precursors
(eg, amino acids) from muscle.

14. Flow phase
Phenomenon Effect
↑ catecholamine
↑ glucagon
↑ cortisol
↑ insulin
↑ cardiac output
↑ core body temperature
↑ aldosterone
↑ ADH
IL1, IL6, TNF
spillage from
wound
↑ consumption
of glucose, FFA,
amino acid
↑ O2 consumption
fluid retention
systemic inflammatory
response
N or ↑ glucose
N or ↑ FFA
normal lactate
↑ CO2 production
↑ heat production
multi-organ
failure

15. Metabolic
response
Sequence of events
surgical problem
± infection
operation
bleeding
tissue trauma
bacterial
contamination
necrotic debris
local
inflammatory
response
wound healing
recovery
hypermetabolism
muscle wasting
immunosuppression
organ failure
mortality
*
*
mortality
food deprivation
wound pain
infection
immobility
Ebb
phase
Flow
phase
Anabolic
phase
*acute stress

16. CRH
TRH
GHRH
ACTH TSH
Injury
Sensory
Nerves
THALAMUS
Nociceptors
ADRENAL
PANCREAS
HYPOTHALAMUS
THYROID
PITUITARY
B&L
16

17. Proteolysis
Lipolysis
Glycogenolysis
Decreased peripheral glucose uptake (insulin
resisance)
Neoglucogenesis
Proteolysis
Lipolysis
Glycogenolysis
Decreased peripheral glucose uptake (insulin
resisance)
Neoglucogenesis
Summary of Metabolic Effects

18. Comparison of metabolic response between ebb and flow
phase
Ebb phase Flow phase
Blood glucose level ↑ N or ↑
Glucose production N ↑
Free fatty acid level ↑ N or ↑
Insulin concentration ↓ N or ↑
Catecholamine ↑ ↑

19. Comparison of metabolic response
between ebb and flow phase (con’t)
Ebb phase Flow phase
Glucagon ↑ ↑
Blood lactate level ↑ N
Oxygen consumption ↓ ↑
Cardiac output ↑ ↑
Core temperature ↓ ↑

20. Strategy to attenuate metabolic response to
surgery
During ebb phase
•Prompt fluid and blood replacement to maintain blood pressure
•Adequate oxygen supply and ventilation
•Cardiovascular support by inotropes
•Antibiotics
During flow phase
•Nutritional support
•Warm room temperature
•Mobilization
•Hemodialysis
•Timely intervention for complication

21. • Neuroendocrine Response
• Lipid Derived Mediators
• Cytokines

22. • Upregulation of sympathoadrenal axis
• ↑ epinephrine inhibition of Glucose
uptake
• ↑nor epinephrine promotes glucagon
secreation
• ↑Vasopressin promotes lipolysis
• ↑ dopamine gluconeogenesis
• Stimulation of hypothalamic – pituitary axix

24. Cytokine Mediated response
• Polypeptide hormones, protein mediators
• Act locally (paracrine)/ systemically (endocrine)
• Responsible for
• Fever
• Leucocytosis
• Hypotension
• malaise
• Important cytokines:
• TNF
• IL-1
• IL-2
• IL-6
• IL-8
• Released by:
• Monocytes
• Lymphocytes
• Marcophages

26. Lipid derived mediators
• Act by:
• Enhanced superoxide production
• Enchanced platelet aggregation
• Changes in endothelial permeability
• Altered pulmonary vascular reactivity

27. Metabolic Response to
Overfeeding
• Hyperglycemia
• Hypertriglyceridemia
• Hypercapnia
• Fatty liver
• Hypophosphatemia, hypomagnesemia,
hypokalemia
Trauma or critically ill patients should not be overfed. Alterations in
serum glucose and lipid levels, development of fatty liver, and
electrolyte shifts have been associated with overfeeding.

28. Factors influencing the Extent and Duration of the
Metabolic Response
• Pain and Fear
• Surgical Factors:
• Type of surgery
• Region
• Duration
• Preoperative support
• Extent of the trauma and degree of resuscitation
• Post traumatic complications:
• Hemorrhage
• Hypoxia
• Sepsis and Fever
• Re-operation
• Pre-existing nutritional status
• Age and sex
• Anaesthetic considerations

29. Methods to Minimize the Metabolic
Response
• Replace blood and fluid losses
• Maintain Oxygenation
• Give adequate nutrition
• Provide Analgesia
• Avoid Hypothermia

30. Consequences of the Response
• Limiting injury
• Initiation of repair processes
• Mobilization of substrates
• Prevention of infection
• Distant organ damage

