Stress response caused by events such as surgical trauma includes endocrine, metabolic and immunological changes. Stress hormones and cytokines play a role in these reactions. More reactions are induced by greater stress, ultimately leading to greater catabolic effects. Cuthbertson reported the characteristic response that occurs in trauma patients: protein and fat consumption and protection of body fluids and electrolytes because of hypermetabolism in the early period. The oxygen and energy requirement increases in proportion to the severity of trauma. The awareness of alterations in amino acid, lipid, and carbohydrate metabolism changes in surgical patients is important in determining metabolic and nutritional support. The main metabolic change in response to injury that leads to a series of reactions is the reduction of the normal anabolic effect of insulin, i.e. the development of insulin resistance. Free fatty acids are primary sources of energy after trauma. Triglycerides meet 50 to 80 % of the consumed energy after trauma and in critical illness. Surgical stress and trauma result in a reduction in protein synthesis and moderate protein degradation. Severe trauma, burns and sepsis result in increased protein degradation. The aim of glucose administration to surgical patients during fasting is to reduce proteolysis and to prevent loss of muscle mass. In major stress such as sepsis and trauma, it is important both to reduce the catabolic response that is the key to faster healing after surgery and to obtain a balanced metabolism in the shortest possible time with minimum loss. For these reasons, the details of metabolic response to trauma should be known in managing these situations and patients should be treated accordingly
2. WHAT IS METABOLIC RESPONSE TO
INJURY
• To maintain homeostatic response after minimal injury and
establish ‘stress free’- pre-operative care.
• For example: surgical treatment of major abdominal sepsis and
provide organ support (critical care) while the patient comes back to a
situation in which homeostasis can achieve are turn to normality.
3. TYPES OF METABOLIC RESPONSE
TO INJURY
• Historically it divided in 2 major phases:
• “Ebb phase”-Initial phase( Shock) which is
reversible
• “Flow Phase”-they are divided into 2 sub-phase
• Catabolic phase (1-2 weeks)
• Anabolic phase (2-4 weeks)
4. EVENTS THAT OCCURS IN ‘EBB’
PHASE
• Acute inflammatory changes
• Endocrine changes in response to injury
• Vascular changes in response to injury
• Neuronal changes in response to injury
• Physiological response to injury
5. PHYSIOLOGICAL RESPONSES
• The natural response to injury includes:
●● Immobility/rest
●● Anorexia
●● Catabolism
• The changes are designed to aid survival of moderate
injury in the absence of medical intervention.
6. ACUTE
INFLAMMATORY
RESPONSE
• Inflammatory cells and cytokines are
the principal mediators of the acute
inflammatory response
• The clinical condition of the patient
depends on the extent to which the
inflammation remains localized and
the balance between these pro-and
anti-inflammatory processes.
8. VASCULAR RESPONSES
• Expression of adhesion molecules leads to
• Leucocyte adhesion
• Transmigration
• Increase local blood flow by
• Vasodilation( kinin, prostaglandin, nitric oxide)
• Increase capillary permeability
• Increase delivery of inflammatory cell, oxygen, nutritional substances.
• Colloid particles; albumin leaks on to the injured tissue leading to oedema
• Exposure of tissue factor promotes coagulation due to
• Platelet activation
• If inflammatory process becomes generalized then
• Microcirculatory thrombosis
• DIC
9.
10. NEURAL RESPONSES
• Tissue injury and inflammation leads to impulses in afferent pain fibers that
reach the thalamus via the dorsal horn of the spinal cord and the lateral
spinothalamic.
• Activation of the sympathetic nervous system leads to the release of
noradrenaline from sympathetic nerve fiber endings and adrenaline from the
adrenal medulla resulting in tachycardia, increased cardiac output, and changes
in carbohydrate, fat and protein metabolism -Interventions that reduce
sympathetic stimulation, such as epidural or spinal anesthesia, may attenuate
these changes.
11.
12. CONSEQUENCES OF METABOLIC RESPONSE
TO INJURY
• Hypovolemia
• Increase energy metabolism and substrate cycling.
• Catabolism and Starvation
• Anabolism---(weeks to months) Recovery cycle
18. STARVATION
• Reduced nutritional intake because of the illness requiring
treatment
• Fasting prior to surgery
• Fasting after surgery, especially to the gastrointestinal tract
• Loss of appetite associated with illness.
19. CHANGES IN RED BLOOD CELL SYNTHESIS
AND COAGULATION
• Anemia following major surgery due to hemorrhage
• Hemodilution following treatment of crystalloid and colloid.
• Impaired red blood cell production by the bone
marrow((because of low erythropoietin production by the kidney and
reduced iron availability due to increased ferritin and reduced transferrin
binding
20. ANABOLISM
• Regaining weight, restoring skeletal muscle mass and replenishing fat stores.
• Pro-inflammatory mediators have subsided.
• Patients, who feel subjectively better and regain their appetite.
• Hormones contributing to this process include insulin, growth hormone, insulin-
like growth factors, androgens and the17-ketosteroids.Adequate nutritional
support and early mobilization also appear to be important in premaintenance
recovery after surgery
22. A PROACTIVE APPROACH TO PREVENT
UNNECESSARY ASPECTS
OF THE SURGICAL STRESS RESPONSE
●● Minimal access techniques
●● Blockade of afferent painful stimuli (e.g. epidural
analgesia, spinal analgesia, wound catheters)
●● Minimal periods of starvation
●● Early mobilization