Trauma of surgery Flashcards
2 phases of physiologic response to trauma
- Ebb phase - first several hours after injury
- Flow phase - days to weeks after injury
Stress response to trauma
- Neuroendocrine-metabolic response
- inflammatory response
What effects the physiological response to trauma?
-site of injury
-severity
-underlying condition of patient
What surgeries are causing the greatest stress reponse?
-abdominal surgery
-orthopedic surgery (surgical arthrodesis)
What factors affect condition of patient?
-age
-sex
-concurrent disease processes (diabetic, cancer, immunocompromised)
-nutritional status/body condition
Neuroendocrine-metabolic response- sympathetic response
Sympathetic response
1. adrenaline (epi) from adrenal medulla which mobilizes carbohydrates and fat for energy
2. Increased blood flow to active muscles, but means reduced flow to organs not used (kidneys, GI)
3. Hepatic and muscle lipolysis and glycogenolysis increased
4. Increased blood coagulability
Neuroendocrine-metabolic response- HPA axis
-adrenocorticotropic hormone increases
-cortisol increases -stays high for 7 days
-growth hormone increases (high hepatic glycogenolysis > hyperglycemia) ; insulin resistance)
Neuroendocrine-metabolic response-HPA volume control
- See hypovolemia and hyperosmolarity= increase in angiotensin II
-release of ADH= urine volume decreases, concentration increases - Release of aldosterone
Clinical signs of trauma in ebb phase
-hypovolemia
-low perfusion
-hypothermia
-acidosis
-shock
-pain
Fear and pain
-increased cortisol
-modulation of pain = control stress response
-control pain early in trauma or surgical patient = minimize wind up
Metabolic response to trauma
Role of aldosterone and ADH
-retention of water and Na helps to maintains blood volume and increase vascular tone
**can be a protective feature = acute loss of plasma volume
Clinical signs of increased aldosterone and ADH
-fluid retention
-oliguria
-accumulation of ECF
Inflammatory-immune stress response
-includes both innate and adaptive immune system
-Stress= excessive production of inflammatory mediators = non-sepcific stress induced response
Cytokines
small proteins
-mediate and maintain local inflammatory response to tissue damage
Acute phase proteins
Produced by hepatocytes in response to cytokine stimulation in response to tissue injury and inflammation
What are the pro inflammatory cytokines?
-IL-6
-IL-1beta
-TNF-alpha
-IL-8
What are the anti-inflammatory cytokines?
-IL-4
-IL-10
-transforming factor-beta
-IL-1 receptor antagonist
-soluble TNF receptors
What happens when pro and anti-inflammatory cytokines are not regulated?
Immunodeficiency and sepsis
Catabolic part of Flow phase
-changes in behaviour
-withdrawal
-reluctance to move
-fear
-anxiety
-aggression
-malaise
Clinical symptoms in catabolic phase
-tachycardia
-tachypnea
-hyperthermia
-hypotension
-decreased perfusion
-decreased urine output
-endotoxemia
-bacteremia
Anabolic period of flow phase
-appetite returns
-body protein is synthesized
-weight restored
-organ function and energy stores
-metabolic demand reduces
-water balance restores
-hormone levels decrease
-generalized feeling of well being develops
Rate of recovery from stress response
-Fast if healthy individuals with no complications
-prolonged if debilitated patients with complications (infection, prolonged catabolic phase)
Use of anesthetic drugs to modulate stress response
OPTIONS:
1. single dose of propofol = suppresses cortisol
- volatile anesthetic agents = inhibits ACTH, cortisol, catecholamines, GH, platelet aggregation, clot stability
- opioids, alpha 2s, benzodiazepines