31. Post-traumatic stress disorder
(PTSD)
• Post-traumatic stress disorder symptoms may start within three months of a
traumatic event, but sometimes symptoms may not appear until years after the
event. These symptoms cause significant problems in social or work situations and
in relationships.
• PTSD symptoms are generally grouped into four types:
intrusive memories, avoidance, negative changes in thinking and mood, or changes
in emotional reactions
• Symptoms of Intrusive memories
• Recurrent, unwanted distressing memories of the traumatic event
• Reliving the traumatic event as if it were happening again (flashbacks)
• Upsetting dreams about the traumatic event
• Severe emotional distress or physical reactions to something that reminds you of the
event
• Avoidance
• Trying to avoid thinking or talking about the traumatic event
• Avoiding places, activities or people that remind you of the traumatic event
• Negative changes in thinking and mood

32. negative changes in thinking and mood
Negative feelings about yourself or other people
Inability to experience positive emotions
Feeling emotionally numb
Lack of interest in activities you once enjoyed
Hopelessness about the future
Memory problems, including not remembering important aspects of the traumatic event
Difficulty maintaining close relationships
Changes in emotional reactions
Changes in emotional reactions (also called arousal symptoms
Irritability, angry outbursts or aggressive behavior, Always being on guard for danger
Overwhelming guilt or shame, Self-destructive behavior, such as drinking too much or
driving too fast, Trouble concentrating, Trouble sleeping, Being easily startled or
frightened

33. Rhabdomyoly
sis• is a syndrome characterized by muscle necrosis and the release of
intracellular muscle constituents into the circulation. Creatine kinase (CK)
levels are typically markedly elevated, and muscle pain and myoglobinuria
may be present.
• The severity of illness ranges from asymptomatic elevations in serum
muscle enzymes to life-threatening disease associated with extreme
enzyme elevations, electrolyte imbalances, and acute kidney injury.
• CAUSES —
• ●Traumatic or muscle compression (eg, crush syndrome or prolonged
immobilization)
• ●Nontraumatic exertional (eg, marked exertion in untrained individuals,
hyperthermia, or metabolic myopathies)
• ●Nontraumatic nonexertional (eg, drugs or toxins, infections, or
electrolyte disorders)
•

34. Pathophysiology of Rhabdomyolysis
• The clinical manifestations and complications of rhabdomyolysis result
from muscle cell death, which may be triggered by any of a variety of
initiating events. The final common pathway for injury is an increase in
intracellular free ionized cytoplasmic and mitochondrial calcium. This may
be caused by depletion of adenosine triphosphate (ATP), the cellular
source of energy, and/or by direct injury and rupture of the plasma
membrane [1,2]. The latter pathway of injury also results in ATP
depletion.
• The increased intracellular calcium leads to activation of proteases,
increased skeletal muscle cell contractility, mitochondrial dysfunction, and
the production of reactive oxygen species, resulting in skeletal muscle cell
death [1]. ATP depletion causes dysfunction of the Na/K-ATPase and
Ca2+ATPase pumps that are essential to maintaining integrity of the
myocyte. ATP depletion leads to myocyte injury and the release of
intracellular muscle constituents, including creatine kinase (CK) and other
muscle enzymes, myoglobin, and various electrolytes.

35. Diabetes
CONCEPTS CONCERNING TRAUMA AND DIABETES
i.The thesis that trauma de novo can cause diabetes has steadily lost support with the expanding knowledge of the nature
of the disease.
2. But evidence has accumulated to show that trauma indirectly can activate, or accelerate the appearance of a latent
diabetes in the hereditarily predisposed, particularly if accompanied by infection, reduced muscular exercise, gain in
weight or overeating.
3. Trauma in the course of diabetes has grown in importance, because the duration of the disease has trebled, thus
lengthening the period of exposure. Moreover, the danger of exposure to trauma is intensified each successive year a
diabetic lives, because time is provided for the disabling complications of the disease to appear and the physical infirmities
of the normally aging process to advance. The tissues of a diabetic are more vulnerable than those of a nondiabetic.
4. Trauma may make the diabetes more severe, but this effect is not necessarily permanent.
5. Emotional, nervous, so-called neurogenic diabetes, as von Noorden well said, was put "into the grave" by the Great
War,
6. To prove that trauma is the cause of diabetes in any individual case evidence must be at hand to show
(a) that the disease did not exist before the trauma;
(b) that the trauma was severe, injuring the pancreas;
(c) that the symptoms and signs of the disease developed within a reasonable period following the trauma, the etiologic
importance of the trauma waning with the prolongation of the interval; and
(d) that the symptoms and signs of diabetes were not transitory but permanent.
7. This question of trauma as the cause of diabetes should be kept absolutely distinct from the question of compensation
of an individual who is found to have diabetes following an accident. Too often, especially in foreign publications
(Lommel, Troell) the two are confused, and for social and governmental insurance reasons the court sitting in judgment
on a case may vote to give the insured the benefit of a doubt which has no factual basis. Many European countries are

