Metabolic response to trauma

Metabolic Response to trauma

1. Metabolic Response to Trauma
Presented by Dr. Mohammed haneef

2. INTRODUCTION
ClASSIFICATION
FEATURES OF METABOLIC RESPONSE
FACTORS MEDIATING METABOLIC RESPONSE
CONSEQUENCES OF METABOLIC RESPONSE
FACTORS MODIFYING METABOLIC RESPONSE
APPLIED ASPECTS

3. •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.

4. •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)
•SIRS, systemic infalmatory response syndrome 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

5. Classification
•Aller and colleagues propose a modern perspective on the
metabolic events associated with the inflammatory response to
major trauma
•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

6. 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 occurs
immediately after trauma and lasts from 24-48 hours
followed by the flow phase. After this, comes the
anabolism phase and finally, the fatty-replacement
phase.

7. •Unmodified metabolic response
•Ebb phase -phase of metabolic response to acute stress
•Flow phase - phase of metabolic response after operation
•Anbolic phase - recovery from operation
Time
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Ebb
Phase

Flow
Phase

8. Metabolic Response to
Trauma:
Ebb Phase (upto 24 hours)
•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
Fonseca : Oral and Maxillofacial Trauma Vol.1

9. 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
Fonseca : Oral and Maxillofacial Trauma Vol.1

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

11. Metabolic Response to
Trauma
Fatty Deposits
Liver & Muscle
(glycogen)
Muscle
(amino acids)
Fatty Acids
Glucose
Amino Acids
Endocrine
Response

12. •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.

13. 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
­ O
2
consumption
fluid retention
systemic inflammatory
response
N or ­ glucose
N or ­ FFA
normal lactate
­ CO
2
production
­ heat production
multi-organ
failure

14. 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

15. 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 ­ ­

16. 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 ¯ ­

17. 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

18. •Neuroendocrine Response
•Lipid Derived Mediators
•Cytokines

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

21. 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

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

24. 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.

25. 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

26. 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

27. 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

28. 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

29. •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.

30. 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

31. •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.

32. 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

33. Key Vitamins and Minerals

Vitamin A
Vitamin C
B Vitamins
Pyridoxine
Zinc
Vitamin E
Folic Acid,
Iron, B
12
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

34. •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.

35. 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

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

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

38. Strategy to attenuate metabolic
response to surgery
Principles
•No effective strategy to attenuate metabolic response
•Supportive measures are available
•Perfect surgery is essential

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

40. Strategy to attenuate metabolic response to
surgery
During flow phase
•Nutritional support
•Warm room temperature
•Mobilization
•Hemodialysis
•Timely surgery for complication

41. 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)