36. Trauma and
Diabetes
• In reality, people who present with persistent hyperglycemia after a traumatic injury
have an underlying defect in glucose metabolism that is laid bare by the metabolic
demands of the body’s response to injury.
• In the case of trauma, the body produces a cascade of hormones that flood the blood
stream. Many of these hormones cause the liver to release glucose to provide energy
as the body tries to heal itself.
• Even people who don’t have diabetes may experience a rise in blood glucose above
the usual limits that the body tries to preserve. However, their pancreases will quickly
take over to produce enough insulin to restore euglycemia. This isn’t the case in
people who already barely meet normal metabolic demands.
• Does trauma cause diabetes? more complex when viewed from a legal
standpoint.
• If the “traumatic event” is an external physical event such as that resulting from a
sudden blow, impact, collision or other substantial continuing traumatic life
experience.
If such external trauma brings forth a level of diabetes that was already lurking in the
individual, then the legal issue arises – has there been an “aggravation of a pre-existing
condition”. The law accepts “aggravation” of a medical condition as a legally
recognized event. Thus, while medically -scientifically – trauma is not a cause of

38. Posttraumatic stress disorder (PTSD) occurs following exposure to a potentially traumatic life event and is
defined in DSM-V by 4 symptom clusters: intrusion, avoidance, negative alterations in cognition and mood,
and alterations in arousal and reactivity. Posttraumatic stress disorder is a common and debilitating disorder
with an estimated lifetime prevalence of 10.4% among women in the United States.1 Posttraumatic stress
disorder has been associated with inflammation,2 neuroendocrine dysfunction,3 poor diet, and low physical
activity,4 all risk factors for type 2 diabetes mellitus (T2D). Research has shown an association of PTSD with
T2D,5- 10 raising important questions about whether women with PTSD are at increased risk of T2D and
whether the treatment of PTSD would prevent T2D.

39. Strategy to attenuate metabolic response to
surgery During ebb phase
• Prompt fluid and blood replacement to maintain blood
pressure
• Adequate oxygen supply and ventilation
• Cardiovascular support by inotropes
• Antibiotics
Strategy to attenuate metabolic response to surgery
During flow phase
• Nutritional support
• Warm room temperature
• Mobilization
• Hemodialysis
• Timely surgery for complication

40. Coagulopathy after traumatic
brain injury.• Traumatic brain injury has long been associated with abnormal coagulation
parameters, but the exact mechanisms underlying this phenomenon are poorly
understood.
• Coagulopathy after traumatic brain injury includes hypercoagulable and
hypocoagulable states that can lead to secondary injury by either the induction of
microthrombosis or the progression of hemorrhagic brain lesions.
• Multiple hypotheses have been proposed to explain this phenomenon, including
the release of tissue factor, disseminated intravascular coagulation,
hyperfibrinolysis, hypoperfusion with protein C activation, and platelet
dysfunction.
• The diagnosis and management of these complex patients are difficult given the
lack of understanding of the underlying mechanisms.

41. Multisystem Organ failure
• Multiple Organ Dysfunction Syndrome MODS
It is a
progressive failure of two or more organ systems, resulting from
acute, severe illnesses or injuries (sepsis, systemic
inflammatory response, trauma, burns) and mediated by the bo
dy's inability to sufficiently activate its defense mechanisms.
• Acute Kidney Failure
• Acute liver failure fulminant hepatic failure;
• Acute respiratory failure
• Acute heart failure
• Gastrointestinal (GI) bleeding

42. 2. SIRS - is a systemic inflammatory response to a
variety of insults including infection, ischemia,
infarction, and injury. It leads to disorders of
microcirculation, organ perfusion and finally to
secondary organ dysfunction.
3. MODS- the presence of altered organ function in
an acutely ill patient such that homeostasis could not
be maintained without intervention.
9/17/2014 4

44. Pathophysiology
Inflammatory response
• Release of mediators
• Direct damage to the endothelium
• Hyper metabolism
• Vasodilation leading to decreased SVR
• Increase in vascular permeability
• Activation of coagulation cascade

45. Initiation of Inflammatory
Response
Toxic stimulus
t
Adhesion
Tumor necrosis factor
lnterleukin-1,6,8,10
Oxygen radicals
Platelet-activating factor
Proteases
Prostaglandins
Leukotrienes
Bradykinin
'■HH
9/17/2014 www.drjayeshpatidar.blogspot.com 1
7

46. • Occurs when altered organ function in an acutely ill patient is present to the
extent that homeostasis can no longer be maintained without intervention. MODS was formerly
known as multiple systemorgan failure.
• The usual sequence of MODS depends somewhat on its cause but often begins with pulmonar
y failure 2 to 3days after surgery, followed, in order, by hepatic failure, stress-
induced gastrointestinal (GI) bleeding, and renal failure.Mortality rates are linearly related to the
number of failed organ systems. Patients with two or more organ systems involvedhave a mortalit
y rate of approximately 75%, and patients with four organ systems involved have a 100% mortali
ty rate.
• MODS was first associated with traumatic injuries in the late 1960s and has subsequently been a
ssociated with infection
and decreased perfusion to any part of the body. The term multiple organ dysfunction syndrom
e was adopted in 1991 at aconsensus conference of the Society of Critical Care Medicine and t
he American College of Chest Physicians as it best
describes the organ dysfunction that precedes complete failure. Primary MODS, the result of a
direct injury or insult to theorgan itself, is initiated by a specific precipitating event, such as a pu
lmonary contusion. The injury or insult causes aninflammatory response within that organ system,
and dysfunction develops.
• Secondary MODS develops as the result of a systemic response to infection or inflammation. Sy
stemic inflammatoryresponse syndrome (SIRS) is an overwhelming response of the normal inflam
matory system, producing systemic effectsinstead of the localized response normally seen. The inf
lammatory response is produced by the activation of a series ofmediators and results in alteratio
ns in blood (selective vasodilation and vasoconstriction), an increase in vascularpermeability, white
blood cell (WBC) activation, and activation of the coagulation cascade. Mortality rates are high
withMODS, and the more organ systems that fail, the higher the mortality. For example, mortali

47. The immune response to trauma.
• The response to trauma begins in the immune system at the moment of injury. The loci are
the wound, with activation of macrophages and production of proinflammatory mediators,
and the microcirculation with activation of endothelial cells, blood elements, and a
capillary leak. These processes are potentiated by ischemia and impaired oxygen delivery
and by the presence of necrotic tissue, each exacerbating the inflammatory response.
Hemorrhage alone may be a sufficient stimulus. Inflammation once was considered to be a
host reaction to bacteria or other irritants. This concept was expanded by the discovery of
autoimmune diseases, and we are now aware that some illnesses are the result of the
body's response to an invader rather than the direct effect of the invader itself. The
discoveries about the response to trauma described here add another dimension, showing
inflammation to be a fundamental life process that begins at the molecular level at the
moment of injury and that, depending on the severity of the stimulus and the
effectiveness of initial treatment, may spread to include every cell, tissue, and organ in the
body, for good or ill. An important part of these expanding concepts is the notion that all
noxious stimuli activate the cytokine system as a final common pathway. Sepsis,
hemorrhage, ischemia, ischemia-reperfusion, and soft tissue trauma all share an ability to
activate macrophages and produce proinflammatory cytokines that may initiate the SIRS.
Second-message compounds and effector molecules mediate the observed clinical
phenomena.

49. • Purpose
• The purpose of the study was to quantify the ability of procalcitonin (PCT) and interleukin-6 (IL-6) to
differentiate noninfectious systemic inflammatory response syndrome (SIRS) and sepsis and to predict
hospital mortality.
• Materials
• We recruited consecutively adult patients with SIRS admitted to an intensive care unit. They were
divided into sepsis and noninfectious SIRS based on clinical assessment with or without positive cultures.
Concentrations of PCT and IL-6 were measured daily over the first 3 days.
• Results
• A total of 239 patients were recruited, 164 (68.6%) had sepsis, and 68 (28.5%) died in hospital. The PCT
levels were higher in sepsis compared with noninfectious SIRS throughout the 3-day period (P < .0001).
On admission, PCT concentration was diagnostic of sepsis (area under the curve of 0.63 [0.55-0.71]),
and IL-6 was predictive of mortality, (area under the curve of 0.70 [0.62-0.78]). Peak IL-6 concentration
improved the risk assessment of Sequential Organ Failure Assessment (SOFA) score for prediction of
mortality among those who went on to die by an average of 5% and who did not die by 2%
• Conclusions
• Procalcitonin measured on intensive care unit admission was diagnostic of sepsis, and IL-6 was predictive
of mortality. Addition of IL-6 concentration to SOFA score improved risk assessment for prediction of
mortality. Future studies should include clinical indices, for example, SOFA score, for prognostic
evaluation of biomarkers.

50. Macronutrients during Stress
Carbohydrate
•At least 100 g/day needed to prevent ketosis
•Carbohydrate intake during stress should be
between 30%-40% of total calories
•Glucose intake should not exceed
5 mg/kg/min
Barton RG. Nutr Clin Pract 1994;9:127-139
ASPEN Board of Directors. JPEN 2002; 26 Suppl 1:22SA

51. Macronutrientes during
Stress
Fat
•Provide 20%-35% of total calories
•Maximum recommendation for intravenous lipid
infusion: 1.0 -1.5 g/kg/day
•Monitor triglyceride level to ensure adequate
lipid clearance
Barton RG. Nutr Clin Pract 1994;9:127-139
ASPEN Board of Directors. JPEN 2002;26 Suppl 1:22SA

52. Macronutrients during Stress
Protein
•Requirements range from 1.2-2.0 g/kg/day
during stress
•Comprise 20%-30% of total calories during
stress
Barton RG. Nutr Clin Pract 1994;9:127-139
ASPEN Board of Directors. JPEN 2002;26 Suppl 1:22SA

53. Determining Protein Requirements for
Hospitalized Patients
Stress Level
Calorie:Nitrogen Ratio
Percent Potein / Total
Calories
Protein / kg Body Weight
No Stress
< 15%
protein
0.8
g/kg/day
Moderate Stress
15-20%
protein
1.0-1.2
g/kg/day
1.5-2.0
g/kg/day
> 20%
protein
Severe Stress

54. • Calorie-to-nitrogen ratios can be used to prevent lean
body mass from being utilized as a source of energy.
Therefore, in the non-stressed patient, less protein is
necessary to maintain muscle as compared to the
severely stressed patient.
• Nitrogen balance can be affected by the biological value
of the protein as well as by growth, caloric balance,
sepsis, surgery, activity (bed rest and lack of muscle use
can promote nitrogen excretion), and by renal function.

55. Role of Glutamine in Metabolic
Stress
•Considered “conditionally essential” for critical
patients
•Depleted after trauma
•Provides fuel for the cells of the immune system
and GI tract
•Helps maintain or restore intestinal mucosal
integrity
Smith RJ, et al. JPEN 1990;14(4 Suppl):94S-99S; Pastores SM, et al. Nutrition 1994;10:385-391
Calder PC. Clin Nutr 1994;13:2-8; Furst P. Eur J Clin Nutr 1994;48:607-616
Standen J, Bihari D. Curr Opin Clin Nutr Metab Care 2000;3:149-157

56. • Glutamine is one of the few nutrients included in the category
of conditionally-essential amino acids.
• Glutamine is the body’s most abundant amino acid and is
involved in many physiological functions. Plasma glutamine
levels decrease drastically following trauma.
• It has been hypothesized that this drop occurs because
glutamine is a preferred substrate for cells of the
gastrointestinal cells and white blood cells.
• Glutamine helps maintain or restore intestinal mucosal
integrity.

57. Role of Arginine in Metabolic
Stress
• Provides substrates to immune system
• Increases nitrogen retention after metabolic stress
• Improves wound healing in animal models
• Stimulates secretion of growth hormone and is a
precursor for polyamines and nitric oxide
• Not appropriate for septic or inflammatory patients.
Barbul A. JPEN 1986;10:227-238; Barbul A, et al. J Surg Res 1980;29:228-235

58. Key Vitamins and Minerals
Vitamin A
Vitamin C
B Vitamins
Pyridoxine
Zinc
Vitamin E
Folic Acid,
Iron, B12
Wound healing and tissue repair
Collagen synthesis, wound healing
Metabolism, carbohydrate utilization
Essential for protein synthesis
Wound healing, immune function, protein
synthesis
Antioxidant
Required for synthesis and replacement of
red blood cells

59. • Micronutrient, trace element, vitamin, and mineral
requirements of metabolically stressed patients seem to
be elevated above the levels for normal healthy people.
• There are no specific dosage guidelines for
micronutrients and trace elements, but there are
plausible theories supporting their increased intake.
• This slide lists some of these nutrients along with the
rationale for their inclusion.

60. References
• Fonseca trauma Vol.1
• Metabolic response to trauma
(The journal of Bone and Joint Surgery)
• Clinical aspects of the metabolic response to trauma
(The american Journal of Clinical Nutrition: Vol.3, Number 3)
• Metabolic response to trauma
( Australian journal of physiotherapy)
• Manipulating the metabolic response to injury
(British medical bulletin 1999;55 (no.1): 181-195)
• The metabolic response to stress: an overview and update
(Anesthesiology 73:308-327, 1980)